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WO2016097831A1 - Traitement du cancer par perfusion chimique électronique, à l'aide d'un nouveau langage adaptatif de communication cellulaire par biosignalement - Google Patents

Traitement du cancer par perfusion chimique électronique, à l'aide d'un nouveau langage adaptatif de communication cellulaire par biosignalement Download PDF

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WO2016097831A1
WO2016097831A1 PCT/IB2015/000426 IB2015000426W WO2016097831A1 WO 2016097831 A1 WO2016097831 A1 WO 2016097831A1 IB 2015000426 W IB2015000426 W IB 2015000426W WO 2016097831 A1 WO2016097831 A1 WO 2016097831A1
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cancer
cells
cell
bio
tumor
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WO2016097831A4 (fr
WO2016097831A9 (fr
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Idris KAMIL
Eltayeb SALIH
Mohammed AMMAR
Abulgasim MAHGOUB
Faisal ALDAWSARI
Amro YOUSIF
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    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61K—PREPARATIONS FOR MEDICAL, DENTAL OR TOILETRY PURPOSES
    • A61K41/00—Medicinal preparations obtained by treating materials with wave energy or particle radiation ; Therapies using these preparations
    • A61K41/0052—Thermotherapy; Hyperthermia; Magnetic induction; Induction heating therapy

Definitions

  • the Invention Name Treatment of Cancer through Electromagnetically Chemical Infusion, using a newly adaptive language of Bio-Signaling Cellular Communications.
  • Hi-Tech Patent of advanced Solar Sonic Communications and Manipulations Technologies as to communicating with all Cells and Pathogens via Propriatery Electromagnetic Frequency Language and Electrochemical Signaling Mechanism of Precision Targeting for the Commencement of Communication, Eradication, Restoration and Triggering Metabolic Homeostasis to maintain it for the life of patient.
  • angiogenesis inhibitors and other cancer therapeutics will be used in combination to reduce cancer morbidity and mortality.
  • Experimental cancer treatments are treatments that are being studied to see whether they work. Typically, these are studied in clinical trials to compare the proposed treatment to the best existing treatment. They may be entirely new treatments, or they may be treatments that have been used successfully in one type of cancer, and are now being tested to see whether they are effective in another type. More and more, such treatments are being developed alongside companion diagnostic tests to target the right drugs to the right patients, based on their individual biology.
  • Agents viruses and events (mutations) which cause or facilitate genetic changes in cells destined to become cancer.
  • Hyper-competition for the financial resources that are required to conduct science appears to suppress the creativity, cooperation, risk-taking, and original thinking required to make fundamental discoveries, unduly favoring low-risk research into small incremental advancements over innovative research that might discover radically new and dramatically improved therapy.
  • Other consequences of the highly pressured competition for research resources appear to be a substantial number of research publications whose results cannot be replicated, and perverse incentives in research funding that encourage grantee institutions to grow without making sufficient in their own faculty and facilities.
  • cancer is largely a disease of older adults, it is not common in pregnant women. Cancer affects approximately 1 in 1,000 pregnant women. The most common cancers found during pregnancy are the same as the most common cancers found in non-pregnant women during childbearing ages: breast cancer, cervical cancer, leukemia, lymphoma, melanoma, ovarian cancer, and colorectal cancer. Diagnosing a new cancer in a pregnant woman is difficult, in part because any symptoms are commonly assumed to be a normal discomfort associated with pregnancy.
  • cancer is typically discovered at a Somewhat later stage than average in many pregnant or recently pregnant women.
  • Some imaging procedures such as MRIs (magnetic resonance Imaging), CT scans, ultrasounds, and mammograms with fetal shielding are considered safe during pregnancy; some others, such as PET scans are not (Positron emission tomography).
  • Treatment is generally the same as for non-pregnant women.
  • radiation and radioactive drugs are normally avoided during pregnancy, especially if the fetal dose might exceed 100 cGy.
  • some or all treatments are postponed until after birth if the cancer is diagnosed late in the pregnancy.
  • Cervical cancer may require birth by Caesarean section. Radiation to the breast reduces the ability of that breast to produce milk and increases the risk of mastitis. Also, when chemotherapy is being given after birth, many of the drugs pass through breast milk to the baby, which could harm the baby. Veterinary oncology, concentrating mainly on cats and dogs, is a growing specialty in wealthy countries, and the major forms of human treatment such as surgery and radiotherapy may be offered.
  • tumors are cancerous; benign tumors do not spread to other parts of the body.
  • Possible signs and symptoms include: a new lump, abnormal bleeding, a prolonged cough, unexplained weight loss, and a change in bowel movements, among others. While these symptoms may indicate cancer they may also occur due to other issues.
  • Cancer is believed to be caused by defective immune system. Many attempts have been made to improve immune system without success. Surprisingly it is found that Mycobacterium w containing compositions which are useful in improving immune status in patients with leprosy are also useful in management of cancer. They are found to be useful in decreasing burden of disease and reducing symptoms associated with cancer. More surprising was their synergy with conventional therapy, in spite of fact that they work through entirely different mechanism. Still surprising was decrease in side effects of other therapy rather than increase in overall side effects, in spite of use in same therapeutic amount along with increase in effect.
  • Electro-poration is a significant increase in the electrical conductivity and permeability of the cell plasma membrane caused by an externally applied electrical field. It is usually used in molecular biology as a way of introducing some substance into a cell, such as loading it with a molecular probe, a drug that can change the cell's function, or a piece of coding DNA. Electroporation is a dynamic phenomenon that depends on the local transmembrane voltage at each point on the cell membrane.
  • E th an electric field magnitude threshold for electroporation
  • bacteria In molecular biology, the process of electroporation is often used for the transformation of bacteria, yeast, and plant protoplasts.
  • bacteria In addition to the lipid membranes, bacteria also have cell walls which are different from the lipid membranes and are made of peptidoglycan and its derivatives. However, the walls are naturally porous and only act as stiff shells that protect bacteria from severe environmental impacts. If bacteria and plasmids are mixed together, the plasmids can be transferred into the cell after electroporation.
  • Electroporation has proven efficient for use on tissues in vivo, for in utero applications as well as in ovo transfection.
  • Adherent cells can also be transfected using electroporation, providing researchers with an alternative to trypsinizing their cells prior to transfection.
  • Fluorescence is the emission of light by a substance that has absorbed light or other electromagnetic radiation. It is a form of luminescence.
  • the emitted light has a longerwavelength, and therefore lower energy, than the absorbed radiation.
  • the most striking examples of fluorescence occur when the absorbed radiation is in the ultraviolet region of the spectrum, and thus invisible to the human eye, and the emitted light is in the visible region.
  • Fluorescence occurs in nature in some minerals and in various biological states in many branches of the animal kingdom. Fluorescence has many practical applications, includingmineralogy, gemology, chemical sensors (fluorescence spectroscopy), fluorescent labeling, dyes, biological detectors, cosmic-ray detection, and, most commonly, fluorescent lamps.
  • cancers In the developing world nearly 20% of cancers are due to infections such as hepatitis B, hepatitis C, and human papilloma virus. These factors act, at least partly, by changing the genes of a cell. Typically many such genetic changes are required before cancer develops. Approximately 5-10% of cancers are due to genetic defects inherited from a person's parents. Cancer can be detected by certain signs and symptoms or screening tests. It is then typically further investigated by medical imaging and confirmed by biopsy.
  • the chance of survival depends on the type of cancer and disease at the start of treatment. In children under 15 at diagnosis the five year survival rate in the developed world is on average 80%.For cancer in the United States the average five year survival rate is 66%. In 2012 about 14.1 million new cases of cancer occurred globally. It caused about 8.2 million deaths or 14.6% of all human deaths.
  • Colorectal cancer A malignant tumor arising from the inner wall of the large intestine (the colon). In the US, colon cancer is the third leading type of cancer in males and the fourth in females. Risk factors for cancer of the colon and rectum (colorectal cancer) include colon polyps, long-standing ulcerative colitis, and genetic family history. Most colorectal cancers develop from polyps.
  • Colon polyps and early colon cancer can have no symptoms. Therefore, regular screening is vitally important, starting at age 50 (or earlier, if added risk factors are present). Diagnosis can be made by barium enema or by colonoscopy, with biopsy confirmation of cancer tissue. Surgery is the most common treatment for colorectal cancer. Cancers are a large family of diseases which involve abnormal cell growth with the potential to invade or spread to other parts of the body. They form a subset of neoplasms. A neoplasm or tumor is a group of cells that have undergone unregulated growth, and will often form a mass or lump, but may be distributed diffusely.
  • Cancers are classified by the type of cell that the tumor cells resemble and are presumed to be the origin of the tumor. These types include:
  • Carcinoma Cancers derived from epithelial cells, this group includes many of the most common cancers, particularly in the aged, and includes nearly all those developing in the breast, prostate, lung, pancreas, and colon.
  • Sarcoma Cancers arising from connective tissue (i.e. bone, cartilage, fat, nerve), each of which develop from cells originating in mesenchymal cells outside the bone marrow.
  • Lymphoma and leukemia These two classes of cancer arise from hematopoietic (blood-forming) cells that leave the marrow and tend to mature in the lymph nodes and blood, respectively.
  • Leukemia is the most common type of cancer in children accounting for about 30%.
  • Germ cell tumor Cancers derived from pluripotent cells, most often presenting in the testicle or the ovary (seminoma and dysgerminoma, respectively).
  • Blastoma Cancers derived from immature "precursor" cells or embryonic tissue. Blastemas are more common in children than in older adults.
  • the radical treatment is a vigorous treatment that aims at the complete cure of a disease rather than the mere relief of symptoms.
  • the underlying SSQF Infusion Resonator Medical Device has been comprehensively designated to radically treat Stage One and Stage Two Cancer.
  • the SSQF Infusion Resonator Medical Device has been knowingly designated to reverse certain cancer conditions within stage Three and Stage Four Cancer, especially those with a prevailing Immune System.
  • the underlying Medical Device is a Legendary Cancer Cure of Precision Targeting in Defeating Cancer by Promoting Cytostasis, Impairing Mitosis, infusing Cytochrome C-Protein and Programming T-Lymphocyte T-Cells, B-Lymphocyte/B-Cells, programming the Thymus Gland, Inducing Apoptosis and Programming Exocytosis, Necrosis, Apoptosis, Cytokinesis, Mitosis, Proteins, Enzymes to respond to SSQF Medical Device.
  • This Highly Sophisticated Technology and its subsequent Medical Device is rated as Solar Sonic Infusion-ably accessible and comprehensively coded for variety of cancer conditions and treatments and offering superior Cancer Disease Management with SSF-Propagation Ratio at Cellular Communications Radius 36556799114
  • the presented Device Diagram is only the construction of the illustrative shell design of Solar Sonic Cancer Therapeutic Infusion Medical Device. All other supporting applications of this Medical Device are detailed in list of 46 items outlining all the exact technical applications within the device which benefit all cancer patients as they receive the most suitable therapeutic protocols via various options offered by SSQF Medical Device.
  • the underlying Medical Device triggers the programmed death of carcinogenic cells, since cell death can be prompted by a signal.
  • This Solar Sonic Curative Cancer Medical Device is proven to work reproducibly as a Super Hi-Tech Solar Sonic Multidimensional Medical Science Technology triggering Cellular / Pathogenic Bio-Signaling Communications and Prompting the adaptive electromagnetic Programming Technology to enhance various electronic circuits and delivery units of digital highways and capsulated energy matrix.
  • This very SSQF Cancer Cure Medical Device converts Multidrug Components from Cytotoxic to Antitoxic safely Electromagnetically Chemical Ignition of Particle Acceleration induces Complete Physiological Infusion intravenously where Bio-Signaling Communication induces Apoptosis, strengthen intracellular/pathogenic Control, Promoting Homeostasis and Impairing Mitosis, Infusing Cytochrome C-Protein and Programming Thymus Gland, T-Lymphocyte/T-Cells, B-Lymphocyte/B-Cells and causing Expeditious Apoptosis Status.
  • AHL can migrate freely through the cell membrane, not just in bacterial cells but also our own cells, which can be influenced to change their functions.
  • white blood cells for example, can be more flexible and effective, but in high concentrations the opposite occurs, which weakens our immune defenses and opens the door for progressive infections and inflammations.
  • Solar Sonic researchers are programming human cells, since the protein can listen in on the bacteria's Signaling communication and change the functions in its host cells. Solar Sonic researchers are showing how bacteria and viruses control processes in human cells the exact same way. Meantime, cells / pathogens are becoming more aggressive and increase their mobility. All these changes are triggered when communication molecules short fatty acids with the designation AHL bind to receptors inside the bacterial cells; as a clear consequence various genes are turned on and off. AHL can migrate freely through the cell membrane, not just in bacterial cells but also our cells, which can be influenced to change their functions. Solar Sonic team is the first research group in the world to show how AHL (cells) can influence their host cells.
  • Intelligent ecologies contain intelligent populations, which contain intelligent organisms, which contain intelligent cells, which contain intelligent compartments, which contain and so forth. If cells are intelligent, we would have to rethink all the cause and effect chains from genes to molecules to cell functions that we somehow believe today to be true.
  • cells are intelligent, molecules and their genes would be the collaborators or even slaves but not the masters of the life functions of cells. If cells are intelligent, medical treatment may involve 'talking to cells rather than to flood the organism with pharmaceuticals as we do today and they are intelligent. If cells respond to signals rather than to exogenous forces, the forces that keep or change direction of their bodies are indeed controlled from within.
  • Solar Sonic Quantum Frequency Waves are systematically inducing self-destruction of cells via Bio-signaling communication eradicating carcinogenic cells within reach.
  • Solar Sonic Technology electromagnetically and chemically infusing Cytochrome C Protein and infusion-ably inducing apoptosis for Eradication Count-down Mechanism, such massive efforts are designed in order to treat infusion-ably accessible diseases with (Solar Sonic Molecularly Therapeutic Resonance Signatures and Quantum SSF Nano-Accelerated Infusion Resonator).
  • Human Cells and Pathogens communicate via Electromagnetic Bio-Chemical Signaling System. Genes involved in transmitting the electrical signal(s) produce channels in a membrane just inside the walls of the cell; the channels maintain electrical potential by regulating the passage of Micro-charged ions at all times. Cancer cells require a mechanism to maintain their telomeric DNA in order to continue dividing indefinitely (immortalization).
  • telomere elongation or maintenance is one of the key steps in cellular immortalization and can be used as a diagnostic marker in the clinic.
  • Telomerase is this enzyme complex that is responsible for elongating telomeres, is activated in approximately 90% of tumors.
  • telomeres a non- conservative telomere lengthening pathway involving the transfer of telomere tandem repeats between sister- chromatids.
  • ALT telomere shortening pathway involving the transfer of telomere tandem repeats between sister- chromatids.
  • Telomerase is the natural enzyme which promotes telomere repair. It is however not active in most cells. It is active in stem cells, germ cells, hair follicles and in 90 percent of cancer cells. Telomerase functions by adding bases to the ends of the telomeres. As a result of this telomerase activity, these cells seem to possess a kind of immortality.
  • Solar Sonic Engineers have demonstrated that the role of telomeres in cancer can both be limited to tumor growth and promote tumorigenesis, depending on the cell type and genomic context.
  • telomeres are stretches of DNA that protect bur genetic data, make it possible for cells to divide, and hold some secrets to how we age and get cancer. Telomeres have been compared with the plastic tips on shoelaces, because they keep chromosome ends from fraying and sticking to each other, which would destroy or scramble an organism's genetic information. Yet, each time a cell divides, the telomeres get shorter. When they get too short, the cell can no longer divide; it becomes inactive or "senescent" or it dies. This shortening process is associated with aging, cancer, and a higher risk of death. So telomeres also have been compared with a bomb fuse, in terms of deactivating cancer.
  • compositions with various Solar Sonic applications is forming a medical device as Cancer Cure in order to treat Infusion-ably Accessible Cancer Conditions with Solar Sonic Molecularly Therapeutic Resonance Signatures and Quantum SSQF Nano-Accelerated Infusion Resonator in all of Solar Sonic Infusion-ably Accessible critical diseases regardless of biological classifications or physiological category such as Neurological, Chromosomal, Hematologic, Cellular, Infectious, Chronic and Terminal Diseases in which all geared up towards Regenerative Bio-Modification, Physiological Restorations and Superior Disease Management Healthcare Services, accommodating different patients with varied needs.
  • Electromagnetically Chemical Ignition of Particle Acceleration induces Complete Physiological Infusion intravenously where Bio-Signaling Communication induces Apoptosis, strengthen intracellular/pathogenic control, Promoting Cytostasis and Impairing Mitosis, Infusing Cytochrome C-Protein and Programming Thymus Gland, T-Lymphocyte/T-Cells, B-Lymphocyte/B-Cells and causing Expeditious Apoptosis Status.
  • the electric eel (Electrophorus electricus) is an electric fish, and the only species in its genus. It is capable of generating powerful electric shocks of up to 650 volts, which it uses for hunting, self-defense and communicating with fellow eels. It is an apex predator; it is not quite an eel, buta knifefish.
  • the genes involved in transmitting the electrical signal(s) produce channels in a membrane just inside the walls of the cell; the channels maintain electrical potential by regulating the passage of Micro-charged ions.
  • Cells must communicate with each other in order to coordinate their functions and maintain the organism. They communicate using their own Language of Bio-Chemical Signals via induction.
  • the protein can listen in on the bacteria's Signaling communication and clearly change functions in its host cells.
  • AHL can migrate freely through the cell membrane, not just in bacterial cells but also our own cells, which can be influenced to change their functions.
  • Solar Sonic team at Linkoping University is the first research group in the world to show how AHL can influence their host cells.
  • the researchers Using biochemical methods, the researchers have identified a protein designated IQGAP, which they single out as the recipient of the bacteria's message, and something of a double agent.
  • Cells must communicate with each other in order to coordinate their functions and maintain the organism. They communicate using their own Language of Bio-Chemical Signals via induction. Intra-Cellular, Extra- Cellular and Pathogenic Bio-Communications and the Non-Human Intelligence's Communications via Solar Sonic Induced Signaling for the treatment of different cancers (Malignancies, Metastasis, Physiological and Cellular Carcinogenicity, Uncontrollable Cellular Reproduction, abnormal growth of Cancer Cells/Tumors, Blood Biochemical Migratory Carcinogenicity).
  • the channels maintain electrical potential by regulating the passage of Micro-charged ions. Cancer cells require a mechanism to maintain their telomeric DNA in order to continue dividing indefinitely (immortalization).
  • telomere elongation or maintenance is one of the key steps in cellular immortalization and can be used as a diagnostic marker in the clinic.
  • Telomerase the enzyme complex responsible for elongating telomeres, is activated in approximately 90% of tumors.
  • telomeres a non- conservative telomere lengthening pathway involving the transfer of telomere tandem repeats between sister- chroma t ids.
  • ALT telomere lengthening pathway involving the transfer of telomere tandem repeats between sister- chroma t ids.
  • Telomerase is the natural enzyme which promotes telomere repair.
  • telomere functions by adding bases to the ends of the telomeres.
  • telomeres As a result of this telomerase activity, these cells seem to possess a kind of immortality. Studies using knockout mice have demonstrated that the role of telomeres in cancer can both be limiting to tumor growth and promote tumorigenesis, depending on the cell type and genomic context.
  • chromosomes Inside the nucleus of a cell, our genes are arranged along twisted, double-stranded molecules of DNA called chromosomes. At the ends of the chromosomes are stretches of DNA called telomeres, which protect our genetic data, make it possible for cells to divide, and hold some secrets to how we age and get cancer.
  • telomeres have been compared with the plastic tips on shoelaces, because they keep chromosome ends from fraying and sticking to each other, which would destroy or scramble an organism's genetic information. Yet, each time a cell divides, the telomeres get shorter.
  • telomeres When they get too short, the cell can no longer divide; it becomes inactive or "senescent" or it dies. This shortening process is associated with aging, cancer, and a higher risk of death. So telomeres also have been compared with a bomb fuse.
  • Electromagnetically Chemical Ignition of Particle Acceleration induces Complete Physiological Infusion intravenously where Bio-Signaling Communication induces Apoptosis, strengthen intracellular/pathogenic control, Promoting Cytostasis and Impairing Mitosis, Infusing Cytochrome C-Protein & Programming Thymus Gland, T-Lymphocyte/T-Cells, B-Lymphocyte/B-Cells and causing Expeditious Apoptosis Status.
  • biological plausibility refers to the proposal of a causal association, a relationship between putative cause and an outcome that is consistent with existing biological and medical knowledge.
  • Biological plausibility is one component of a method of reasoning that can establish a cause-and- Effect relationship between a biological factor and particular disease or adverse event. It is also an important part of the process of evaluating whether a proposed therapy (drug, vaccine, surgical procedure, etc.) has a real benefit to a patient.
  • the Solar Sonic Molecularly Therapeutic Resonance Signature and Quantum EMF Nano-Accelerated Infusion Resonator as a Therapeutic intravenous Infusion Regimen for treating all types of cancers by inducing, stimulating and infusing cancerous cells as well as inducing biological charging of the critical super-paramagnetic Nano-Particles in treatment and removal of cells throughout very sophisticated Electromagnetic frequency waves with capsulated energy output. This causes instantaneous cellular imbalance of carcinogenic cells.
  • cancerous cells will begin to eradicate, terminate and die down without affecting healthy cells, as the system is designed for precision targeting of only cancerous cells after marking the resonance signatures of cancerous cells in the body via SSQF waves.
  • Solar Sonic electromagnetic frequency waves along with the SSQF intravenous Nano infusion and the highly proprietary infused electromagnetic SSQF solution for cellular regeneration and cellular communications. As such, they collectively provide several methods of treating cancer through this particular medical device. One of which is paving the way to administer cell cycle arresting frequency waves impeded within a composition of valid and pharmaceutically approved carrier with calculated lazing procedure and stabilizing agent(s).
  • Electromagnetic Frequency Wave(s) intravenously in order to methodically terminate carcinogenic cells in developed tumors and the overall cancerous conditions, as the system is also programmed for all cancer stages.
  • the above stated technology is a highly proprietary discovery, it is a phenomenon that was never ever scientifically introduced, given the structuring of the composition of the EMF Nano therapeutic infusion and the superior eradication of carcinogenic cells, viciously roaming within the entire body, the system also master environmental development of tumor growth and identical cell replication mechanism in late stages of the disease.
  • This Abstract covers multiple functions of the medical device presented and various composition options of Nano-infusion-therapy for various cancer treatments and superior disease management, suiting all different patients.
  • This system is to treat infusion-ably accessible diseases with (Solar Sonic Molecularly Therapeutic Resonance Signature and Quantum SSF Nano-Accelerated Infusion Resonator) in all of Solar Sonic Infusion- ably Accessible diseases.
  • biological classifications or physiological category such as Neurological, Chromosomal, Cellular, Infectious, Chronic Terminal & Hematologic Diseases, upon which all are geared up towards Regenerative Bio-Modifications, Physiological Restorations and Superior Hi-Tech Disease Management.
  • the present invention introduces a multi-function medical device, we entertain new technological methodology in battling all types of cancers which is Bio-communication, Bio-signaling, Electromagnetically Chemical Intracellular / Extracellular Bio-Signaling Communications. Leading to programming the cells to follow biological instructions or face deprivation and eradication of their carcinogenic environment. Whereas their critically vital components will be forcefully converted as programmed by the device.
  • This Highly Sophisticated Technology and its subsequent Medical Device is rated as Solar Sonic Infusion-ably accessible and comprehensively coded for variety of cancer conditions and treatments and offering superior Cancer Disease Management with SSF-Propagation Ratio at Cellular Communications Radius 36556799114.
  • the Device Diagram is only the construction of the illustrative shell design of Solar Sonic Cancer Therapeutic Infusion Medical Device. All other supporting applications of this Medical Device are detailed in a list of 45 items, outlining all the exact technical applications within the device that which benefit all cancer patients as they receive the most suitable medicinal and therapeutic protocol via various options offered by the device.
  • the invention relates to a medical device especially designed to treat cancer patients with their various needs.
  • the invention also relates to varied tumor treatment methods, the medical device with all of its accompanying therapeutic infusion composition and other varied supporting capabilities can be used in oncology for the treatment of primary and metastatic tumors.
  • the medical device and the infusion composition are specifically designed to positively interact in all cancer treatments, in early or late stages, in metastasis or malignancies.
  • the medical device presented is utilized for destroying cancerous cells and destroying all of its Synergistic pathogens and immunity suppressing moieties (ISM) in humans.
  • ISM Synergistic pathogens and immunity suppressing moieties
  • a single intravenous injection of the device is all that is required for efficacy at levels of about 40 PPM of human blood.
  • the device When administered into the bloodstream, the device electrons will be triggered by carcinogenic cells and all pathogens.
  • the medical device Upon a single intravenous injection the medical device will simultaneously trigger an infusion reaction of the entities and begin communicating with them directly to either convert them to healthy cells or begin to eradicate them.
  • the underlying program of the device contains electromagnetic frequency waves of highly proprietary resonance signature cloning-resonator that gives an imaginary electromagnetic signature of a virus, a cell, a pathogen or any other organism for that matter of an identical biological structure (cancer cells, pathogens).
  • this medical device will analyze the resonance signature of all healthy and carcinogenic cells and all pathogens. Once biological analysis is completed the process of intracellular communications and signaling will then begin. The final results of the intracellular communications at this very point in time are to attempt to terminate the carcinogenic cells and to instantaneously begin eradication of the carcinogenic cells at once.
  • This is also a method of treatment of a tumor comprising the steps of catheterization of the arterial vessel that feeds the tumor and trans-catheter administration of therapeutic pharmacological agents, pharmaceutically acceptable carriers with other simultaneous applications of approved pharmaceutical and chemotherapeutic agents onto tumor, bearing in mind that all Cytotoxic elements are converted to Antitoxic by medical device.
  • the tumor is subjected to heat from ultra-low to ultra-medium of a local radio frequency electromagnetic field or ultrasonic waves to produce heating of the tumor tissue to a moderate temperature of 43.0°-43.5° C for a period of 15-45 minutes, all done simultaneously, illustrated here below are a list of our applicable chemical compositions / agents, this approved list was specifically selected as they all are Solar Sonic Infusion-ably Accessible as chemical resonance signature that can be electromagnetically /chemically manipulated for an expeditious intracellular redirection and penetration leading to intracellular Bio-signal Communications of carcinogenic cells / pathogens, upon such contact countdown will begin for an immediate initiation to systematically eradicate cancer cells, as a biological matter of intracellular-connectivity.
  • the invention comes with a medicament delivery device including medicament housing with a drug delivery reservoir and a membrane coupled to the medicament housing.
  • the invention further includes a medicament selected from highly proprietary pharmaceutically infused therapeutic Compositions and immunotherapeutic agent, immune-modulators, anti-antigenic agent, angiogenesis inhibitor, vascular sealing agent, gene therapy agent, antibiotic, resistance modification agent and a photodynamic therapy agent.
  • the invention also specifically provides a method for treating cancer in both humans and animals alike, administering to the human a dose of a pharmaceutical composition comprising pharmaceutically acceptable carrier and an adenoviral vector comprising a nucleic acid sequence encoding a human TNF-a and operably linked to a promoter.
  • adenovirus-based vectors Due to the efficient nuclear entry mechanism of adenovirus and its low pathogencity for humans, adenovirus- based vectors become gene delivery vehicles that are widely used for transduction of different cell types, especially for quiescent, differentiated cells, in research, in gene therapy applications, and in vaccine development.
  • adenoviral vectors can be produced in high titers, they can transducer cells in vivo with transgenes of more than 30 kb, and they do not integrate into the host cell genome.
  • tissue Through irradiation within the Solar Sonic Medical Device we sterilize tissue completely, sterilizing tissue to reduce the level of one or more active biological contaminants or pathogens therein, such as viruses, bacteria, (including inter- and intracellular bacteria, such as mycoplasmas, ureaplasmas, nanobacteria, chlamydia, rickettsias), yeasts, molds, fungi, prions or similar agents responsible, alone or in combination, for TSEs or multi-cellular parasites, the methods involve sterilizing one or more tissues with irradiation.
  • active biological contaminants or pathogens therein such as viruses, bacteria, (including inter- and intracellular bacteria, such as mycoplasmas, ureaplasmas, nanobacteria, chlamydia, rickettsias), yeasts, molds, fungi, prions or similar agents responsible, alone or in combination, for TSEs or multi-cellular parasites
  • the methods involve sterilizing one or more tissues with irradiation.
  • the invention also relates to the use of a pharmacological multi-combination composition and their chemical equivalents and pharmacologically compatible carrier or diluents.
  • a pharmacological multi-combination composition for the treatment of cancer by inducing apoptosis and/or reversing apoptosis-resistance in a cell preferably, the dosage is 10-100 mg/kg.
  • the pharmacological multi-combination composition may be optionally given in combination with a pro-apoptotic agent.
  • the cancers treated are non-small cell lung cancer, glioblastoma and breast carcinoma.
  • the invention also relates to micro-particles that may be used for antigen delivery and vaccine immunization strategies.
  • the invention in particular relates to micro-particles that are useful in the prophylaxis and the underlying treatment of cancer.
  • One of the main challenges in cancer research is the development of vaccines that induce effective and long-lived protective immunity against tumors. Significant progress has been made in identifying members of the cancer testis antigen family as potential vaccine candidates. However, an ideal form for antigen delivery that induces robust and sustainable antigen-specific T-cell responses.
  • Local symptoms may occur due to the mass of the tumor or its ulceration.
  • mass effects from lung cancer can cause blockage of the bronchus resulting in cough or pneumonia; esophageal cancer can cause narrowing of the esophagus, making it difficult or painful to swallow; and colorectal cancer may lead to narrowing or blockages in the bowel, resulting in changes in bowel habits.
  • Masses in breasts or testicles may be easily felt. Ulceration can cause bleeding which, if it occurs in the lung, will lead to coughing up blood, in the bowels to anemia or rectal bleeding, in the bladder to blood in the urine, and in the uterus to vaginal bleeding.
  • localized pain may occur in advanced cancer, the initial swelling is usually painless.
  • Some cancers can cause buildup of fluid within the chest or abdomen.
  • General symptoms occur due to distant effects of the cancer that are not related to direct or metastatic spread. These may include: unintentional weight loss, fever, being excessively tired, and changes to the Skin.
  • Hodgkin disease, leukemia, and cancers of the liver or kidney can cause a persistent fever of unknown origin.
  • Some cancers may cause specific groups of systemic symptoms, termed paraneoplastic phenomena. Examples include the appearance of myasthenia gravis in thymoma and clubbing in lung cancer.
  • Cancer can spread from its original site by local spread, lymphatic spread to regional lymph nodes or by blood (haematogenous spread) to distant sites, known as metastasis.
  • haematogenous route When cancer spreads by a haematogenous route, it usually spreads all over the body.
  • cancer 'seeds' grow in certain selected site only ('soil') as hypothesized in the soil and seed hypothesis of cancer metastasis.
  • the symptoms of metastatic cancers depend on the location of the tumor, and can include enlarged lymph nodes (which can be felt or sometimes seen under the skin and are typically hard), enlarged liver or enlarged spleen, which can be felt in the abdomen, pain or fracture of affected bones, and neurological symptoms.
  • cancer is generally not a transmissible disease.
  • Tobacco smoking causes 90% of lung cancer. It also causes cancer in the larynx, head, neck, stomach, bladder, kidney, esophagus and pancreas. Tobacco smoke contains over fifty known carcinogens, including nitrosamines and polycyclic aromatic hydrocarbons. Tobacco is responsible for about one in three of all cancer deaths in the developed world, and about one in five worldwide. Lung cancer death rates in the United States have mirrored smoking patterns, with increases in smoking followed by dramatic increases in lung cancer death rates and, more recently, decreases in smoking rates since the 1950s followed by decreases in lung cancer death rates in men since 1990.
  • Aflatoxin Bl a frequent food contaminate, causes liver cancer. Betel nut chewing causes oral cancer.
  • the differences in dietary practices may partly explain differences in cancer incidence in different countries. For example, gastric cancer is more common in Japan due to its high-salt diet and colon cancer is more common in the United States. Immigrants develop the risk of their new country, often within one generation, suggesting a substantial link between diet and cancer. Worldwide approximately 18% of cancer deaths are related to infectious diseases. This proportion varies in different regions of the world from a high of 25% in Africa to less than 10% in the developed world. Viruses are the usual infectious agents that cause cancer but bacteria and parasites may also have an effect. Oncovirus is a virus that can swiftly cause cancer.
  • human papillomavirus cervical carcinoma
  • Epstein-Barr virus B-cell lympho-proliferative disease and nasopharyngeal carcinoma
  • Kaposi's sarcoma herpesvirus Kaposi's sarcoma herpesvirus
  • hepatitis B and hepatitis C viruses hepatocellular carcinoma
  • human T-cell leukemia virus-1 T-cell leukemias.
  • Bacterial infection may also increase the risk of cancer, as seen in Helicobacter pylori-induced gastric carcinoma.
  • Parasitic infections strongly associated with cancer include Schistosoma haematobium (squamous cell carcinoma of bladder) and the liver flukes, Opisthorchis viverrini and Clonorchis sinensis (cholangio-carcinoma).
  • invasive cancers Up to 10% of invasive cancers are related to radiation exposure, including both ionizing radiation and nonionizing ultraviolet radiation. Additionally, the vast majority of non-invasive cancers are non-melanoma skin cancers caused by non-ionizing ultraviolet radiation, mostly from sunlight. Sources of ionizing radiation include medical imaging and radon gas. Ionizing radiation is not a particularly strong mutagen. Residential exposure to radon gas, for example, has similar cancer risks as passive smoking. Radiation is a more potent source of cancer when it is combined with other cancer-causing agents, e.g.radon gas exposure and tobacco.
  • Radiation can cause cancer in most parts of the body, in all animals, and at any age. Children and adolescents are twice as likely to develop radiation-induced leukemia as adults; radiation exposure before birth has ten times the effect. Medical use of ionizing radiation is a small but growing source of radiation-induced cancers. Ionizing radiation may be used to treat other cancers, but this may, in some cases, induce a second form of cancer. It is also used in some kinds of medical imaging. Prolonged exposure to ultraviolet radiation from the sun can lead to melanoma and other skin malignancies.
  • Some of these syndromes include: certain inherited mutations in the genes BRCA1 and BRCA2 with a more than 75% risk of breast cancer and ovarian cancer, and hereditary nonpolyposis colorectal cancer (HNPCC or Lynch syndrome) which is present in about 3% of people with colorectal cancer, among others.
  • HNPCC hereditary nonpolyposis colorectal cancer
  • Non-fibrous particulate materials that cause cancer include powdered metallic cobalt and nickel, and crystalline silica (quartz, cristobalite, and tridytnite). Usually, physical carcinogens must get inside the body (such as through inhaling tiny pieces) and require years of exposure to develop cancer.
  • oncogenes are known to build up an inflammatory pro-tumorigenic microenvironment.
  • Some hormones play a role in the development of cancer by promoting cell proliferation.
  • Insulin-like growth factors and their binding proteins play a key role in cancer cell proliferation, differentiation and apoptosis, suggesting possible involvement in carcinogenesis.
  • Hormones are important agents in sex-related cancers such as cancer of the breast, endometrium, prostate, ovary, and testis, and also of thyroid cancer and bone cancer.
  • the daughters of women who have breast cancer have signiflcantly higher levels of estrogen and progesterone than the daughters of women without breast cancer.
  • men of African ancestry have significantly higher levels of testosterone than men of European ancestry, and have a correspondingly much higher level of prostate cancer.
  • Other factors are also relevant: obese people have higher levels of some hormones associated with cancer and a higher rate of those cancers.
  • Cancer is fundamentally a disease of tissue growth regulation failure. In order for a normal cell to transform into a cancer cell, the genes which regulate cell growth and differentiation must be altered. The affected genes are divided into two broad categories.
  • Oncogenes are genes which promote cell growth and reproduction.
  • Tumor suppressor genes are genes which inhibit cell division and survival. Malignant transformation can occur through the formation of novel oncogenes, the inappropriate over-expression of normal oncogenes, or by the under-expression or disabling of tumor suppressor genes.
  • changes in many genes are required to transform a normal cell into a cancer cell. Genetic changes can occur at different levels and by different mechanisms. The gain or loss of an entire chromosome can occur through errors in mitosis. More common are mutations, which are changes in the nucleotide sequence of genomic DNA. Large-scale mutations involve the deletion or gain of a portion of a chromosome. Genomic amplification occurs when a cell gains many copies (often 20 or more) of a small chromosomal locus, containing one or more oncogenes and adjacent genetic material.
  • Translocation occurs when two separate chromosomal regions become abnormally fused, often at a characteristic location.
  • a well-known example of this is the Philadelphia chromosome, or translocation of chromosomes 9 and 22, which occurs in chronic myelogenous leukemia, and results in production of the BCR-ablfusion protein, an oncogenic tyrosine kinase.
  • Small-scale mutations include point mutations, deletions, and insertions, which may occur in the promoter region of a gene and affect its expression, or may occur in the gene's coding sequence and alter The function or stability of its protein product.
  • Disruption of a single gene may also result from integration of genomic material from a DNA virus or retrovirus, leading to the expression of viral oncogenes in affected cell and its descendants. Replication of the enormous amount of data contained within the DNA of living cells will probabilistically result in some errors (mutations). Complex error correction and prevention is built into the process, and safeguards the cell against cancer. If significant error occurs, the damaged cell can "self-destruct" through programmed cell death, termed apoptosis. If the error control processes fail, then the mutations will survive and be passed along to daughter cells. Some environments make errors more likely to arise and propagate, they can include the presence of disruptive substances called carcinogens, repeated physical injury, heat, ionizing radiation, or hypoxia. The errors which cause cancer are self- amplifying and compounding, for example:
  • a mutation in the error-correcting machinery of a cell might cause that cell and its children to accumulate errors more rapidly.
  • a further mutation may cause loss of a tumor suppressor gene, disrupting the apoptosis signaling pathway and resulting in the cell becoming immortal.
  • a further mutation in signaling machinery of the cell might send error-causing signals to nearby cells.
  • Characteristic abilities developed by cancers are divided into a number of categories. Six categories were originally proposed, in a 2000 paper called "The Hallmarks of Cancer" by Douglas Hanahan and Robert Weinberg: evasion of apoptosis, self-sufficiency in growth signals, insensitivity to anti-growth signals, sustained angiogenesis, limitless replicative potential, and metastasis.
  • cancer has been viewed as a set of diseases that are driven by progressive genetic abnormalities that include mutations in tumor-suppressor genes and oncogenes, and chromosomal abnormalities.
  • progressive genetic abnormalities that include mutations in tumor-suppressor genes and oncogenes, and chromosomal abnormalities.
  • epigenetic alterations that include mutations in tumor-suppressor genes and oncogenes, and chromosomal abnormalities.
  • Epigenetic alterations refer to functionally relevant modifications to the genome that do not involve a change in the nucleotide sequence. Examples of such modifications are changes in DNA methylation (hypermethylation and hypomethylation) and histone modification and changes in chromosomal architecture (caused by inappropriate expression of proteins such as HMGA2 or HMGA1). Each of these epigenetic alterations serves to regulate gene expression without altering the underlying DNA sequence. These changes may remain through cell divisions, last for multiple generations, and can be considered to be epimutations (equivalent to mutations). Epigenetic alterations occur frequently in cancers. As an example, Schnekenburger and Diederich listed protein coding genes that were frequently altered in their methylation in association with colon cancer. These included 147 hypermethylated and 27 hypomethylated genes. Of the hypermethylated genes, 10 were hypermethylated in 100% of colon cancers, and many others were hypermethylated in more than 50% of colon cancers.
  • MiRNAs do not code for proteins, can "target" protein-coding genes and reduce their expression.
  • Cancers usually arise from an assemblage of mutations and epimutations that confer a selective advantage leading to clonal expansion. Mutations, however, may not be as frequent in cancers as epigenetic alterations.
  • An average cancer of the breast or colon can have about 60 to 70 protein-altering mutations, of which about 3 or 4 may be “driver” mutations, and the remaining ones may be “passenger” mutations.
  • cancer is caused by failure to regulate tissue growth, when the genes which regulate cell growth and differentiation are altered. It has become clear that these alterations are caused by both DNA sequence mutation in oncogenes and tumor suppressor genes as well as by epigenetic alterations.
  • Metastasis is the spread of cancer to other locations in the body.
  • the new tumors are called metastatic tumors, while the original is called the primary tumor.
  • Almost all cancers can metastasize.
  • Most cancer deaths are due to cancer that has spread from its primary site to other organs (metastasized).
  • Metastasis is very common in the late stages of cancer, and it can occur via the blood or the lymphatic system or both.
  • the typical steps in metastasis are local invasion, intravasation into the blood or lymph, circulation through the body, extravasation into the new tissue, proliferation, and angiogenesis.
  • cancers tend to metastasize to particular organs, but overall the most common places for metastases to occur are the lungs, liver, brain, and the bones. Most cancers are initially recognized either because of the appearance of signs or symptoms or through screening. Neither of these lead to a definitive diagnosis, which requires the examination of a tissue sample by a pathologist. People with suspected cancer are investigated with medical tests. These commonly include blood tests, X-rays, CT scans and endoscopy.
  • Cancers are classified by the type of cell that the tumor cells resemble and is therefore presumed to be the origin of the tumor. These types include:
  • Carcinoma Cancers derived from epithelial cells. This group includes many of the most common cancers, particularly in the aged, and include nearly all those developing in the breast, prostate, lung, pancreas, and colon.
  • Lymphoma and leukemia These two classes of cancer arise from hematopoietic (blood-forming) cells that leave the marrow and tend to mature in the lymph nodes and blood, respectively.
  • Leukemia is the most common type of cancer in children accounting for about 30%.
  • Germ cell tumor Cancers derived from pluripotent cells, most often presenting in the testicle or the ovary (seminoma and dysgerminoma, respectively).
  • Blastema Cancers derived from immature "precursor" cells or embryonic tissue. Blastemas are more common in children than in older adults. Cancers are usually named using -carcinoma, -sarcoma or -blastoma as a suffix, with the Latin or Greek word for the organ or tissue of origin as the root. For example, cancers of the liver parenchyma arising from malignant epithelial cells is called hepatocarcinoma, while a malignancy arising from primitive liver precursor cells is called a hepatoblastoma, and a cancer arising from fat cells is called a liposarcoma.
  • the English organ name is used.
  • the most common type of breast cancer is called ductal carcinoma of the breast.
  • the adjective ductal refers to the appearance of the cancer under the microscope, which suggests that it has originated in the milk ducts.
  • Benign tumors (which are not cancers) are named using -oma as a suffix with the organ name as the root.
  • a benign tumor of smooth muscle cells is called aleiomyoma (the common name of this frequently occurring benign Tumor in the uterus is fibroid).
  • cancer use the -noma suffix, examples including melanoma and seminoma.
  • Some types of cancer are named for the size and shape of the cells under a microscope, such as giant cell carcinoma, spindle cell carcinoma, and small-cell carcinoma.
  • the tissue diagnosis given by the pathologist indicates the type of cell that is proliferating, its histological grade, genetic abnormalities, and other features of the tumor. Together, this information is useful to evaluate the prognosis of the patient and to choose the best treatment.
  • Cytogenetics and immuno-histochemistry are other types of testing that the pathologist may perform on the tissue specimen. These tests may provide information about the molecular changes (such as mutations, fusion genes, and numerical chromosome changes) that have happened in the cancer cells, and may thus also indicate the future behavior of the cancer (prognosis) and best treatment.
  • Cancer prevention is defined as active measures to decrease the risk of cancer.
  • the vast majority of cancer cases are due to environmental risk factors, and many, but not all, of these environmental factors are controllable lifestyle choices. Thus, cancer is considered a largely preventable disease. Greater than 30% of cancer deaths could be prevented by avoiding risk factors including: tobacco, overweight / obesity, an insufficient diet, physical inactivity, alcohol, sexually transmitted infections, and air pollution.
  • risk factors including: tobacco, overweight / obesity, an insufficient diet, physical inactivity, alcohol, sexually transmitted infections, and air pollution.
  • Not all environmental causes are controllable, such as naturally occurring background radiation, and other cases of cancer are caused through hereditary genetic disorders, thus it is not possible to prevent all cases of cancer.
  • NSAIDs reduce the risk of colorectal cancer, however due to the cardiovascular and gastrointestinal side effects they cause overall harm when used for prevention.
  • Aspirin has been found to reduce the risk of death from cancer by about 7%.
  • COX-2 inhibitor may decrease the rate of polyp formation in people with familial adenomatous polyposis, however it is associated with the same adverse effects as NSAIDs.
  • Daily use of tamoxifen or raloxifene has been demonstrated to reduce the risk of developing breast cancer in high-risk women.
  • Vitamins have not been found to be effective at preventing cancer, although low blood levels of vitamin D are correlated with increased cancer risk. Whether this relationship is causal and vitamin D supplementation is protective is not determined.
  • Beta-Carotene supplementation has been found to increase lung cancer rates in those who are high risk.
  • Folic acid supplementation has not been found effective in preventing colon cancer and may increase colon polyps. It is unclear if selenium supplementation has an effect.
  • Vaccines have been developed that prevent infection by some carcinogenic viruses. Human papillomavirus vaccine (Gardasil and Cervarix) decreases the risk of developing Cervical Cancer.
  • the Hepatitis B vaccine prevents infection with hepatitis B virus and thus decreases the risk of liver cancer.
  • the administration of human papillomavirus and hepatitis B vaccinations is recommended when resources allow.
  • cancer screening involves efforts to detect cancer after it has formed, but before any noticeable symptoms appear. This may involve physical examination, blood or urine tests, or medical imaging. Cancer screening is currently not possible for many types of cancers, and even when tests are available, they may not be recommended for everyone. Universal screening or mass screening involves screening everyone. Selective screening identifies people who are known to be at higher risk of developing cancer, such as people with a family history of cancer.
  • the U.S. Preventive Services Task Force strongly recommends cervical cancer screening in women who are sexually active and have a cervix at least until the age of 65. They recommend that Americans be screened for colorectal cancer via fecal occult blood testing, sigmoidoscopy, or colonoscopy starting at age SO until age 75. There is insufficient evidence to recommend for or against screening for skin cancer, oral cancer, lung cancer, or prostate cancer in men under 75. Routine screening is not recommended for bladder cancer, testicular cancer, ovarian cancer, pancreatic cancer, or prostate cancer.
  • the U.S. Preventive Services Task Force recommends mammography for breast cancer screening every two years for those 50-74 years old; however, they do not recommend either breast self-examination or clinical breast examination.
  • a 2011 Cochrane review came to slightly different conclusions with respect to breast cancer screening stating that routine mammography may do more harm than good.
  • Genetic testing for individuals at high-risk of certain cancers is recommended. Carriers of these mutations may then undergo enhanced surveillance, chemoprevention, or preventative surgery to reduce their subsequent risk.
  • the treatment intent may be curative or not curative.
  • Chemotherapy it is the treatment of cancer with one or more cytotoxic antineoplastic drugs (chemotherapeutic agents) as part of a standardized regimen.
  • chemotherapeutic agents cytotoxic antineoplastic drugs
  • the term encompasses any of a large variety of different anticancer drugs, which are divided into broad categories such as alkylating agents and antimetabolites.
  • Traditional chemotherapeutic agents act by killing cells that divide rapidly, one of the main properties of most cancer cells.
  • Targeted therapy is a form of chemotherapy which target specific molecular differences between cancer and normal cells.
  • the first targeted therapies to be developed blocked the estrogen receptor molecule, inhibiting the growth of breast cancer.
  • Another common example is the class of Bcr-Abl inhibitors, which are used to treat chronic myelogenous leukemia (CML).
  • CML chronic myelogenous leukemia
  • CML chronic myelogenous leukemia
  • the efficacy of chemotherapy depends on the type of cancer and the stage. In combination with surgery, chemotherapy has proven useful in a number of different cancer types including: breast cancer, colorectal cancer, pancreatic cancer, osteogenic sarcoma, testicular cancer, ovarian cancer, and certain lung cancers.
  • the overall effectiveness ranges from being curative for some cancers, such as some leukemia, to being ineffective, such as in some
  • Radiotherapy involves the use of ionizing radiation in an attempt to either cure or improve the symptoms of cancer.
  • Surgery is the primary method of treatment of most isolated solid cancers and may play a role in palliation and prolongation of survival. It is typically an important part of making the definitive diagnosis and staging the tumor as biopsies are usually required. In localized cancer surgery typically attempts to remove the entire mass along with, in certain cases, the lymph nodes in the area.
  • Palliative care refers to treatment which attempts to make the person feel better and may or may not be combined with an attempt to treat the cancer.
  • Palliative care includes action to reduce the physical, emotional, spiritual, and psycho-social distress experienced by people with cancer. Unlike treatment that is aimed at killing cancer cells, the primary goal of palliative care is to improve the person's quality of life.
  • Palliative care is often confused with hospice and therefore only involved when people approach end of life. Like hospice care, palliative care attempts to help the person cope with the immediate needs and to increase The person's comfort. Unlike hospice care, palliative care does not require people to stop treatment aimed at prolonging their lives or curing the cancer. Multiple national medical guidelines recommend early palliative care for people whose cancer has produced distressing symptoms (pain, shortness of breath, fatigue, nausea) or who need help coping with their illness. In people who have metastatic disease when first diagnosed, oncologists should consider a palliative care consult immediately. Additionally, an oncologist should consider a palliative care in any person has less than 12 months of life even if continuing aggressive treatment.
  • Cancer has a reputation as a deadly disease. About half of people receiving treatment for invasive cancer (excluding carcinoma in situ and non-melanoma skin cancers) die from cancer or its treatment. Survival is worse in the developing world, partly because the types of cancer that are most common there are at present harder to treat than those associated with the lifestyle of many developed countries. However, the survival rates vary dramatically by type of cancer, and by the stage at which it is diagnosed, with the range running from the great majority of people surviving to almost no one surviving as long as five years after diagnosis. Once a cancer has metastasized or spread beyond its original site the prognosis normally becomes much worse.
  • Those who survive cancer are at increased risk of developing a second primary cancer at about twice the rate of those never diagnosed with cancer.
  • the increased risk is believed to be primarily due to the same risk factors that produced the first cancer, partly due to the treatment for the first cancer, and potentially related to better compliance with screening. Predicting either short-term or long-term survival is difficult and depends on many factors. The most important factors are the Particular kind of cancer and the patient's age and health.
  • cancer is largely a disease of older adults, it is not common in pregnant women. Cancer affects approximately 1 in 1,000 pregnant women. The most common cancers found during pregnancy are the same as the most common cancers found in non-pregnant women during childbearing ages: breast cancer, cervical cancer, leukemia, lymphoma, melanoma, ovarian cancer, and colorectal cancer.
  • the invention relates to a process/composition for the diagnosis or killing of cancer cells and inactivation of susceptible bacterial, parasitic, fungal, and viral pathogens by chemically generating heat, and/or free radicals or hyperthermia-inducible immunogenic determinants by using mitochondrial uncoupling agents, especially 2,4 dinitrophenol and, their conjugates, in combination with other drugs, hormones and cytokines.
  • the present invention also has the capabilities to prognosticate cancer.
  • a particle-based electronic brachytherapy device can include an applicator (catheter) and a high energy particle, such as but not limited to, laser plasma accelerator.
  • the laser plasma accelerator can be a compact, miniature laser-based plasma accelerator with a voltage gradient suitable to generate particles having energies in the range of 570 MeV. Electrons, protons, and heavy ions with acceleration gradients of 30 GeV/m to 200 GeV/m can be obtained through Solar Sonic Cancer Cure Medical Device via laser plasma accelerator, circuit equivalents, integrated circuits and central delivery unit of energy output fluctuations.
  • the present invention also relates to therapeutic compositions for treating cancer or preventing the growth of cancer cells, tumor growth, in a subject.
  • the present invention relates to methods for treating cancer, inhibiting tumor growth, in a subject who has become resistant to treatment, by administering to a subject an effective amount of a proteasome inhibitor and an effective amount of therapeutic agent, chemotherapeutic agent.
  • the present invention further relates to methods for purging bone marrow, removing cancer cells from Bone marrow, by exposing the bone marrow cells to a proteasome inhibitor and a therapeutic agent, and a chemotherapeutic agent.
  • the present invention also promotes methods for improving the efficiency of electroporation protocols and methods to enhance the permeabilized state, to improve the intracellular delivery of therapeutic substances, involve the use of at least one agent which is capable of prolonging the permeability of the cell membranes in the tissue exposed to an electroporation-inducing electrical field.
  • the present invention also contains an anti adhesion therapy which uses the compound as a mediator or inhibitor of adhesion proteins and angiopoietins. It inhibits excess adhesion and inhibits cell attachment. It modulates angiogenesis.
  • the compounds also use as mediator of cell adhesion receptor, cell circulating, cell moving and inflammatory.
  • This invention provides a method of synthesizing new active compounds for pharmaceutical uses including cancer treatment, wherein the cancers comprise breast, leukocytic, liver, ovarian, bladder, prostatic, skin, bone, brain, leukemia, lung, colon, C S, melanoma, renal, cervical, esophageal, testicular, spleenic, kidney, lymphatic, pancreatic, stomach and thyroid cancers.
  • the present invention also relates to novel photoactivable rhodamine derivatives for enhancing high quantum-yield production and singlet oxygen generation upon irradiation with light while maintaining desirable differential retention of rhodamine between normal and cancer cells, said derivatives are selected from the group consisting of dibromorhodamine dibromo-6-amino-3-imino-3H-xanthen-9-yl-benzoic acid methyl ester hydrochloride; dibromorhodamine dibromo-6-amino-3-imino-3H-xanthen-9-yl-benzoic acid ethyl ester hydrochloride; and photoactivable derivatives; whereby photoactivation of the derivatives induces cell killing while unactivated derivatives are substantially non-toxic to cells.
  • the present invention relates to the use of photoactivable derivatives of the present invention for photodynamic therapy of a cancer patient by destroying human cancer cells, wherein appropriate intracellular levels of the derivatives are achieved and irradiation with light of a suitable wavelength is applied.
  • the present invention also relates to a method for the photodynamic therapy of a patient suffering from leukemias, disseminated multiple myelomas or lymphomas.
  • the present invention also concerns methods and compositions for forming anti-cancer chemical complexes using Solar Sonic Anti-Cancer Multidimensional electrochemical therapeutic infusion technologies.
  • the anti-cancer chemical complex comprises an antibody moiety that binds to dendritic cells, such as an anti-CD74 antibody or antigen-binding fragment thereof, attached to an AD (anchoring domain) moiety and a xenoantigen, such as CD20, attached to a DDD (dimerization and docking domain) moiety, wherein two copies of the DDD moiety form a dimer that binds to the AD moiety, resulting in the formation of the SSOF Chemical Complex.
  • an antibody moiety that binds to dendritic cells such as an anti-CD74 antibody or antigen-binding fragment thereof
  • AD anchoring domain
  • CD20 a xenoantigen
  • DDD dimerization and docking domain
  • the anti-cancer chemical complex is capable of inducing an immune response against xenoantigen expressing cancer cells, such as CD138 neg CD20 + MM stem cells, and inducing apoptosis of and inhibiting the growth of carcinogenic cells and eliminating the cancer cells.
  • the present invention also presents an antibody for targeted induction of Apoptosis, CDC and ADCC mediated killing of Cancer cells, TBL-CLN1, is disclosed.
  • the antibodies, TBL-CLN1 are monoclonal antibodies which can specifically target and bind to the epitope of SEQ ID expressed on cancer cells which further leads to killing of cancer cells.
  • TBL-CLN1 is not conjugated to toxin or cytotoxic molecules, and provides selective killing of cancer cells just by binding to cancer cell surface.
  • the present invention also illustrates that biological organism suffering from cancer can be treated by administering a cancer cell cycle arresting drug; optionally administering a microtubule stabilizing agent; and exposing the cell cycle arrested cells to mechanical vibrational energy, the method selectively induces apoptosis in cancer cells.
  • the Present invention also relates to multiple targeting protocols and methods of treating all cancer at all stages, Wherein a pharmaceutical composition made from 'Mycobacterium (M w ) is found to be useful in the management of cancer. We have now found that the same therapeutic agent is useful in management of cancer.
  • M w Mycobacterium
  • the present invention also relates to the use of dichloroacetate and chemical equivalents thereof for the treatment of cancer by inducing apoptosis or reversing apoptosis- resistance in a cell.
  • the dosage is 10-100 mg/kg.
  • sodium dichloroacetate is selected from the Active Solar Sonic Infusion-ably Accessible Pharmacological Agents.
  • Dichloroacetate may optionally be given in combination with a pro-apoptotic agent and/or a chemotherapeutic agent.
  • the cancers treated are non-small cell lung cancer, glioblastoma and breast carcinoma.
  • the present invention also provides a combined frequency therapy and hyperthermia therapy including inducing hyperthermia in at least a portion of a target area, a tumor or targeted cancerous cells.
  • Bio- molecules labeled with at least one radionuclide suitable for radiotherapy are provided and introduced into a patient; targeted frequency absorption enhancers provided and introduced into a patient; and a hyperthermia generating frequency signal is directed toward the target cells, warming the radionuclide- labeled bio-molecules and target frequency absorption enhancers bound to target cells.
  • Targeted frequency absorption enhancers may, in a manner of speaking, add one or more frequency absorption frequencies to cells in the target area, which permit a hyperthermia generating frequency signal at that frequency or frequencies to heat the targeted cells.
  • Bio-molecules labeled with at least one radionuclide suitable for radiotherapy may be used for both radiotherapy and as frequency absorption enhancers for the hyperthermia generating frequency signal.
  • the present invention also comprises a charged particle beam path coupling an injector, synchrotron accelerator, beam transport system, targeting system, and/or patient interface method and apparatus.
  • the injector comprises: a negative ion beam source, a two phase ion source vacuum system, an ion beam focusing lens, and/or a tandem accelerator.
  • the synchrotron comprises turning magnets, edge focusing magnets, magnetic field concentration magnets, winding and correction coils, flat magnetic field incident surfaces, and/or extraction elements.
  • the synchrotron, beam transport system, targeting system, and patient interface combine to allow multi-axis/multi-field irradiation, where multi-axis control comprises control of horizontal and vertical beam position, beam energy, and/or beam intensity and multi-field control comprises control of patient rotation and distribution of delivered energy in and about the tumor in a time controlled, targeted, accurate, precise, dosage controlled, and/or efficient manner.
  • the present invention also relates to the use of phytocannabinoids, either in an isolated form or in the form of a botanical drug substance (BDS), as a prophylactic or in the treatment of cancer.
  • the cancer to be treated is a cancer of the: prostate, breast, skin, glioma, colon, lung or a bone or lymph metastasis.
  • the phytocannabinoids is safely used in combination with other Solar Sonic cancer treatment methodologies.
  • the present invention also relates to compositions of immunotoxins, Monoclonal antibody, CD22, CD25, interleukin. More particularly this invention relates to the use of antibody to potentiate the vital activity of the immunotoxins for treatment of cancer.
  • Immunotoxins are antibody-toxin bifunctional molecules that rely on intracellular toxin action to kill target cells.
  • Target specificity is determined via the binding attributes of the chosen antibody.
  • immunotoxins are purpose-built to kill cancer cells as part of novel treatment approaches.
  • Other applications for immunotoxins include immune regulation and the treatment of viral or parasitic diseases.
  • protein toxins of both bacterial and plant origin, joined to antibodies for targeting cancer cells.
  • the invention presents a method for treating a patient suffering from cancer comprising administeringto said patient an amount of a cell cycle arresting drug sufficient to synchronize cell cycles of a plurality of cancer cells in said patient; and subjecting said cellsto mechanical vibrational energy, wherein the cell cycle arresting drug from the group consisting of: gemcytabine, cisplatin, carboplatin, cyclophosphamide, topoisomerase inhibitor, etoposide, 5-fluorouracil, doxorubicin, methotrexate, hydroxyurea, and 3'-azido-3'- deoxythymidine, wherein the mechanical vibrational energy is ultrasound energy having a frequency of about 50 megahertz to about 2 gigahertz, wherein the exposure to mechanical vibrational energy is repeated or sustained over a period of at least one typical cell cycle.
  • the cell cycle arresting drug from the group consisting of: gemcytabine, cisplatin, carboplatin, cyclophosphamide, topo
  • the invention provides a method of treating a patient suffering from cancer comprising administering to said patient an amount of a cell cycle arresting drug sufficient to synchronize cell cycles of a plurality of cancer cells in the patient; administering to the patient a microtubule stabilizing agent; and exposing the patient to mechanical vibrational energy, wherein the microtubule stabilizing agent is selected from the group consis of:taxanes, magnetic taxanes; coumarins, magnetic coumarins, and combinations thereof, wherein the microtubule stabilizing agent is selected from the group consisting of paclitaxel, docetaxel, magnetic derivatives thereof, and combinations thereof, wherein the cell cycle arresting drug is selected from the group consisting of: gemcytabine, cisplatin, carboplatin, cyclophosphamide, topoisomerase inhibitor, etoposide, 5- fluorouracil, doxorubicin, methotrexate, hydroxyurea, and 3'-azido-3'-deoxythym
  • the cell cycle arresting drug is gemcytabine and the microtubule stabilizing agent is a taxane, a coumarin, magnetic derivatives, and combinations thereof, wherein the mechanical vibrational energy is ultrasound energy having a frequency of 50 megahertz to about 2 gigahertz, wherein exposure to mechanical vibrational energy is repeated or sustained over a period of one typical cell cycle and exposure to mechanical Vibrational energy is performed at least 60 minutes after administration of the cell cycle arresting drug, wherein the microtubule stabilizing agent is administered from a drug eluting implant, wherein the implant is a drug eluting stent.
  • the invention provides a process for treating a patient suffering from cancer comprising administering to said patient an amount of a cell cycle arresting drug sufficient to synchronize cell cycles of a plurality of the cancer cells in said patient; administering to the said patient radiation therapy sufficient to stabilize microtubule assembly in said cancer cells; and subjecting said cancer cells to mechanical vibrational energy.
  • the invention provides a method of treating a patient suffering from cancer comprising administering to said patient a cancer cell cycle arresting amount of gemcytabine; administering a microtubule stabilizing agent selected from the group consisting of taxanes, coumarins, magnetic derivatives thereof, and combinations thereof; and exposing the patient to mechanical vibrational energy of frequency of about 50 megahertz to about 2 gigahertz, wherein the microtubule stabilizing agent is selected from the group consisting of paclitaxel, docetaxel, magnetic derivatives thereof, and combinations thereof.
  • the invention provides a method of treating a patient suffering from cancer comprising administering to said patient an amount of a cell cycle arresting drug sufficient to synchronize cell cycles of a plurality of cancer cells in patient; administering to the patient a magnetic microtubule stabilizing agent; applying a localized Magnetic field toincrease the concentration of magnetic microtubule stabilizing agent at a predetermined location in the patient; and exposing the patient to mechanical vibrational energy, wherein the magnetic microtubule stabilizing agent is a magnetic taxane or a magnetic coumarin, wherein the mechanical vibrational energy is ultrasound energy of frequency of about 50 megahertz to about 2 gigahertz, wherein the ultrasound energy is administered to the patient by an intracorporeal device.
  • the invention provides method for treating a cancer associated with hyperpolarized mitochondria which comprising: selecting a patient having a cancer comprising hyperpolarized mitochondria and/or an elevated survivin to Kvl.5 protein ratio relative to a normal control; and administering to said patient in need thereof a therapeutically effective amount of dichloroacetate (DCA) or an acid or salt thereof, wherein the intended dichloroacetate or acid or salt thereof is a salt of dichloroacetic acid.
  • DCA dichloroacetate
  • the dichloroacetate or acid or salt thereof is sodium dichloroacetate
  • the cancer comprising hyperpolarized mitochondria and/or an elevated survivin to Kvl.5 protein ratio relative to a normal control is selected from the group consisting of non-small cell lung cancer, glioblastoma and breast carcinoma
  • the dichloroacetate or acid or salt thereof is administered in the form of a pharmaceutical composition comprising dichloroacetate or acid or salt thereof and a pharmaceutically acceptable carrier, wherein the dichloroacetate or acid or salt thereof is administered orally, wherein 10-100 mg/kg of DCA or acid or salt thereof is administered per day, wherein 10-100 mg/kg of DCA or acid or salt thereof is administered twice per day.
  • a dose is 25-50 mg/kg, wherein a dose is 25-50 mg/kg, wherein the dichloroacetate or acid or salt thereof is administered in combination with another pro-apoptotic agent and/or chemotherapeutic agent, and/or other cancer therapy, wherein the administering of an effective amount of dichloroacetate or acid or salt thereof induces apoptosis and/or reverses apoptosis resistance in a cancer cell of the patient, wherein the administering of an effective amount of dichloroacetate or acid or salt thereof inhibits proliferation ofcancer cells of the patient, wherein the administering of an effective amount of dichloroacetate or acid or salt thereof decreases level of survivin in a cancer cell of the patient.
  • the administering of an effective amount of dichloroacetate or acid or salt thereof increases level of Kvl.5 protein in a cancer cell of the patient, wherein the administering of an effective amount of dichloroacetate or acid or salt thereof increases level of apoptosis-inducing factor (AIF) in a cancer cell of the patient, wherein the administering of an effective amount of dichloroacetate or acid or salt thereof increases level of ⁇ 2 ⁇ 2 ⁇ a cancer cell of the patient, wherein cancer cells, but not normal or non-cancerous cells, of the patient are affected b the administration of dichloroacetate or acid or salt thereof, wherein the dichloroacetate or acid or salt thereof has the formula CH(Cl 2 )-COO-X, wherein X is selected from the group consisting of Na + , K + , CH 3 and OH, wherein the dichloroacetate or acid or salt thereof has the formula CH(C1 2 )— COO ⁇ K + .
  • AIF apoptos
  • the invention also provides a method for delivering a therapeutic substance to a region of tissue in a patient comprising: providing a therapeutic substance to a patient in need of said substance; establishing electrical Field which encompasses a region of tissue within said patient; exposing said region of tissue to said electrical field for a time and under conditions sufficient to permit the permeation of said substance across the cell membranes of cells located within said region of tissue; and administering to said patient at least one agent which is capable of prolonging the permeability of the cell membranes in the tissue exposed to said electrical field in a manner so that said agent does not contact said region of tissue until after the tissue's exposure to the electrical field.
  • the invention also provides a method for delivering a therapeutic substance as recited in claim wherein said agent comprises at least one compound which temporarily decreases cell membrane fluidity.
  • the invention also provides a method for delivering a therapeutic substance as recited in claims wherein said agent comprises at least dexamethasone.
  • a method for delivering a therapeutic substance as recited in claims wherein said therapeutic substance is provided to the patient by direct administration to the region of tissue within said patient _A method for delivering a therapeutic substance as recited in claims.
  • said therapeutic substances are provided to the patient by systemic administration.
  • a method for delivering a therapeutic substance to a region of tissue located in a patient wherein said tissue has been exposed to an electroporation-inducing electrical field the improvement comprising: Contacting said tissue after it has been exposed to said electrical field with at least one agent which is capable of prolonging the permeability of the cell membranes in the tissue exposed to said electrical field.
  • said agent comprises at least one compound which temporarily decreases cell membrane fluidity.
  • said agent comprises at least one member selected from the group consisting of dexamethasone, prednisone, methylprednisolone, progesterone, Angiotensin II and Vitamin E.
  • a method for delivering a therapeutic substance as recited in claims wherein said therapeutic substance is provided to the patient by direct administration to the region of tissue within said patient.
  • a method for delivering a therapeutic substance as recited in claims wherein said therapeutic substance is provided to the patient by systemic administration to the patient.
  • a method for delivering a therapeutic substance as recited in claims wherein said therapeutic substance is provided to the patient by a combination of systemic administration to the patient and direct administration to the region of tissue within said patient.
  • the invention also provides a method for treating multiple myeloma or breast cancer in a subject wherein the subject's multiple myeloma or breast cancer cells are resistant to treatment with a proteasome inhibitor, comprising administering to the subject an effective amount of a second proteasome inhibitor and an effective amount of a therapeutic agent, wherein the therapeutic agent is doxorubicin, such that the multiple myeloma or breast cancer is treated, wherein the treatment of cancer is due to the inhibition of tumor growth, wherein the proteasome inhibitor and/or the second proteasome inhibitor is PS-341.
  • the second proteasome inhibitor is administered prior to the administration of the therapeutic agent, simultaneously with the administration of the therapeutic agent, or after the administration of the therapeutic agent, wherein the second proteasome inhibitor inhibits NF- ⁇ activity or abolishes cell adhesion mediated drug-resistance, wherein the administration of an effective amount of the second proteasome inhibitor and an effective amount of the therapeutic agent results in cancer cell death, apoptosis of cancercells, or modulation of the response to genotoxic stress, wherein the second proteasome inhibitor modulates a DNA-dependant protein kinase, wherein the second proteasome inhibitor and the therapeutic agent are administered intravenously, intraperitoneally.
  • the second proteasome inhibitor is administered at a dose of about 0.001 mg/m 2 body surface area/day to about 4.0 mg/m 2 body surface area/day, wherein the treatment of cancer is due to the inhibition of tumor growth, wherein the proteasome inhibitor and/or the second proteasome inhibitor is PS-341, wherein the second proteasome inhibitor is administered prior to the administration of the therapeutic agent, simultaneously with the administration of the therapeutic agent, or after the administration of the therapeutic agent.
  • the second proteasome inhibitor inhibits NF- ⁇ activity or abolishes cell adhesion mediated drug- resistance, wherein the administration of an effective amount of the second proteasome inhibitor and an effective amount of the therapeutic agent results in cancer cell death, apoptosis of cancer cells, or modulation of the response to genotoxic stress, wherein the second proteasome inhibitor modulates a DNA-dependant protein kinase, wherein the second proteasome inhibitor and the Therapeutic agent are administered intravenously, intraperitoneally, or orally, wherein the proteasome inhibitor and the second proteasome inhibitor are the same, wherein the proteasome inhibitor and the second proteasome inhibitor are the same, wherein the proteasome inhibitor and the second proteasome inhibitor are different, wherein the proteasome inhibitor and the second proteasome inhibitor are different.
  • Immunotoxins are proteins contain a toxin along with an antibody or growth factor that binds specifically to target cells. Nearly all protein toxins work by enzymatically inhibiting protein synthesis. And so, for the immunotoxin to work, it must bind to and be internalized by the target cells, and the enzymatic fragment of the toxin must translocate to the cytosol. Once in the cytosol, 1 molecule is capable of killing a cell, making immunotoxins some of the most potent killing agents.
  • Various plants and bacterial toxins have been genetically fused or chemically conjugated to ligands that bind to cancer cells. Among the most active clinically are those that bind to hematologic tumors.
  • the inventive method further comprises administering a dose of one or more therapeutic pharmacological agents, a pharmaceutically acceptable carrier with other simultaneous applications of approved pharmaceutical agents and chemotherapeutic agents onto the area of the tumor to a patient over the therapeutic period.
  • Suitable Agents are the ones that are Solar Sonic Infusion-ably accessible and compatible to the patient's present condition and needs.
  • Solar Sonic Laboratories have systematically divided the most suitable therapeutic pharmacological agents to be intravenously infused into all cancer patients into Seven Substantial Group List (SSGL), each group represents certain types of cancer.
  • SSGL Seven Substantial Group List
  • CCD Chemical Common Denominators
  • CCD Chemical Common Denominators
  • Natural tissues are composed of functionally diverse cell types that are organized in spatially complex arrangements. Organogenesis of complex tissues requires a coordinated sequential transformation process, with individual stages involving time-dependent expression of cell-cell, cell-matrix, and cell-signal interactions in three dimensions.
  • PTA precursor tissue analog
  • the goal of PTA in tissue engineering is not to fabricate the final transplantable tissue but rather to guide the dynamic organization, maturation, and remodeling leading to the formation of normal and functional tissues.
  • Structural, mechanical, physiological requirements of the PTA as a temporary scaffold must be met by a fabrication method with flexibility.
  • the fabrication incorporating biological materials like living cells/plasmid DNA has been addressed.
  • the PTA concept is considered suitable for future tissue engineering and the use of undifferentiated stem cells, and may possess a capability.
  • Solar Sonic Technologies have perfected the science of Electromagnetically Bio-Chemical Intracellular and pathogenic communication and signaling, to the extent that we can affect intracellular and pathogenic programming, signaling, Pathogenic communication and manipulation leading to Homeostasis or Apoptosis.
  • Fiber-Optic Micro-needle is utilized with Solar Sonic Cancer Cure Device to deliver pharmacologically infused composition or for the swift delivery of advanced Nano-particles or entertaining as such Solar Sonic DNA and Cell Reprogramming Via Epigenetic Information swiftly Delivered by Magnetic Fields, Sound Vibration and Coherent Hydrogen Molecules.
  • Solar Sonic Therapeutic Infusion Medical Device chemically promotes Pulsed Suppression of Mitochondrials Channel Axis in Cancer, Inducing Apoptosis and Inhibiting Cancer Growth.
  • Solar Sonic Curative Cancer Medical Device is proven to work reproducibly as a Super Hi-Tech Solar Sonic Multidimensional Medical Science of the Paranormal Cellular/Pathogenic Bio-Signaling Communications and Programming Technology, the medical device converts Multi-Drug Components from Cytotoxic to Antitoxic.
  • Solar Sonic Laser Needles and pulsed electromagnetic fields are permeating for the administration of the SSF Therapeutic Infusion Composition Protocols for the eradication of carcinogenic cells.
  • the intracellular and pathogenic Bio-communications, and regenerative human physiology via SSF Paranormal Homeostasis and Induced Apoptosis are leading the way in combating pathogens.
  • Solar Sonic Therapeutic Infusion Medical Device Electrochemically promotes Pulsed Suppression of Mitochondria-K + Channel Axis in Cancer, Inducing Apoptosis and Inhibiting Cancer Growth.
  • cells are intelligent, molecules and their genes would be the collaborators or even slaves but not the masters of the life functions of cells. If cells are intelligent, medical treatment may involve 'talking to cells rather than to flood the organism with pharmaceuticals as we do today and they are intelligent. If cells respond to signals rather than to exogenous forces, the forces that keep or change the direction of their bodies must be controlled from within.
  • Solar Sonic Quantum Frequency Waves induce self- destruction of cells via Bio-signaling communications eradicating carcinogenic cells.
  • BCG vaccine is used for boosting of immunity of individuals with cancer. This has not been well accepted as a mode of therapy due to inconclusive results. The only accepted method of BCG is to use it for bladder cancer by way of intravesicular therapy.
  • the disadvantage associated with use of BCG is practical development of systemic tuberculosis caused by BCG. This is related to the fact that BCG contain live organism and they can be pathogenic to immunocompromised host.
  • the present invention relates to a medical device especially designed to treat cancer patients with their various needs.
  • the invention also relates to varied tumor treatment methods, the medical device with all of its accompanying therapeutic infusion composition and other supporting capabilities can be used in oncology for the treatment of primary and metastatic tumors.
  • the medical device and the infusion composition are specifically designed to positively interact in all treatments related to cancer, either early or late stages, metastasis & malignancies.
  • the present invention relates to the design and generation of dendritic cell-based, in vivo antigen targeting vaccines for therapy of cancer, such as multiple myeloma.
  • the vaccines are generated by the SSQFV method, in which effector moieties are attached to anchoring domain, derived from AKAP proteins and dimerization and docking domain moieties derived from protein kinase A (PKA).
  • SSQFV complexes are generated when dimerization and docking domain moieties spontaneously dimerize and bind to an anchoring domain moiety, resulting in a complex with a 2:1 stoichiometry between-linked effectors.
  • the effector moieties comprise a humanized anti-CD74 antibody and a tumor-associated xenoantigen, such as a CD20 xenoantigen.
  • the anti-CD74 antibody is an hLLl antibody.
  • the SSQF/CC constructs are of use for preparation of pharmaceutical compositions, for generation of chemical complex against cancers, such as multiple myeloma (MM), and for induction of an immune response against tumor antigen-expressing cells, such as CD20 positive cancer cells in patients with multiple myeloma or other CD20-expressing cancers.
  • the present invention also relates to the a process for treating a biological organism in which a cell cycle arresting drug is administered to the organism to produce synchronized cells, optionally the microtubules within the synchronized cells are stabilized by means of microtubule stabilizing agent & synchronized cells with the optionally stabilized microtubules are then contacted with mechanical vibrational energy, such as ultrasound energy.
  • mechanical vibrational energy such as ultrasound energy.
  • Multiple myeloma is a hematological malignancy characterized by clonal proliferation of neoplastic plasma cells in the bone marrow. Although responsive to many chemotherapeutic agents, MM remains largely incurable and the majority of patients ultimately relapse.
  • MM cancer stem cells are refractory to multiple chemotherapeutic drugs and responsible for tumor re-growth and relapse.
  • cancer stem cells such as MM stem cells
  • immunotherapy and vaccination may offer a potential modality to eradicate these cells, particularly after standard therapies and/or stem cell transplantation, the time when tumor load is greatly reduced.
  • the present invention also relates to the field of immunotherapy for cancers, and more particularly to monoclonal antibodies which specifically target an epitope expressed on cancer cells.
  • Cancer is a class of diseases which occurs because cells become immortalized; they fail to heed customary signals to turn off growth which is a normal function of remodeling in the body that requires cells to die on cue. Apoptosis or programmed cell death, can become defective, when this happen malignant transformation can take place.
  • the immortalized cells grow beyond their normal limits and invade adjacent tissues. The malignant cells may also metastasize and spread to other locations in the body via the bloodstream or lymphatic system. Cancer cells often form a mass known as a tumor.
  • cancers can start in any type of body tissue although many cancers will metastasize into other body tissues.
  • causes of cancer include; carcinogens, age, genetic mutations, immune system problems, diet, weight, lifestyle, environmental factors such as pollutants, some viruses for example the human papilloma virus (HPV) is implicated in cervical cancer and some bacterial infections are also known to cause cancers.
  • HPV human papilloma virus
  • treatment options for cancer is often determined by the type and stage of the cancer.
  • Treatment options include; chemotherapeutic drug treatment, hormonal drug treatment, radiotherapy, surgery, complementary therapies and combinations thereof.
  • Prostate cancer is the most common type of cancer in men and accounts for 24% of all UK male cancers. In 2006 there were over 35,000 new cases of prostate cancer diagnosed in the UK alone. The prostate is a gland in the male reproductive system and symptoms of cancerin the prostate can include pain, difficulty urinating, problems with sexual intercourse and erectile dysfunction. Prostate cancer may metastasise to the bones and or lymph nodes.
  • Treatment options for prostate cancer include surgery, radiation therapy, and Chemotherapy and hormone treatment.
  • Hormone treatment usually involves treatment with an anti-androgen such as cyproterone acetate, flutamide or bicalutamide, either alone or in combination with a chemotherapeutic agent. These treatments work to stop the production of testosterone (androgen) which can slow down tumor growth or even shrink the tumor.
  • an anti-androgen such as cyproterone acetate, flutamide or bicalutamide, either alone or in combination with a chemotherapeutic agent.
  • prostate cancer cells While the prostate cancer cells are responding to anti-androgens, they are referred to as 'hormone-sensitive' prostate cancer. Unfortunately, after a few years of treatment with anti-androgens the prostate cancer stops responding to hormone treatment and is termed 'hormone-insensitive' prostate cancer, and at this stage the cancer growth cannot be controlled by the hormone treatment.
  • the cell line LNCaP is hormone- sensitive prostate cancer cells which were derived from a supraclavicular lymph node metastasis in a 50 year.
  • the cell line DU-145 is hormone-insensitive prostate cancer cells which were derived from a brain metastasis. It is known that expression levels of both cannabinoid receptors, CB1 and CB2, were significantly higher in CA-human papillomavirus-10 (virally transformed cells derived from adeno-carcinoma of human prostate tissue), and other human prostate cells LNCaP, DU-145, PC3, and CWR22RN1 than in human prostate epithelial and PZ-HPV-7 (virally transformed cells derived from normal human prostate tissue) cells.
  • CB1 and CB2 cannabinoid receptors
  • Cannabis has been ascribed to be both a carcinogen and anti-cancer agent.
  • smoking cannabis is known to be carcinogenic as the cannabis smoke contains at least 50 different known carcinogenic compounds, many of which are the same substances found in smoked tobacco.
  • benzopyrene is known to cause cancer as it alters a gene called p53, which is a tumor suppressor gene.
  • Cannabis contains the substance tetrahydrocannabinol (THC) which has been shown to cause benzopyrene to promote the p53 gene to change.
  • THC tetrahydrocannabinol
  • cannabinoids including THC and cannabidiol (CBD) are able to promote re-emergence of apoptosis so that some tumors will heed the signals, stop dividing, and die.
  • CBD cannabidiol
  • the process of apoptosis is judged by observation of several phenomena including: reduced cellular volume, condensation of nuclear chromatin, changes in distribution of phospholipids in plasma membrane phospholipids, and cleavage of chromatin into DNA fragments called DNA ladders.
  • Another method by which tumours grow is by ensuring that they are nourished: they send out signals to promote angiogenesis, the growth of new blood vessels.
  • Cannabinoids may turn off these signals as well. Cannabinoids have been shown to have an anti-proliferative effect on different cancer cell lines.
  • the cannabinoids THC, THCA, CBD, CBD A, CBG and CBC and the cannabinoid BDS THC and CBD were tested on eight different cell lines including DU-145 (hormone- sensitive prostate cancer), MDA-MB-231 (breastcancer), CaCo-2 (colorectal cancer) and C6 (glioma cells).
  • TRPM8 transient receptor potential channels have been implicated in survival, growth and spread of prostate and other cancers.
  • TRPM8 is expressed in sensory neurons, where it responds to cold and to cooling agents, notably menthol, but it is also abundantly expressed in the prostate.
  • TRPM8 is over-expressed in hormone-sensitive prostate cancer cells, expression of TRPM8 is almost completely ablated once the cancer becomes hormone-insensitive and in patients receiving anti- androgen therapy.
  • TRPM8 is stimulated by androgens in hormone-sensitive prostate cancer cell lines (LNCaP). There is evidence that expression of TRPM8 is required for survival of prostate cancer cells. The mechanism of such an action of TRPM8 is likely to relate to its ability to modulate intracellular calcium, and possibly even the distribution of calcium within the cell. The latter point may be important because of the localization of TRPM8 in the prostate cancer cell.
  • TRPM8 receptor While found on the cell membrane, it is also found on the endoplasmic reticulum; thus any potential therapeutic agent which targets the TRPM8 receptor must be able to gain good access to the intracellular space.
  • the endogenous cannabinoid anandamide has been shown to antagonise TRPM8. The authors also showed stimulation of CBl receptors transiently antagonised TRPM8 receptors expressed on the same cells.
  • the diseases/conditions to be prevented or treated include: neuropathic pain, inflammation, vasoconstriction or cancer.
  • the TRPM8 receptor has also been found in breast, colon and skin cancers. It has been shown that CBD is able to able to down-regulate the expression of the DNA binding protein inhibitor, Id-1 in human breast cancer cells.
  • the CBD concentrations effective at inhibiting Id-1 expression correlated with those used to inhibit the proliferative and invasive phenotype of breast cancer cells. CBD was able to inhibit Id-1 expression at the mRNA and protein level in a concentration-dependent fashion.
  • CBD has also been shown to inhibit human cancer cell proliferation and invasion through differential modulation of the ERK and ROS pathways and that sustained activation of the ERK pathway leads to down-regulation of Id-1 expression. It was also demonstrated that CBD up-regulates the pro-differentiation agent, Id-2. Using a mouse 4T1 cell line and a model of metastatic breast cancer, CBD significantly reduced metastatic spread. As such CBD may represent a promising treatment of breast cancer in patients with secondary tumours. Recent evidence indicates that CBD is a GPR55 antagonist; this raises the possibility that this receptor may underlie the effects of CBD on breast and other tumour cells.
  • GPR55 couples to G12/13 and the downstream activation of the RhoA, racl and cdc42 small GTPases; this pathway is crucial in cytoskeletal reorganisation and cell migration.
  • Increased G 12/13 expression has been found in early stage human breast cancer cells taken by biopsy and inhibition of G13 decreases the level of breast cancer cell metastasis in vivo.
  • the anti-proliferative effects of CBD have also been evaluated on U87 and U373 human glioma cell lines.
  • the anti-proliferative effect of CBD was correlated to induction of apoptosis, as determined by cytofluorimetric analysis and single-strand DNA staining, which was not reverted by cannabinoid antagonists.
  • CBD administered s.c. to nude mice at the dose of 0.5 mg mouse, significantly inhibited the growth of subcutaneously implanted U87 human glioma cells.
  • CBD was able to produce a significant anti-tumour activity both in vitro and in vivo, thus suggesting a possible application of CBD as a chemotherapeutic agent.
  • CBD caused a concentration-dependent inhibition of the migration of U87 glioma cells, quantified in a Boyden chamber. Since these cells express both cannabinoid CBl and CB2 receptors in the membrane, the group also evaluated their engagement in the anti-migratory effect of CBD.
  • Cannabinoids have been shown to play a fundamental role in the control of cell survival / cell death. It has been reported cannabinoids may induce proliferation, growth arrest, or apoptosis in a number of cells, including neurons, lymphocytes, and various transformed Neural and non-neural cells, and that cannabinoids induce apoptosis of glioma cells in culture and regression of malignant gliomas in vivo.
  • the cancer to be treated is a brain tumour, more particularly a glioma; more particularly still a glioblastoma multiforme (GBM).
  • the non- cannabinoid chemotherapeutic agent may be a selective estrogen receptor modulator or an alkylating agent.
  • a platform of data representing the use of isolated phytocannabinoids and phytocannabinoid botanical drug substances (BDS) in different aspects of the treatment of cancer is provided and the results extrapolated to identify groups of phytocannabinoids, whether isolated or in the form of a BDS, which appear more promising than others in specific treatments.
  • electroporation may provide a feasible method for the transfection of genetic material into living cells in tissue.
  • electroporation therapy for the transmembrane delivery of therapeutic substances is dependent on achieving two necessary and sufficient conditions in the region to be treated:
  • Threshold level electrical fields must be generated throughout the target tissue. While a significant amount of research has been performed demonstrating the utility of electroporation in the treatment of various animal and human tumor models. There is limited understanding regarding the best methods for the clinical application of electroporation therapy. In the field of cancer treatment, delivery of therapeutic substances is made more difficult by the anatomical characteristics of solid tumors such as non uniform vasculature and high interstitial pressure. These properties make it difficult to achieve uniform, high concentrations of therapeutic substances within the tumor. The tortuous, non-uniform vasculature prevents blood borne substances from reaching all parts of the tumor.
  • membrane permeability occurs as a result of exposing a cell to threshold level electric field strengths, an electroporation therapy is dependent on propagating these fields throughout a target region of tissue and allowing concentrations of the desired substances to accumulate intracellularly.
  • the invention provides methods to facilitate the intracellular delivery of substances via electroporation. In particular, these methods can be applied to improve benefit derived from the application of electroporation therapy to diseased tissue.
  • the invention provides for delivering a therapeutic substance to a predetermined location in a patient comprising providing a therapeutic substance to a patient in need of the substance, establishing an electrical field which encompasses a predetermined region of tissue within the patient.
  • Use of the invention facilitates the transport of certain therapeutic substances to their site of action, inside the cell. Even under unfavorable conditions, such as low concentrations of therapeutic substance within the target tissue and substance with a large or irregularly shaped molecular structure, the present techniques can be effective in the delivery of therapeutic substances.
  • this invention provides a method for the concentration of therapeutic substances within a diseased region of tissue. Utilization of this technique improves the efficacy of electroporation mediated delivery while minimizing side effects associated with the administration of cytotoxic substances.
  • a further aspect of this invention provides a method for the use of substances capable of prolonging the permeabi!ized state of the cell membrane, dramatically improving the intracellular delivery of therapeutic substances.
  • Electro-poration is a significant increase in the electrical conductivity and permeability of the cell plasma membrane caused by an externally applied electrical field. It is usually used in molecular biology as a way of introducing some substance into a cell, such as loading it with a molecular probe, a drug that can change the cell's function, or a piece of coding DNA. Electroporation is a dynamic phenomenon that depends on the local trans-membrane voltage at each point on the cell membrane. It is generally accepted that for a given pulse duration and shape, a specific transmembrane voltage threshold exists for the manifestation of the electroporation phenomenon (from 0.5 V to 1 V). This leads to the definition of an electric field magnitude threshold for electroporation (E, h ).
  • E ir irreversible electroporation
  • the walls are naturally porous and only act as stiff shells that protect bacteria from severe environmental impacts. If bacteria and plasmids are mixed together, the plasmids can be transferred into the cell after electroporation. Several hundred volts across a distance of several millimeters are typically used in this process.
  • transfection The process of introducing foreign DNAs into eukaryotic cells is known as transfection. Electroporation is highly effective for transfecting cells in suspension using electroporation cuvettes. Electroporation has proven efficient for use on tissues in vivo, for in utero applications as well as in ovo transfection. Adherent cells can also be transfected using electroporation, providing researchers with an alternative to trypsinizing their cells prior to transfection.
  • the present invention relates to the field of immunotherapy for cancers, and more particularly to monoclonal antibodies which specifically target an epitope expressed on cancer cells.
  • ADCC antibody-dependent cell- mediated cytotoxicity
  • CDC complement-dependent cytotoxicity
  • therapy-resistance in cancer is frequently associated with de-regulation in the mechanisms that control apoptosis.
  • cancer cells are often reliant on these molecular aberrations for survival. Therefore, selective induction of apoptosis, CDC and ADCC in cancer cells but not normal cells is a challenge to be addressed.
  • TRAIL tumor necrosis factor
  • TNF tumor necrosis factor
  • TRAIL tumor necrosis factor-related apoptosis-inducing ligand
  • mAb monoclonal antibodies
  • Fab fragment antigen binding
  • Monoclonal antibody drugs are a relatively new innovation in cancer treatment. While several Monoclonal antibody drugs are available for treating certain cancers, the best way to use these new drugs isn't always clear. The immune system attacks foreign invaders in our body, but it doesn't always recognize cancer cells as enemies. A monoclonal antibody can be directed to attach to certain parts of a cancer cell. In this way, the antibody marks the cancer cell and makes it easier for the immune system to find. Monoclonal antibody developed to the specific cancer cell surface target can kill the cell with or without toxin attached just by binding to cell surface target.
  • the antibody can initiate lysis of the cancer cell through apoptosis, CDC and ADCC.
  • Monoclonal antibody therapy can be used to destroy malignant tumor cells and prevent tumor growth by- blocking specific cell receptors or by delivering a conjugated toxin.
  • Paclitaxel is a complex diterpenoid that is widely used as an anti-mitotic agent; it consists of a bulky, fused ring system and an extended side chain that is required for its activity.
  • paclitaxel Trigger Anticancer Agents: Basic Science and Current Status
  • the aqueous solubility of paclitaxel is relatively low, estimates of paclitaxel solubility vary widely, ranging from about 30 micrograms per milliliter and about 7 micrograms per milliliter to less than 0.7 micrograms per milliliter.
  • the molecular weight of paclitaxel is in excess of 700; this relatively high molecular weight is one factor according to the well-known "rule of 5,” contributes to paclitaxel poor water solubility. It is an object of this invention invention to provide such an agent, in particular, and in one embodiment, it is an object of this to provide a magnetic anti-mitotic composition that can be directed to be more toxic to cancer cells than normal cells.
  • Important breakthroughs in cancer therapy include clinical application of antibodies.
  • the therapeutic strategy relies on the deliberate and selective induction of apoptosis or killing by ADCC and CDC of malignant cells.
  • TRAIL tumor necrosis factor
  • mAb monoclonal antibodies
  • Such mAb could, also be modified for delivery of a toxin, radioisotope, cytokine or other active conjugate.
  • bispecific antibodies that can bind with their Fab regions both to target antigen and to a conjugate or effector cell.
  • Monoclonal antibody drugs are a relatively new innovation in cancer treatment. While several monoclonal antibody drugs are available for treating certain cancers, the best way to use these new drugs isn't always clear.
  • a monoclonal antibody can be directed to attach to certain parts of a cancer cell. In this way, the antibody marks the cancer cell and makes it easier for the immune system to find.
  • Monoclonal antibody developed to the specific cancer cell surface target can kill the cell with or without toxin attached by binding to cell surface target. The antibody can initiate lysis of the cancer cell through apoptosis, complement dependent cytotocxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC).
  • Monoclonal antibody therapy can be used to destroy malignant tumor cells and prevent tumor growth by blocking specific cell receptors or by delivering a conjugated toxin.
  • the principal tumor treatment methods include surgical, chemotherapeutic, and radiation approaches. Surgical approach is efficient in cases of early diagnosis and smaller tumors without remote metastases. Large, advanced tumors may be removed only in rare cases, and this approach is often impossible.
  • the preferred method of conservative treatment of malignant tumors includes selective chemotherapy performed by injection of antitumor preparations into the blood vessels that supply the tumor, or directly into the tumor tissue or peritumoral region.
  • Known in the art is the method of treatment of malignant kidney tumors including chemoembolization of arterial network of the diseased kidney using an oil solution containing 100 mg of the anticancer substance Dioxadet, followed by occlusion of the main branch of the renal artery by a metal coil.
  • Such chemoembolization leads to a reliable increase in the corrected indices of 3- and 5-year cumulative survival in patients with inoperable cancer of kidney parenchyma to 33.0 ⁇ 6.9% and 24.5 ⁇ 6.75 respectively, in comparison with the convenient embolization methods without a chemotherapeutic component, where these indices are 10.6 ⁇ 4.2% and 0%.
  • Intra-arterial infusion of chemo-therapeutic agents provides better results as compared to intraportal infusion, since malignant tumors of the liver are supplied mainly by the arterial blood system. Therefore the intra-arterial injection received wider application. According to the inventors' data, remissions last up to 6-8 months, and one-year survival in patients with unresectable malignant tumors was 56.2%. The duration of remissions reported in the world medical literature for selective chemotherapy is 4-12 months. Anticancer substances are known to be toxic, especially when used systemically.
  • Chemotherapeutic agent is administered into hepatic artery within the mixture containing a solution of carboxymethylcellulose or dextrane in a saline aqueous medium, and magnetically soft substance, metal iron, in the form of particles 30-50 mem in size.
  • the composition is confined within the tumor area by a local magnetic field. Hyperthermia is performed by induction heating of the magnetic particles. However, the large size of particles necessary for efficient induction heating (30-50 mem) causes occlusion of the precapillary zone of the tumor. Therefore the prerequisites are created for preservation of viable parts of the tumor. Magnetically soft material may migrate out of the tumor area and dissipate in the course of tumor degradation. This phenomenon may lead to undesirable micro-embolizations.
  • the use of water-based solutions of chemotherapeutic agents is known to provide a less pronounced prolongation effect because of the faster diffusion into tissues with consequent washing out of the organ. This process is increased by preserved organ blood flow.
  • the principal object of this invention is to provide a method for targeted and selective killing of cancer cells, wherein the killing' may be induced by apoptosis, ADCC and CDC of cancer cells.
  • Another object of the invention is to provide a method for selective elimination of cancer cells without affecting the normal cell, population.
  • the main objective of the present invention is to reduce the probability of recurrence of a tumor and of the off spread of metastases.
  • Another objective of the invention is to reduce systemic toxicity of the treatment.
  • the main and other objectives are achieved by the method for tumor treatment which involves first catheterization of the vessel that supplies a tumor of interest. Then, a suspension of a magnetically hard ferromagnetic substance in an oil solution of oil-soluble antitumor agent is injected through the catheter under fluoroscopic control and, at the same time, local magnetic field is applied onto the tumor-bearing area.
  • the tumor is subjected to oscillating power field selected from ultrahigh radio frequency electromagnetic field and the field of ultrasonic contraction waves until the temperature of 43.0°-43.5° C. is reached within the tumor, this temperature is maintained for 5-45 minutes.Jn cases of large size tumors it is preferable, according to the invention, to reduce the blood flow in the tumor-feeding blood vessel after the administration thereto of the said suspension.
  • oscillating power field selected from ultrahigh radio frequency electromagnetic field and the field of ultrasonic contraction waves until the temperature of 43.0°-43.5° C. is reached within the tumor, this temperature is maintained for 5-45 minutes.Jn cases of large size tumors it is preferable, according to the invention, to reduce the blood flow in the tumor-feeding blood vessel after the administration thereto of the said suspension.
  • the magnetically hard ferromagnetic substance preferably includes non-toxic non-corrosive iron containing material such as strontium hexaferrite (Sr0.6Fe 2 0 3 ) in the form of particles 0.5-7 mem in size, which allow the ferromagnetic to penetrate also into capillary part of a tumor vasculature.
  • strontium hexaferrite Sr0.6Fe 2 0 3
  • the application of local magnetic field serves not only to confine the embolization within the tumor area, but also to form a compact, porous body of the ferromagnetic particles held together by magnetic forces, owing to the high residual magnetism of the hard ferromagnetic material.
  • Such a compact magnetic system can withstand considerable hydrostatic pressure and provides reliable retention of the liquid phase of the embolizate within the tumor vasculature for a long time, without recanalization and dissipation of both ferromagnetic and liquid phase throughout the body. Therefore the antitumor agent is uniformly distributed within the tumor, while its systemic concentration is strongly reduced, and therapeutic index is improved.
  • This advantage is supported by the delivery of the antitumor agent in the form of an oil solution which is better retained within the embolizate due to its Immiscibility with tissue and body fluids.
  • the stability of embolizate within the whole tumor-feeding vasculature in combination with prolonged chemotherapy and hyperthermia of a tumor reduces the proportion of viable tumor cells, prevents their migration outside the embolized area and therefore decreases the metastatic off spread.
  • the antitumor agent as well as the products of tumor tissue degradation, are prevented from migration outside the tumor focus; therefore toxic effects of the antitumor chemotherapeutic agent and of the tumor degradation products are substantially reduced.
  • a process for treating a biological organism in which a cell cycle arresting drug is administered to the organism to produce synchronized cells, optionally the microtubules within the Synchronized cells are stabilized by means of a microtubule stabilizing agent, and the synchronized cells with the optionally stabilized microtubules are then contacted with mechanical vibrational energy.
  • the present invention also discloses methods and compositions for vaccines against cancer stem cells, such as MM stem cells, that are prepared using the SSQF method.
  • the SSQF technique has been used to generate a variety of stable and defined complexes suitable for in vivo applications.
  • the SSQF complexes comprise an anti-CD74 antibody or antigen binding fragment thereof, such as the hLLl antibody, attached to a dimerization and docking domain or anchor domain moiety.
  • the dimerization and docking domain moieties spontaneously dimerize and each dimer binds to an anchoring domain moiety.
  • a complementary moiety is attached to a CD20 xenoantigen, as described, resulting in formation of SSQF complexes comprising anti-CD74 moieties and CD20 xenoantigen moieties.
  • the antibody component directs the SSQF complex to antigen presenting cells (APCs), such as dendritic cells (DCs), while the xenoantigen component is processed to invoke an immune response against cells expressing the target antigen.
  • APCs antigen presenting cells
  • DCs dendritic cells
  • CD20 xenoantigens suitable for use in the anti-cancer vaccine SSQF complex are known in the art, such as the murine CD20 sequence.
  • Other CD20 amino acid sequences of potential use are readily available to the skilled artisan through well-known public databases as the NCBI protein database.
  • CD20 amino acid sequences are known and readily available from a wide variety of species and can be incorporated into the anti-cancer vaccine SSQF complex.
  • TAAs tumor-associated antigens
  • the Antibody binds to an antigen expressed by APCs, more preferably dendritic cells.
  • a variety of antigens associated with dendritic cells are known in the art, including but not limited to CD209 (DC-SIGN), CD34, CD74, CD205, TLR 2, TLR 4, TLR 7, TLR 9, BDCA-2, BDCA-3, BDCA-4, and HLA-DR.
  • the target antigen is CD74.
  • other types of target antigen are known to be associated with dendritic cells and anti-cancer vaccine SSQF constructs incorporating antibodies that target any such alternative antigen may be utilized in the claimed methods and compositions.
  • the anti-cancer vaccine SSQF comprise an anti-CD74 antibody or antigen-binding fragment thereof and another anti-dendritic cell antibody or fragment.
  • the use of chimeric antibodies is preferred because they possess human antibody constant region sequences and therefore do not elicit as strong a human anti-mouse antibody (HAMA) response as murine antibodies.
  • HAMA human anti-mouse antibody
  • the use of humanized antibodies is even more preferred, in order to further reduce the possibility of inducing a HAMA reaction.
  • the anti-cancer vaccine SSQFV constructs may be administered in combination with at least one therapeutic agent administered before, simultaneously with or after the anti-cancer vaccine construct.
  • the therapeutic agent is administered before the anti-cancer vaccine.
  • the therapeutic agent may be co-administered with or even conjugated to the SSQFV construct.
  • Any therapeutic agent known in the art, as discussed in more detail below, may be utilized in conjunction with an anti-cancer vaccine SSQFV, including but not limited to radionuclides, immunomodulators, anti-angiogenic agents, cytokines, chemokines, growth factors, hormones, drugs, prodrugs, enzymes, oligonucleotides, siRNAs, pro-apoptotic agents, photoactive therapeutic agents, cytotoxic agents, chemotherapeutic agents, toxins, other antibodies or antigen binding fragments thereof.
  • the therapeutic agent is a cytotoxic agent, such as a drug or a toxin.
  • the drug is selected from the group consisting of nitrogen mustards, ethylenimine derivatives, alkyl sulfonates, nitrosoureas, gemcitabine, triazenes, folic acid analogs, anthracyclines, taxanes, COX-2 inhibitors, pyrimidine analogs, purine analogs, antibiotics, enzyme inhibitors, epipodophyllotoxins, coordination complexes, vinca alkaloids, substituted ureas, methyl hydrazine derivatives, adrenocortical suppressants, hormone antagonists, endostatin, taxols, camptothecins, SN-38, doxorubicins /analogs, Antimetabolites, alkylating agents, antimitotics, anti-angiogenic agents, tyrosine kinase inhibitors, mTOR inhibitors, heat
  • the therapeutic agent is a toxin selected from the group consisting of ricin, abrin, alpha toxin, saporin, ribonuclease (R ase), DNase I, Staphylococcal enterotoxin-A, pokeweed antiviral protein, gelonin, diphtheria toxin, Pseudomonas exotoxin, and Pseudomonas endotoxin and combinations thereof, or an immunomodulator selected from the group consisting of a cytokine, a stem cell growth factor, a lymphotoxin, a hematopoietic factor, a colony stimulating factor (CSF), an interferon (IFN), a stem cell growth factor, erythropoietin, thrombopoietin and a combinations thereof.
  • ricin abrin, alpha toxin, saporin, ribonuclease (R ase), DNase I, Staphylococcal enter
  • the therapeutic agent is a photoactive therapeutic agent selected from the group consisting of chromogens and dyes.
  • the therapeutic agent is an enzyme selected from the group consisting of ma late dehydrogenase, staphylococcal nuclease, delta-V-steroid isomerase, yeast alcohol dehydrogenase, alpha-glycerophosphate dehydrogenase, triose phosphate isomerase, horseradish peroxidase, alkaline phosphatase, asparaginase, glucose oxidase, beta-galactosidase, ribonuclease, urease, catalase, glucose-6-phosphate dehydrogenase, glucoamylase and acetylcholinesterase.
  • Such enzymes may be used, for example, in combination with prodrugs that are administered in relatively non-toxic form and converted at the target site by the enzyme into a cytotoxic agent.
  • a drug may be converted into less toxic form by endogenous enzymes in the subject but may be reconverted into a cytotoxic form by the therapeutic enzyme.
  • the anti-cancer vaccine SSQFV complexes are of use for therapy of multiple myeloma
  • a CD20/anti-CD74 construct may potentially be of use for other types of diseases, such as other forms of CD20 + cancer like B-cell lymphoma, B-cell leukemia, acute lymphoblastic leukemia, chronic lymphocytic leukemia, follicular lymphoma, mantle cell lymphoma, small lymphocytic lymphoma, diffuse B-cell lymphoma, marginal zone lymphoma, Burkitt lymphoma, Hodgkin's lymphoma or non-Hodgkin's lymphoma.
  • a tumor-associated xenoantigen other than CD20 is used, the skilled artisan will realize that any type of cancer with an associated TAA may be targeted using the SSQFV. Still other embodiments relate to DNA sequences encoding fusion proteins, such as antibody-DDD or xenoantigen-DDD fusion proteins or antibody- AD or xenoantigen-AD fusion proteins, vectors and host cells containing the DNA sequences, and methods of making fusion proteins for the production of anti-cancer vaccine SSQFV constructs.
  • fusion proteins such as antibody-DDD or xenoantigen-DDD fusion proteins or antibody- AD or xenoantigen-AD fusion proteins
  • fusion proteins of use for making anti-Cancer Vaccine SSQFV constructs include fusion proteins of use for making anti-Cancer Vaccine SSQFV constructs, antibody-DDD or xenoantigen-DDD fusion proteins or antibody-AD or xenoantigen-AD fusion proteins.
  • the subunit components of the SSQFV complex may be formed by chemical cross- linking of, an antibody or antibody fragment and a DDD peptide, or a CD20 xenoantigen and an AD peptide for example.
  • the diagnostic agent is a fluorescent labeling compound selected from the group consisting of fluorescein isothiocyanate, rhodamine, phycoerytherin, phycocyanin, allophycocyanin, o- phthaldehyde and fluoresce mine, a chemiluminescent labeling compound selected from the group consisting of luminol, isoluminol, an aromatic acridinium ester, an imidazole, an acridinium salt and an oxalate ester, or a bioluminescent compound selected from the group consisting of luciferin, luciferase and aequorin.
  • Embodiments of the present invention are directed towards An antibody and. a method for targeting and killing of cancer cells including; Colon cancer, Multiple Myeloma and Non-Hodgkin's lymphoma cancer cells.
  • the main focus of the present invention is to selectively target and kill cancer cells by monoclonal antibodies produced against a unique surface antigen over expressed on Colon cancer (CC), Multiple Myeloma(MM) and Non-Hodgkin's lymphoma (NHL) cancer cells.
  • the invention focuses on enhancing the immunogenicity of surface antigen by adding a cysteine residue to the carboxyl end of the 14 amino acid long extra- cellular antigenic peptide epitope.
  • Tumor necrosis factor receptors are single transmembrane- spanning glycoproteins that bind cytokines and trigger multiple signal transduction pathways.
  • Tumor necrosis factor (TNF) is a proinflammatory cytokine whose role is established in the pathogenesis of malignant diseases like cancer.
  • TNF has been found to have a pro-cancerous effect and gene polymorphisms which increase or decrease TNF production results either in increased risk or protective effect on a number of different cancers and precancerous diseases including gastric cancer, lymphoma and cervical cancer, certain TNFR member proteins are expressed on specific cancer cells.
  • TNF has been detected in a number of different tumor types such as ovarian and breast tissue as well as hematological malignancies. Both mRNA expression and TNF protein has been found in human epithelial ovarian tumor cells as well as within the infiltrating macrophages. The p55 TNFR has also been detected within ovarian tumor cells and infiltrating macrophages but not stromal macrophages while the p75 TNFR has only been found within the infiltrating macrophages.
  • TNF is a cytokine that is produced early in the inflammatory cascade and has been shown to promote carcinogenesis. TNF has a wide range of activities in cancer.
  • the main component of the device is "Solar Sonic Therapeutic Infusion Composition Mix”.
  • Device convert/redirect/expel Toxic Chemical as form of physiological genetic reverse engineering in the body.
  • Device is capable of injecting cancer cells with imaginary (sensory) accessive flow of highly oxygeneted blood, since cancer cells are proven to be anaerobic, such injection will be done via various Solar Sonic Electromagnetic Chemical Infusion Intracellular Evaporation, whereby the Solar Sonic Phenomenon of physiological genetic reverse engineering will simultaneously occur, at the end of which gradual rate of cancer cells eradication countdown will literally begin.
  • the main component of the device is Solar Sonic Therapeutic Infusion Composition Mix.
  • invention Device is equipped with advanced electronic linkage capabilities & miscellaneous.
  • Multi-faceted distribution system air suctioning, air blowing, air pressure, air compression.
  • Solar Sonic Therapeutic Infusion Medical Device chemically promotes Pulsed Suppression of Mitochondria-K + Channel Axis in Cancer, Inducing Apoptosis and Inhibiting Cancer Growth.
  • the mitochondria is a natural cancer fighting human organelle, the mitochondria is never a cell, it is an organelle. It certainly cannot be accurately characterized as a cancer fighting cell, since its primary function is to provide nucleoside triphosphates such as ATP for cell structure.
  • Solar Sonic Laboratories were able to precisely program the mitochondria organelle to communicate with carcinogenic cells and systematically cause their irreversible eradication and the inevitable methodical deprivation to cancer cells from vital carcinogenic environment.
  • a medical device and a pharmaceutically acceptable carrier for therapeutic infusion in cancer treatments We present this medical device for selectively removing a target cell, pathogen, or virus expressing a binding partner on its surface, the device comprising various Solar Sonic Circuits, wherein the SSQF Circuit comprises a magnetic filter comprising a magnet capable of generating a magnetic field sufficient to capture magnetic nanomaterials in the magnetic field and a removable, magnetizable substrate capable of capturing magnetic nanomaterials; and a pump in fluid communication with the magnetic filter, wherein the pump moves fluid through the Solar Sonic Circuit.
  • the SSQF Circuit comprises a magnetic filter comprising a magnet capable of generating a magnetic field sufficient to capture magnetic nanomaterials in the magnetic field and a removable, magnetizable substrate capable of capturing magnetic nanomaterials; and a pump in fluid communication with the magnetic filter, wherein the pump moves fluid through the Solar Sonic Circuit.
  • the magnetizable substrate is a screen
  • the device of claim further comprising a reservoir in fluid communication with the magnetic filter
  • the device of claim further comprising a mixing chamber between the reservoir and the magnetic filter and in fluid communication with the reservoir and the magnetic filter
  • the device of claim further comprising a heater for heating fluid moving through the device.
  • the device of claim further comprising a management component in electrical communication or wireless communication with the pump for monitoring or maintaining flow rate of the fluid, the device of claim, further comprising a management component in electrical communication or wireless communication with the heater for maintaining the fluid at a predetermined temperature, the device of claim, wherein the magnetizable substrate is removable from the magnetic filter, the device of claim, wherein the reservoir and magnetizable substrate are sterilizable, the device of claim wherein the reservoir systematically comprises superparamagnetic nanoparticles functionalized with a first binding partner that binds to the binding partner on the surface of the target cell, pathogen or virus, the device of claim, wherein the binding partner on the target cell comprises a tumor specific antigen or fragment thereof capable of binding to the first binding partner.
  • the first binding partner on the superparamagnetic nanoparticles is selected from the group consisting of nucleic acid aptamers, peptide aptamers, pseudo peptide, synthetic ligands selected for the target, and antibodies or antigen binding fragments thereof.
  • a method for removing a target cell, organism, or virus from a subject in need of treatment comprising removing a biofluid from the patient and transporting the biofluid into the device passing the mixture of the superparamagnetic nanoparticles and biofluid through the magnetic filter, and either returning the filtrate to the reservoir or the patient, wherein the target cell is a cancer cell, the method of claim, further comprising administering replacement fluids to the subject.
  • biofluid is a fluid selected from the group consisting of blood, blood serum, cerebrospinal fluid, lymph, and peritoneal fluid.
  • infected cell is infected by a virus, bacterium, protozoan, or fungus
  • the method of claim further comprising administering replacement fluids to the subject wherein the binding partner on the superparamagnetic nanoparticles is selected from the group consisting of nucleic acid aptamers, peptide aptamers, pseudo peptide, and synthetic ligands selected for the target.
  • a method for removing a target cell organism, or virus from a subject comprising obtaining a biofluid from the subject; transporting the biofluid into the device of passing a mixture of the superparamagnetic nano particles and biofluid through the magnetic filter.
  • a method for removing nanomaterials having magnetic properties from a subject comprising obtaining a biofluid containing a nanomaterial having magnetic properties from the subject; transporting the biofluid into the device of any one of claims wherein nanomaterials in the biofluid are captured by the magnetic filter, and either returning the filtrate to the reservoir or the patient.
  • a method of treating or managing cancer comprising administering to a patient a pharmaceutical composition comprising an effective amount of mycobacterium W or constituents of mycobacterium W Wherein the method is for decreasing the burden of cancer tissues, a method of claim, wherein the method is for improving the cancer treating effect of radiotherapy or chemotherapy.
  • the method is for reducing the side-effects of radiotherapy or chemotherapy wherein the side effects are mostly hematological side effects, the method of claim, wherein the side effects are reduced to avoid postponement of chemotherapy, the method of claim, wherein the side effects are leucopenia, thrombocytopenia, anaemia, nausea, vomiting or mucositis, wherein the mycobacterium W is dead mycobacterium w, wherein the mycobacterium w has been killed by a physical method, wherein the physical method is the application of heat, wherein the heat is applied by means of autoclaving.
  • the pharmaceutical composition comprises constituents of mycobacterium w that have been obtained by sonication, wherein the pharmaceutical composition comprises constituents of mycobacterium w that have been obtained by extraction.
  • a method of improving the quality of like in a patient suffering from cancer comprising: administering to a patient a pharmaceutical composition comprising an effective amount of mycobacterium w or constituents of mycobacterium w. Wherein the improvement in quality of life is obtained in the absence of other modes of treatment, wherein the improvement in quality of life is obtained with the addition of other modes of treatment.
  • a method of amelioration of symptoms associated with cancer comprising: administering to a patient a pharmaceutical composition comprising an effective amount of mycobacterium W or constituents of mycobacterium W.
  • Said nanomagnetic material has a saturation magentization of from about 2 to about 3000 electromagnetic units per cubic centimeter, and (b) Said nanomagnetic material is comprised of nanomagnetic particles with an average particle size of less than about 100 nanometers, wherein the average coherence length between adjacent nanomagnetic particles is less than 100 nanometers.
  • said magneto-resistive material when exposed to a direct current field of 1.5 Tesia and a radio frequency field of 64 megahertz increase its resistance by at least two orders of magnitude
  • said device is a medical device, wherein said medical device is comprised of a first therapeutic agent, wherein said first therapeutic agent is an anti-cancer drug, wherein said nanomagnetic material has average particle size of less than about 20 nanometers and a phase transition temperature of less than about 200 degrees Celsius, wherein said assembly further comprises a cytotoxic radioactive material, wherein said assembly is comprised of a material that is absorbable in living tissue.
  • said material that is absorbable in living tissue is selected from the group consisting of polyester amides from glycolic acids, polyester amides from lacitic acids, polymers and copolymers of gylcolate, polymers and copolymers of lactatate, and poolydioxanone, wherein said medical device is comprised of a polymeric material, wherein said polymeric material is comprised of said first therapeutic agent, wherein said polymeric material is comprised of a second therapeutic agent, wherein said polymeric material is comprised of a third therapeutic agent, wherein said polymeric material is a drug-eluting polymer, wherein said polymeric material is a synthetic absorbable copolymer formed by copolymereizing glycolide with trimethylene carbonate, wherein said polymeric material is selected from the group of silk, polyester, polytetrafluoroethylene, polyurethane silicone-based material, and polyamide.
  • said therapeutic agent is selected from the group consisting of antithrombogenic agents, antiplatelet agents, prostaglandins, thrombolytic drugs, antiproliferative drugs, antirejection drugs, antimicrobial drugs, growth factors, anticalcifying agents, and mixtures thereof
  • said reservoir is formed by a polymer selected from the group consisting of polyurethanes and its copolymers, silicone and its copolymers, ethylene vinylacetat, thermoplastic elastomers, polyvinylchloride, polyolefins, cellulosics, polyamides, polytetrafluoroethylenes, polyesters, polycarbonates, polysulfones, acrylics, and acrylonitrile butadiene styrene copolymers, wherein said polymeric material is a bioabsorbable polymer selected from group consisting of poly (L-lactic acid), polycaprolactone, poly (lactide-co-glycolide) Poly (hydroxybuty
  • said polymeric material is a biomolecule,wherein said biomolecule is selected from the group consisting of fibrin, fibrogen, cellulose, starch, collagen, and hyaluronic acid, wherein said polymeric material is selected from the group consisting of polyolefin, acrylic polymer, acrylic copolymer, vinyl halide polymer, vinyl halide copolymer, polyvinyl ether, polyvinylidene halide, polvinylketone, polyvinyl aromatic polymer, copolymers of vinyl monomer, acrylonitrile-styrene copolymer, ethylene-vinyl acetate copolymer, polyamide, Alkyd resin, polyoxymethylene, polyimide, polyether, epoxy resin, rayon, rayon-tracetate, cellulose, cellulose acetate, cellulose butyrate, cellulose acetate butyrate, cellophane, cellulose nitrate, cellulose propionate, cellulose ether, and carboxymethyl cellulose, wherein said first
  • said polymeric material is a multi-layered polymeric material, wherein said polymeric material is a porous polymeric material, wherein said polymeric material has a thermal processing temperature of less than about 100 degrees Celsius, wherein said polymeric material is comprised of a porosigen, wherein said porosigen is selected from the group of microgranules of sodium chloride, lactose, sodium heparin, polyethyelen glycol, polyethylene oxide/polypropylene oxide copolymer, and mixtures thereof, wherein said polymeric material is a thermoplastic polymer, wherein said polymeric material is an elastomeric polymer, wherein said polymeric material is in the form of a layer of material with a thickness of from about 0.002 to about 0.02 inches, wherein said polymeric material is a controlled release polymer, wherein said controlled release polymer is comprised of a congener of an endothelium-derived bioactive composition.
  • said congener of an endothelium-derived bioactive agent is selected from the group consisting of nitric oxide, nitric L-arginine, sodium nitroprusside, and nitroglycerine
  • said polymeric material is a transparent polymeric materialwherein said polymeric material is a hydrophobic elastomeric material
  • said polymeric material is a hydrophilic polymer
  • said first therapeutic agent is a water- soluble therapeutic agent
  • said first therapeutic agent is an anti-microtubule agent that impairs functioning of microtubules, wherein said anti-microtuble agent is paclitaxel
  • said polymeric material is a pH-sensitive polymer, wherein said pH-sensitive polymer is selected from the group consisting of poly(acrylic acid), poly (aminocarbox lic acid), poly (acrlic acid), poly (methyl acrylic acid), cellulose acetate phthalate, hydroxypropylmethylcellulose phthalate, hydroxypropylmethylcellulose acetate
  • thermogelling polymer is selected from the group consisting of poly(-methyl-N-n-propylacrlamide), poly(-methyl-N-n-propylacrylamide), poly(N-n-propylacrylamide), poly(N-methyl-N-isopropylacrylamide), poly(N-n-propylmethacrylamide), poly(N-isopropylacrylamide), poly(N,n-diethylacrylamide), poly(N-isopropylmethacrylamide), poly(N-cyclopropylacrylamide), poly(N- ethylmethyacrylamide), poly(N-methyl-N-ethylacrylamide), poly(N-cyclopropylmethacrylamide), and poly(N- ethylacrylamide), hydroxypropyl cellulose, methyl cellulose, hydroxypropylmethyl cellulose, as well as ethylhydroxyethyl cellulose, wherein the average particle size of such nanom
  • particles of said nanomagnetic material are at least triatomic, being comprised of a first distinct atom, a second distinct atom, and a third distinct atom, wherein said first distinct atom is an atom selected from the group consisting of atoms of actinium, americium, berkelium, californium, cerium, chromium, cobalt, curium, dysprosium, einsteinium, erbium, europium, fermium, gadolinium, holmium, iron, lanthanum, lawrencium, lutetium, manganese, mendelevium, nickel, neodymium, neptunium, nobelium, plutonium, praseodymium, promethium, protactinium, samarium, terbium, thorium, thulium, uranium, and ytterbium, wherein said First distinct atom is a cobalt atom, wherein said particles of nanom
  • said particles of nanomagnetic material are comprised of a said first distinct atom, said second distinct atom, said third distinct atom, and a fourth distinct atom, wherein said particles of nanomagnetic Material are comprised of a fifth distinct atom, wherein said particles of nanomagnetic material have a sqareness of from about 0.1 to about 0.9, wherein said particles of nanomagnetic material have a squarenesss is from about , 0.2 to about 0.8, wherein said particles of nanomagnetic material have an average size of less of less than about 3 nanometers.
  • said particles of nanomagnetic material have an average size of less than about 15 nanometers, wherein said particles of nanomagnetic material have an average size is less than about 11 nanometers, wherein said particles of nanomagnetic material have a phase transition temperature of less than 46 degrees Celsius, wherein said particles of nanomagnetic material have a phase transition temperature of less than about 50 degrees Celsius, wherein said nanomagnetic material has a coercive force of from about 0.1 to about 10 Oersteds, wherein particles of nanomagnetic material haa a relative magnetic permeability of from about 1.5 to about 2,000, wherein particles of nanomagnetic material have a saturation magnetization of at least lOOelectromagnetic units per cubic centimeter.
  • said particles of nanomagnetic material have a saturation magnetization of at least about 200 electromagnetic units (emu) per cubic centimeter, wherein particles of nanomagnetic material have a saturation magnetization of about 1,000 electromagnetic units per cubic centimeter, wherein said particles of nanomagnetic material have a coercive force of from about 0.01 to about 5,000 Oersteds, wherein said particles of nanomagnetic material have a coercive force of from about 0.01 to about 3,000 Oersteds, wherein said particles of nanomagnetic material are disposed within a film that has a heat shielding factor of at least 0.2, wherein said particles of nanomagnetic material have a relative magnetic permeability of from about 1 to about 500,000, wherein said particles of nanomagnetic material have a relative magnetic permeability of from about 1.5 to about 260,000, wherein said assembly is comprised of antithrombogenic material, wherein said particles of nanomagnetic material have a mass density of about 0.001 grams per cubic centimeter.
  • said particles of nanomagnetic material have a mass density of at least about 1 gram per cubic centimeter, wherein said particles of nanomagnetic material have a mass density of at least about 3 grams per cubic centimeter, wherein said particles of nanomagnetic material have a mass density of at least about 4 grams per cubic centimeter, wherein said second distinct atom has a relative magnetic permeability of about 1.0, wherein said second distinct atom is an atom selected from the group consisting of aluminum, antimony, barium, beryllium, boron, bismuth, calcium, gallium, germanium, gold, indium, lead, magnesium, palladium, platinum, silicon, silver, strontium, tantalum, tin, titanium, tungsten, yttrium, zirconium, magnesium, and zinc, wherein said third distinct atom is an atom selected from the group consisting of argon, bromine, carbon, chlorine, fluorine, helium, helium, hydrogen, iodine, krypton
  • said nanomagnetic material is disposed within a ceramic binder, wherein said ceramic binder is selected from the group consisting of a clay binder, an organic colloidal particle binder, and a molecular organic binder, wherein said nanomagnetic material is disposed within a synthetic polymeric binder, wherein said nanomagnetic material is disposed within a fiber, wherein said nanomagnetic material is disposed within a fabric, wherein said particles of nanomagnetic material are disposed within an insulating matrix, wherein said Particles of nanomagnetic material are present in the form of a coating with a thickness of from about 400 to about 2000 nanometers, wherein said coating has a thickness of from about 600 to about 1200 nanometers.
  • said coating has a morphological density of at least about 98 percent, wherein said coating has a morphological density of at least about 99 percent, wherein said coating has a morphological density of at least about 99.5 percent, wherein said coating has an average surface roughness of less than about 100 nanometers, wherein said coating has an average surface roughness of less than about 10 nanometers, wherein said coating is hydrophilic, biocompatiable, hydrophobic and presenting various methods therein, one of which is a method of eliciting an immune response in a subject directed against a polypeptide sequence selected from the above listed pharmacological groups and acceptable carriers, comprising, administering to the subject an immunologically sufficient amount of a polypeptide sequence selected from the above listed Pharmacological groups and acceptable carriers.
  • the system is a method of treating cancer comprising, administering a therapeutically effective amount of antibody that binds to a polypeptide, wherein said cancer is selected from a group consisting of Multiple Myeloma, Colon Cancer and Non- Hodgkin's Lymphoma.
  • a therapeutically effective amount of antibody that binds to a polypeptide wherein said cancer is selected from a group consisting of Multiple Myeloma, Colon Cancer and Non- Hodgkin's Lymphoma.
  • the use of an antibody as claimed, wherein said cancer is selected from a group consisting of Multiple myeloma, Colon cancer and Non- Hodgkin's lymphoma.
  • the SSQF technology presents a medical device and pharmacologically infused therapeutic composition complex of claims, wherein the xenoantigen is selected from the group consisting of
  • said mechanical vibrational energy has an excitation source frequency in the range of from about 1 hertz to about 10 Gigahertz
  • cell cycle arresting drug synchronizes tumor cells with respect to cell cycle progression
  • said cell cycle arresting drug is selected from the group consisting of gemcitabine, cisplatin, carboplatin, cyclophosphamide, topoisomerase inhibitor, etoposide, 5-fluoroacil, doxorubicin, methotrexate, hydroxyurea, 3'-azido-3'-deoxythymidine, and mixtures thereof
  • said cell cycle arresting drug is gemcitabine
  • said cell cycle arresting drug synchronizes said cells in metaphase
  • said cell cycle arresting drug synchronizes said cells in anaphase, wherein at least about 30 percent of said cells are synchronized in metaphase, wherein 50 percent of said cells are synchronized in metaphase.
  • At least about 70 percent of said cells are synchronized in metaphase, wherein said mechanical vibrational energy is ultrasound, wherein said synchronized cells are contacted with said ultrasound only after at least 25 minutes after said cell cycle arresting drug has been administered to said organism, wherein said synchronized cells are contacted with said ultrasound only after at least 60 minutes after said cell cycle arresting drug has been administered to said organism, wherein synchronized cells are contacted with said ultrasound only after at least 240 minutes after said cell cycle arresting drug has been administered to said organism, wherein said synchronized cells are contacted with said ultrasound only after at least 48 hours after said cell cycle arresting drug has been administered to said organism, wherein said microtubule stabilizing drug is a laulimalidge microtubule stabilizing agent, wherein said microtubule stabilizing drug is a coumarin compound, wherein said ultrasound has a frequency of from about 270 to about 420 kilohertz.
  • said ultrasound has an intensity of from about 10 to about 30 watts per square meter, wherein said microtubule stabilizing drug is paclitaxel, wherein said ultrasound has a frequency of from about 50 megahertz to about 2 gigahertz, wherein said ultrasound has a frequency of from about 100 megahertz to about 1 gigahertz, wherein the power of said ultrasound is at least about 0.01 watts per square meter, wherein the power of said ultrasound is at least about 0.1 watts per square meter, wherein said ultrasound has a frequency of form about 100 kilohertz to about 500 kilohertz, wherein said ultrasound has a frequency of from about 110 to about 200 kilohertz, wherein said ultrasound has a frequency of from about 130 to about 170 kilohertz, wherein the power of said ultrasound is from about 1 to about 30 watts per square meter, wherein the power of said ultrasound is from about 5 to about 15 watts per square meter.
  • SSQF is creating several programs for each one to induce Apoptosis and/or trigger Metabolic Homeostasis:
  • Solar Sonic Effects use special frequency arrays to decode and extract Logistical Data contained in the holographic matrix of the universe as the Unified Field.
  • At the core of Solar-Sonic-Discovery is a complex matrix of light, heat, sound, reflection, refraction, attenuation, kinetics, and resonance. These matrices obey the mathematical principals of frequencies. All vibration frequencies are mathematically represented on a graph as a waveform as all matters visible or invisible emits unique frequency signatures.
  • Solar Sonic possesses intellectual knowledge, crucial frequency array coding technology and algorithms that Together detect, capture, emit, enhance and modulate any waveform frequency. Such Effects generate results when the master waveforms are manipulated and sonically photonic configured within specific proprietary parameters where it produces two events.
  • the first event is "IPAST Image Penetration and Stimulation Technology", which is matrix imaging of the elected target and override its physical entity with compatible elements, enhancing its resolution with multidimensional imaging technology and dominating its elements.
  • FPAST Frequency Penetration And Stimulation Technology FPAST inserts frequencies that penetrate and stimulate other waveforms, such as Any Organism, Atoms, Cells, Molecules, Particles, Air, Water, Heat, Sonic-Patterns, Solar-Patterns.
  • FPAST inserts frequencies that penetrate and stimulate other waveforms, such as Any Organism, Atoms, Cells, Molecules, Particles, Air, Water, Heat, Sonic-Patterns, Solar-Patterns.
  • Ultrasonic, Infrasonic, Hypersonic, Supersonic and Solar-Sonic thereby greatly enhancing and enriching the data gathered and strengthening its principal extraction potential in a very methodical manner.
  • Solid tumors including the aggressive primary brain cancer glioblastoma multiforme, develop resistance to cell death, in part as a result of a switch from mitochondrial oxidative phosphorylation to cytoplasmic glycolysis.
  • This metabolic remodeling is accompanied by mitochondrial hyperpolarization.
  • DCA small-molecule and orphan drug dichloroacetate
  • Freshly isolated glioblastomas from 49 patients showed mitochondrial hyperpolarization which was rapidly reversed by DCA.
  • DCA therapy also inhibited the hypoxia-inducible factor-la, promoted p53 activation, and suppressed angiogenesis both in vivo and in vitro.
  • the dose-limiting toxicity was a dose-dependent, reversible peripheral neuropathy, and there was no hematologic, hepatic, renal, or cardiac toxicity. Indications of clinical efficacy were present at a dose that did not cause peripheral neuropathy and at serum concentrations of DCA sufficient to inhibit the target enzyme of DCA, pyruvate dehydrogenase kinase II, which was highly expressed in all glioblastomas.
  • Metabolic modulation may be a viable therapeutic approach in the treatment of glioblastoma.
  • the function of the apoptotic pathway in cancer cells is extremely critical for all cancer research and for all new inventions in treating cancer.
  • the intrinsic (self) and extrinsic(from the outside) pathways of cell suicide are activated by mitochondrial cytochrome C release, which cascade with other enzymes activating the caspase 8, 9 pathways which cleave all the cells protein, killing it.
  • mitochondrial cytochrome C release which cascade with other enzymes activating the caspase 8, 9 pathways which cleave all the cells protein, killing it.
  • a cancer cell being a cancer cell, will have this pathway cut off—irreversibly— simply because it otherwise would have been killed before it became cancer.
  • the extrinsic pathway will be cut off due to faulty receptors or cascading proteins, and the intrinsic pathway- -even if the mitochondria are "activated” and cytochrome C is released, because the cell either won't listen to the death signal that has an amplification of repressors to the apoptotic signal (BCL2, BCL XL), or the DNA coding for the proteins necessary to carry out the caspase activity of cleaving proteins has been mutated/deleted/rendered non-functional.
  • a Mitochondria-K+ Channel Axis is Suppressed in Cancer and its Normalization Promotes Apoptosis and Inhibits Cancer Growth
  • the unique metabolic profile of cancer might confer apoptosis resistance and be therapeutically targeted.
  • apoptosis resistance Compared to normal cells, several human cancers have high mitochondrial membrane potential and low expression of the K + channel Kvl.5, both contributing to apoptosis resistance.
  • DCA Dichloroacetate
  • PDK mitochondrial pyruvate dehydrogenase kinase
  • PDK mitochondrial pyruvate dehydrogenase kinase
  • PDK mitochondrial pyruvate dehydrogenase kinase
  • DCA upregulates Kvl.5 by an NFATl-dependent mechanism.
  • DCA induces apoptosis, decreases proliferation, and inhibits tumor growth, without apparent toxicity.
  • siRNA mimics DCA.
  • the mitochondria-NFAT-Kv axis and PDK are important therapeutic targets in cancer; the orally available DCA is a promising selective anticancer agent.
  • Apoptosis is the death of cells which occurs as a normal and controlled part of an organism's growth or development. Apoptosis is the process of programmed cell death (PCD) that may occur in multi-cellular organisms. Biochemical events lead to characteristic cell changes (morphology) and death. These changes include blebbing, cell shrinkage, nuclear fragmentation, chromatin condensation, and chromosomal DNA fragmentation. In contrast to necrosis which is form of traumatic cell death that results from cellular injury?
  • Necrosis is the death of most or all of the cells in an organ or tissue due to disease, injury, or failure of the blood supply. Necroptosis is a programmed form of necrotic cell death and Necrotic cell death has been considered a form of passive cell death. Mitotic catastrophe is an event in which a cell is destroyed during mitosis. This is believed by some to occur as a result of an attempt at aberrant chromosome segregation early in mitosis, or as a result of DNA damage later.
  • Mitosis is a type of cell division that results in two daughter cells each having the same number and kind of chromosomes as the parent nucleus, typical of ordinary tissue growth. Cytostasis is the inhibition of cell growth and multiplication. Cytostatic refers to a cellular component or medicine that inhibits cell growth. Cytostasis is an important prerequisite for structured multi-cellular organisms.
  • necrosis in general apoptosis confers advantages during an organism's lifecycle. For example, the separation of fingers and toes in a developing human embryo occurs because cells between the digits undergo apoptosis. Unlike necrosis, apoptosis produces cell fragments called apoptotic bodies that phagocytic cells are able to engulf and quickly remove before the contents of the cell can spill out onto surrounding cells and cause damage. Between 50 and 70 billion cells die each day due to apoptosis in the average human adult.
  • Nanotechnology can be applied in a variety of bio-medical and bio-engineering proceedings and is called Nano-medicine.
  • Magnetic nano-particles of different sizes with tailored surface chemistry are used in a routine setting for cell Separation and in as magnetic resonance imaging contrast agents, hyperthermia and drug delivery, for SSF applications these particles coated by different materials to receive biocompatibility.
  • One major hurdle that underlies the use of nano-particles in the treatment of diseases is the problem of getting the particles to a specific body compartment; Solar Sonic Laboratories have completely solved that.
  • a potential benefit of using these particles is the application of external magnetic fields/gradients to focus the particles to the particular site in the body and to hold them until the therapy is complete. All these efforts point to an aim in which drugs are only delivered to specific sites and at therapeutic levels. Magnetic drug targeting, in which magnetic nano-particles bound to a chemotherapeutic agent and concentrated in a tumor region by an external magnetic field after intra-arterial injection could be a promising tool in cancer therapy.
  • Intracellular distributions of the anticancer drug doxorubicin (DR) and nucleic acid dyes 4',6-diamidino-2- phenylindole (DAPI) and ethidium (£) bromide were investigated and modified by Solar Sonic Laboratories. By visual inspection, it was observed that yeast cell culture was heterogeneous in stainability by DAPI, DR £.
  • Preosteoclastic behaviour is also reflected in the functional properties of cancer cells, that is: matrix-resolving properties, hormone / neuronal dependence, coupling with mesenchymal cells, migrating and transmigrating properties, neurogenetic properties, trafficking to the bone, immune deviation, sensitivity to antirheumatics, bisphosphonates, polyphenols and steroids.
  • preosteoclasts fuse to osteoclasts they over-express certain intracellular signaling pathways which are likewise over-expressed in cancer cells during their proliferation.
  • the following clusters of differentiation commonly expressed by myeloid, including preand osteoclast cells are surface markers of various cancer cells as well: CD9, CD10, CDllb, CD13, CD14, CD24, CD26, CD31, CD34, CD35, CD36, CD37, CD40, CD44, CD46, CD 47, CD49, CD51, CD53, CD54, CD55, CDS6, CDS9, CD61, CD63, CD68, CD71, CD73, CD75, CD80/86, CD 81, CD87, CD90, CD97, CD 98, CD 105, CD115, CD117, CD151, CD133, CD147, CD163, CD164, CD166, CD184, CD200.
  • cancer cells Due to epithelial markers, cancer cells seem likely to be of epithelial origin. But certain cells of the myeloid lineage, the Langerhans cells, usually adopt epithelial markers as well. Langerhans cells show a high level of epithelial surface markers CD326 (EpCAM), CD 227(Mucinl) and E-Cadherin in the epidermis, through which they are connected with keratinocytes. Whether they may also adopt a local cytokeratin scaffold has not so far been ascertained to our knowledge. MTA transgenic mice offer further evidence that myeloid lineage cells in the epidermis, rather than epithelial cells, are required for carcinogenesis.
  • EpCAM epithelial surface markers
  • MTCadherin epithelial surface markers
  • MTA transgenic mice offer further evidence that myeloid lineage cells in the epidermis, rather than epithelial cells, are required for carcinogenesis.
  • mice are deficient in MHC-II positive cells in the epidermis, and Langerhans cells or any other myeloid cells are therefore completely absent in the epidermis. These mice are resistant to squamous cell carcinoma induction in the skin, which can be explained by the hypothesis that cells of myeloid origin, rather than epithelial cells alone, are a prerequisite for carcinogenesis.
  • cancer cells can be seen as different stages of the myeloid lineage, from bone marrow stem cells through monocytes to pre- and osteoclasts with the additional feature of malignancy.
  • osteomimetic properties of cancer cells are inherent properties of these cells and consequently cannot be interpreted as an epiphenomenon or as opportunistic features for the sole purpose of metastasis in the bone.
  • fusogenic properties of macrophages and preosteoclasts or their plasticity allow them to adopt local cytokeratin characteristics, and how these aspects may be connected with their malignancy, is the subject of intense research by various research groups. If there is a transition between the different phenotypes of cancer cells, it is more epithelial-myeloid transition and less epithelialmesenchymal transition.
  • Hypericin a photosensitive pigment occurs in the plant Hypericum perforatum L. It is a substance which, Thanks to its exceptional properties, has attracted for the decades interest of experts in the field of biology and medicine. Attention is given to its anti-retroviral, antidepressant, anti-inflammatory, antineoplastic, and antibacterial effects.
  • PDT photodynamic therapy
  • Halichondrin B was isolated from the black sponge, Halichondria okadai. Interestingly, this polyether macrolide exhibited antitumor activity both in vitro and in vivo. The mechanism of action of halichondrin B was shown to be a novel one that disrupts the polymerization dynamics of tublin, which makes this Natural product an interesting candidate for the treatment of cancer. However, the difficulty of collecting sufficient material (only 12.5 mg from 600 kg of sponge) impaired studies for its development.
  • halichondrin B represented a breakthrough.
  • the total synthesis also facilitated the structure-activity relationship study, and which revealed that the activity resides in the macrocyclic lactone C1-C38 moiety.
  • the moiety derivative was approved for the treatment of breast cancer in several countries and is now available on the market as anti-cancer drug Halaven.
  • Cyanobacteria are photosynthetic prokaryotes and that are widely distributed throughout marine and terrestrial environments.
  • the vitamin D axis includes vitamin D, vitamin D receptor (VDR) and vitamin D-binding protein (VDBP; also known as Gcglobulin) that is the precursor of the Gc globulin-derived Macrophage Activating Factor a protein that proved effective as an anticancer agent in a variety of experimental and spontaneous tumours.
  • VDR vitamin D receptor
  • VDBP vitamin D-binding protein
  • MAF precursor activity and serum Nagalase activity have been used as diagnostic indices for a variety of cancer patients and as prognostic indices during radiation therapy, surgical resection of tumors and GcMAF therapy of tumor bearing mice.
  • the well demonstrated anti-cancer efficacy of GcMAF can be ascribed to different biological properties of the molecule that include activation of tumoricidal macrophages, inhibition of tumor-induced angiogenesis and direct inhibition of cancer cell proliferation, migration and metastatic potential.
  • GcMAF-activated macrophages induce the apoptosis of human breast cancer cells and inhibit their proliferation in vitro.
  • Macrophages (cell line Raw 264.7, HPA Culture Collection) were activated by culturing them in the presence of 100 ng/ml GcMAF for 72 h prior to addition to the human breast cancer cell culture (cell line MCF-7, HPA Culture Collection). Cell cultures were fixed and stained with Haematoxylin Eos in or with Papanicolau staining after 18 and 40 h of co-incubation. It could be swiftly observed that GcMAF-activated macrophage surrounded MCF-7 cells and emitted pseudopods that appeared to "search for" contact with the cancer cells.
  • MCF-7 cells in contact with activated macrophages showed a significantly altered morphology with large and irregular cytoplasm and with nuclei where the chromatin appeared fragmented, almost as if the cells were undergoing apoptosis.
  • the GcMAF-activated macrophages appeared to disaggregate the MCF- 7 cytoplasm.
  • ErbB2 Human epidermal growth factor receptor 2
  • Trastuzumab which interacts with the ErbB2 extracellular domain (ErbB2-ECD).
  • the fruiting bodies of G.gargal cultivated at Solar Sonic Laboratories were used.
  • the lyophilized sample was extracted with hot water, and then a crude extract was obtained, and then it was separated by Sephacryl gel permeation chromatography.
  • the monocyte cell-line, THP-1 was induced differentiation to a macrophage by PMA, then stimulated with various concentrations of each fraction.
  • cytokine proteins and mRNAs produced in the macrophages were examined by western blotting and qRT-PCR, respectively. Moreover, after HeLa cells were co-cultivated with the stimulated cells, a tumorcidal effect was examined. A crude extract of G. gargal induced to activate a macrophage. And then, it was shown that a growth of HeLa was inhibited by co-cultivation with it. We obtained three fractions from a crude extract. A polysaccharide fraction (Mw 400 kDa) showed the strongest immunomodulating effect on cytokines productions. These cytokines were recognized as type 1, inflammatory, cytokine, such as TNF-, IL- 1, IL-6, and IL-12. Moreover, we also elucidate that other polysaccha ride-related complex (Mw 20 kDa) played as a same immunomodulator.
  • Mw 400 kDa polysaccharide fraction
  • G. gargal a hot water extract from G. gargal possessed a tumorcidal activity against HeLa. And, polysaccharide and polysaccharide-related complex fraction from it showed an immune-modulating effect on inflammatory cytokine production from stimulated macrophages. These results suggested that G. gargal induced a tumorcidal action of macrophages via type 1 cytokines network. It can be considered that G. gargal become a source of a novel medicinal material. Glycosylation is one of the major post-translational modifications of biotherapeutics that depends on the cell line used for production.
  • GlycoExpress toolbox GEX
  • Glycol-engineered human cell lines for the high yield production of fully human glycoproteins to optimize the glycosylation of antibodies and non antibody biotherapeutics.
  • non antibody molecules three glycooptimized antibodies are presently in clinical development and further in the pipeline. Two of these are Biobetter antibody molecules directed against approved targets and glycooptimized with respect to manifold improvement of anti-cancer activity, half-life elongation, and removal of immunogenic components and broadening of the patient and indication coverage.
  • the receptor is present on natural killer cells (NK cells) which are involved in antibody dependent cellular anti tumor cytoxicity (ADCC) and are thought to be the effector cells for cancer cell killing.
  • ADCC antibody dependent cellular anti tumor cytoxicity
  • CetuGEX which is an improved 2 nd generation GEX-glycooptimized antibody of ErbituxR, is improved by ⁇ 10-fold for patients carrying the V/V allotype and up to 250 fold for the other allotypes (>80% of patients). Thereby all allotypes reach an anti tumor activity about 10-fold higher than that of the V/V allotype with conventional non-GEX-glycooptimized antibodies.
  • CetuGEX revealed a ⁇ 1.5-2 fold improvement of serum half live in PK studies within cynomolgus monkeys due to the optimization of its sialylation.
  • the mean terminal serum elimination half-life of CetuGEX was 110 hours while the terminal half-life of ErbituxR was 67.5 hours, respectively, resulting in an improved area under the curve for the CetuGEX molecule.
  • TrasGEX is a Trastuzumab similarly GEX-glycoopotimized as CetuGEX with a 10- 140 fold improved ADCC suitable for all patient ADCC receptor allotypes.
  • PankoMab- GEX is a highly potent anti-tumor antibody for up to 100% of the patients of Ovarian, Breast NSCLC and other endometrial cancers.
  • SPM sternness phenorype model
  • CSCs Cancer stem cell s
  • SPM and the 2PT may provide the basis for a more rational approach to develop effective anticancer therapies for gliomas and this varied strategy can be extrapolated to other tumors.
  • Cancer stem cell s usually stays in the stationary phase so that they are resistant against the ordinal Chemothrapies because these treatments are effective to growing cells, upon some stimuli or environmental alterations, CSCs are activated & induced proliferation, then finally form secondary cancer cells. If we could modulate stem cell-like properties of CSCs by small organic molecule, it is expected that we could eliminate cancers from human body.
  • stem cells possess a molecular mechanism that guarantees undifferentiated state while they can proliferate well.
  • One of the factors related to this mechanism is transcription factor, Hairy and Enhancer of Split 1 (Hesl). This helix-loop-helix type transcriptional repressor is expressed in all undifferentiated cells, and inhibits differentiation.
  • Hesl inhibitor could take stem celllike property away from CSCs through induction of their differentiation, Hesl functions through association with a co-repressor, Grocho /transducing-like Enhancer of Split (Gro/TLE) family of proteins.
  • Trp-Arg-Pro-Trp WRPW
  • a WRPW motif mimicking compound binds to Hesl binding site of Gro/TLE, interfere the association between Hesl and Gro TLE, and then inhibit Hesl function.
  • the motif is 1) only four amino acids long, 2) composed of characteristic amino acids, and 3) shown to be turn conformation, at Pro residue.
  • Hesl expression vector introduction of Hesl expression vector into the cells results in decrease of Luc activity because of transcriptional repression activity of Hesl when using Luc plasmid containing actin promoter and Hesl binding site, N-Box.
  • Luc activity should be restored by inhibiting the interaction between Hesl and Gro/TLE.
  • Hypericin is a substance isolated from Hypericum perforatum L. It is mainly known for its benefitial effects on human body such as antibacterial, anti-inflammatory, anti-depressant effects. Solar Sonic researchers have shown an increasing interest in hypericin mediated photodynamic therapy which is known for its tumour-seeking ability/minimal toxicity in dark. Our objective was to determine the effects of different concentrations of photoactivated hypericin to inhibit the growth of the A549 cell line and also to determine the mechanism inducing this effect.
  • NMSC nonmelanoma skin cancers
  • BCC basal cell carcinoma
  • SCC squamous cell carcinoma
  • ugonin K expressed less toxic to human keratinocytes (HaCaT cells) and human skin fibroblasts (Hs68 cells) than BCC cells, suggesting that ugonin K may have potential to be developed effective drugs for skin cancer cells without damaging skin normal cells.
  • ugonin K After treatment with ugonin K in BCC cells, cell cycle arrested in S-G2/M phase with a markedly increased apoptotic sub- Gl peak, the expression of p53 and p21 revealed a more significant increased than the untreated control.
  • ugonin K was found to increase reactive oxygen species generation on SCC25 and BCC cells. In this study, we expected ugonin K has potential for an effective and specific drug to cancer cell, can minimize the damage to normal cell and provide a better therapeutic method to skin carcinoma.
  • Leukemia is the general term for some different types of blood cancer. There are four main types of leukemia called: Acute lymphoblastic (lymphocytic) leukemia (ALL), Acute myeloid (myelogenous) leukemia (AML), chronic lymphocytic leukemia (CLL), chronic myeloid (myelogenous) leukemia (CML). It is important to know that patients are affected and treated differently for each type of leukemia. These four types of leukemia do have one thing in common; they begin in a cell in the bone marrow. The cell undergoes a change and becomes a type of leukemia cell. The first job is to form myeloid cells.
  • lymphocytes which are a part of the immune system. Lymphocytic leukemia can arise in these cells.
  • the leukemia is called lymphocytic or lymphoblastic if the cancerous change takes place in a type of marrow cell that forms lymphocytes.
  • the leukemia is called myelogenous or myeloid if the cell change takes place in a type of marrow cell that normally goes on to form red cells, some kinds of white cells and platelets.
  • ALL and AML acute leukemias
  • Acute leukemias are each composed of young cells, known as !ymphoblasts or myeloblasts. These cells are sometimes called blasts. Acute leukemias progress rapidly without treatment. Patients who relapse after treatment and Patients who continue treatment after remission (maintenance), a carefully conducted clinical trial may provide the best available therapy.
  • CML chronic myeloid leukemia
  • a process called its life cycle can help Solar Sonic scientists design new drugs that are more effective at suppressing the virus & have fewer side effects.
  • Viruses cannot reproduce without the aid of a living cell.
  • HIV can infect a number of cells in the body, the main target is an immune cell called a lymphocyte, precisely a CD4 helper cell, a type of T-cell.
  • T-cells are an important part of the immune system because they help facilitate the body's response to many common but potentially fatal infections. Without enough T-cells, the body's immune system is unable to defend itself against many infections. By ways that are not yet understood, HIV's life cycle directly or indirectly causes a reduction in the number of T-cells in the body and resulting in increased risk of infections.
  • HIV After HIV enters the body through unsafe sex, contaminated needles, and blood transfusions or from mother to child (vertical or perinatal transmission) it comes in contact with its favorite host cell - the T-cell. When this happens, HIV will hijack the host cell's cellular machinery to reproduce thousands of copies of it. HIV has to complete many steps in order for this to happen. At each step of HIV's life cycle, it is possible to design a drug that will stop the virus. Designing drugs to interfere with specific steps in the viral life cycle is called rational drug design.
  • the urine test successfully identified cancerous cells in urine samples in patients with a history of the disease, with reported sensitivity of 84.4% and specificity of 82.7% for the study's primary endpoint.
  • the technology is being developed by Solar Sonic Laboratories as cancer diagnostics subsidiary, and allows an accurate diagnosis of cancerous and precancerous cells, based on a unique combination of color and morphology by utilizing a proprietary kit containing unique extract and dyes.
  • Bladder cancer is the fourth most prevalent cancer among males in the U.S. and the seventh most prevalent among males worldwide, with nearly 430,000 new case of the disease diagnosed globally in 2012.
  • the rate of recurrence is the highest of all cancers and ranges from 50% to 80%.
  • the technology may be implemented in screening tests and monitoring tests of disease recurrence in cancer patients after being treated.
  • Solar Sonic Laboratories have proven the efficacy in diagnosing cervical cancer and bladder cancer in the framework of clinical trials, and estimates that the technology underlying the products may be implemented for use in additional cancer indications.
  • the cervical cancer detection screening diagnostic test kit is in the initial commercial stage and has recently completed a clinical trial to prove its ability to monitor bladder cancer recurrence, while the underlying Solar Sonic Technologies are also adapted for other types of cancer as well, after a long history of extensively vigorous clinical trials in Africa.
  • the MDD 93/42/EEC, Annex IX makes provisions for software that functions as a medical device. Basically, it states that any software that drives a device or influences the use of a device falls automatically in the same classification.
  • software may be viewed as a medical device or an accessory to a medical device or as a component and integral part of a medical device (automatically in the same class as the medical device and subject to the conformity assessment of medical device).
  • the function of the software guides the classification of the software medical device. If the software is a medical device, it may be classified as Class I; however, if software medical device is an integral component of a device as indicated above, it assumes the classification of the device. For example, software that is part of a Class III medical device is viewed as a Class III device.
  • Class I medical device software may be subject to classification as a Class I medical device with a measuring function. And, if the software now is viewed as such, Notified Body involvement is required for CE Marking.
  • the Guidance MEDDEV 2.1.5, Medical Devices with a Measuring Function may be relevant to some software. Software with a measuring function must meet a few characteristics: measure quantitatively a physiological function or anatomical parameter; measurement displayed in legal units or other acceptable units as described within European Directive 80/181/EEC; and the intended purpose implies accuracy, and failing to comply with the "measurement" could result in a significant adverse effect on the patient's health and safety.
  • the software provides instructions for an instrument for the purpose of diagnosis, prevention, monitoring, treatment or alleviation of disease.
  • Conformity Assessment procedures require consideration of the development lifecycle; procedures for document control and configuration management; and control of combinations between software versions and intended hardware.
  • Published software medical device standards include I EC 62304, Medical Device Software- Software Life Cycle Processes, ISO/IEC 90003 and IEC 60601 series.
  • Software is a component of many complicated medical devices or is an independent medical device or accessory, and as such, it is important for manufacturers to appreciate that their software may require CE Marking.
  • the 1st mode of action is manifested by interference with the proper formation of the mitotic spindle, while the 2nd mode of action results in rapid disintegration of the dividing cells. Both effects are consistent with the computed directional forces exerted by these specific fields on charges and dipoles within the dividing cells.
  • In-vivo treatment of tumors in C57BL/6 and BALB/c mice resulted in significant slowing of tumor growth and extensive destruction of tumor cells within 3 to 6 days.
  • Electric tumor treating fields also known as alternating electrical field therapy, are low-intensity (1 to 2 V/cm), intermediate-frequency (100 to 200 kHz), alternating electric fields employed for the treatment of malignant tumors.
  • This novel treatment modality has shown promise in pilot clinical trials in patients with advanced stage solid tumors including glioblastoma (GBM).
  • GBM glioblastoma
  • Current published evidence is primarily from a single investigator group. The findings of a pilot clinical trial examining the effects of ETTF in 10 patients with recurrent GBM.
  • TTP Median time to progression
  • OS median overall survival
  • ETTF are a safe and effective new treatment modality that effectively slows down tumor growth in-vitro, in-vivo, as well as in human cancer patients.
  • ETTF significantly improved median OS compared with standard therapy (7.8 versus 6.1 months) for the patients treated per protocol.
  • quality-of-life was also better in the ETTF group
  • a phase II study of second-line treatment of non-small cell lung cancer where ETTF was administered concomitantly with pemetrexed.
  • ETTF is an emerging and promising novel treatment concept.
  • the system is intended as treatment for adult patients (22 years of age or older) with histologically confirmed glioblastoma multiforme (GBM), following histologically or radiologically confired recurrence in the supra- tentorial region of the brain after receiving chemotherapy.
  • GBM glioblastoma multiforme
  • the device is intended to be used as a monotherapy, and is intended as an alternative to standard medical therapy for GBM after surgical and radiation options have been exhausted.
  • the first randomized clinical study of electric tumor treatment fields did not reach its primary end-point of improved survival compared to active chemotherapy. This study was funded and sponsored by the device manufacturer; Novocure, Ltd. Subjects for this study were age 18+ years with histologically confirmed glioblastoma (World Health Organization grade IV astrocytoma) with radiologically disease progression.
  • Prior therapy must have included radiotherapy (with / without concomitant and/or adjuvant temozolomide).
  • Chemotherapy agents considered as best standard of care (BSC) during the study included platinum-based chemotherapy (i.e., carboplatin); nitrosureas; procarbazine; combination of procarbazine, lomustine and vincristine; temozolomide; and bevacizumab.
  • platinum-based chemotherapy i.e., carboplatin
  • nitrosureas i.e., carboplatin
  • procarbazine i.e., carboplatin
  • nitrosureas nitrosureas
  • procarbazine combination of procarbazine, lomustine and vincristine
  • temozolomide temozolomide
  • bevacizumab temozolomide
  • the trial did not reach its primary end-point of improved survival compared to active chemotherapy. In addition, differences in response rates, progression-free survival at 6 months, and reduction in risk of death were not statistically significant. Quality of life analyses favored ETTF therapy in most domains. The differences in median overall survival between patients in the NovoTTF-lOOA group and the BSC group were not statistically significant.
  • survival was not significantly affected by the choice of chemotherapy.
  • the survival curve for the two treatment groups appeared to be very similar during the first 12 months of followup. Between 12 and 24 months, the survival curves separated slightly in favor or the BSC control group.
  • Symptom scale analysis is in accordance to treatment-associated toxicity; appetite loss, diarrhea, constipation, nausea and vomiting were directly related to the chemotherapy administration. Increased pain/fatigue was reported in the chemotherapy-treated patients and not in the ETTF treatment. Commenting on the trial by Solar Sonic Laboratories stated that the study was designed for superiority; Although well conducted, it might not have shown it for a limited compliance in the ETTF group. Stated that, even with this limitation, the trial has shown at least equivalence of ETTF to chemotherapy, with a decreased toxicity and increased quality of life favoring ETTF.
  • the manufacturer has initiated a subsequent randomized clinical trial enrolling diagnosed glioblastoma patients after completion of standard radiochemotherpy, parallel to starting the adjuvant or maintenance temozolomide chemotherapy Patients randomized to the experimental arm will receive ETTF in addition to maintenance temozolomide.
  • Comprehensive Cancer Network has a Category 2B recommendation to consider the use of ETTF for persons with local, diffuse or multiple recurrences of glioblastoma.
  • Electric tumor treating field's technology is also being studied as a treatment for other solid tumors (e.g., melanoma and non-small cell lung cancer).
  • solid tumors e.g., melanoma and non-small cell lung cancer
  • TTFields tumor treating fields
  • Ongoing and future trials will evaluate TTFields in newly diagnosed glioblastoma, solid tumor brain metastases, non-small cell lung cancer, and ovarian and pancreatic cancers.
  • Efficacy is the capacity to produce an effect: It has different specific meanings in different fields. In medicine, it is the ability of an intervention or drug to produce a desired effect.
  • efficacy indicates the capacity for beneficial change (or therapeutic effect) of a given intervention (e.g. a drug, medical device, surgical procedure, or a public health intervention). If efficacy is established, an intervention is likely to be at least as good as other available interventions, to which it will have been compared. Comparisons of this type are typically made in 'explanatory' randomized controlled trials, whereas 'pragmatic' trials are used to establish the effectiveness of an intervention.
  • a given intervention e.g. a drug, medical device, surgical procedure, or a public health intervention.
  • efficacy refers to the maximum response achievable from a drug.
  • Intrinsic activity is a relative term that describes a drug's efficacy relative to a drug with the highest observed efficacy. Effectiveness refers to the ability of a drug to produce a beneficial effect.
  • Cancers are usually named using -carcinoma, -sarcoma or -blastoma as a suffix, with the Latin or Greek word for the organ or tissue of origin as the root.
  • cancers of the liver parenchyma arising from malignant epithelial cells is called hepatocarcinoma
  • a malignancy arising from primitive liver precursor cells is called a hepatoblastoma
  • a cancer arising from fat cells is called a liposarcoma.
  • the English organ name is used.
  • the most common type of breast cancer is called ductal carcinoma of the breast.
  • the adjective ductal refers to the appearance of the cancer under the microscope, which suggests that it has originated in the milk ducts.
  • Benign tumors (which are not cancers) are named using -oma as a suffix with the organ name as the root.
  • a benign tumor of smooth muscle cells is called a leiomyoma (the common name of this frequently occurring benign tumor in the uterus is fibroid).
  • cancer uses the -noma suffix, examples including melanoma and seminoma.
  • Some types of cancer are named for the size and shape of the cells under a microscope, such as giant cell carcinoma, spindle cell carcinoma, and small-cell carcinoma.
  • the brain perceives the world and registers it by means of wave pulses.
  • Cytochrome C complex is a small hemeprotein found loosely associated with the inner membrane of the mitochondrion. It belongs to the cytochrome c family of proteins. Cytochrome c is a highly water soluble protein, unlike other cytochromes, with a solubility of about 100 g/L and is an essential component of the electron transport chain, where it carries one electron. It is capable of undergoing oxidation/reduction, but does not bind oxygen. It transfers electrons between Complexes III (Coenzyme Q - Cyt C reductase) and IV (Cyt C oxidase). In humans, cytochrome c is encoded by the CYCS gene.
  • Cytochrome c is a component of the electron transport chain in mitochondria.
  • the heme group of cytochrome c accepts electrons from the bcj complex and transfers electrons to the complex IV.
  • Cytochrome c is also involved in initiation of apoptosis. Upon release of Cytochrome c to the cytoplasm, the protein binds apoptotic protease activating factor-1 (Apaf-1).
  • Cytochrome c can catalyze several reactions such as hydroxylation and aromatic oxidation, and shows peroxidase activity by oxidation of various electron donors such as 2,2-azino- bis(3-ethylbenzthiazoline-6-sulphonic acid) (ABTS), 2-keto-4-thiomethyl butyric acid and 4-aminoantipyrine. Cytochrome c is a highly conserved protein across the spectrum of species, found in plants, animals, and many unicellular organisms. This, along with its small size (molecular weight about 12,000 daltons), makes it useful in studies of cladistics.
  • cytochrome c Its primary structure consists of a chain of about 100 amino acids. Many higher order organisms possess a chain of 104 amino acids.
  • the cytochrome c molecule has been studied for the glimpse it gives into evolutionary biology. Its amino acid sequence is highly conserved in mammals differing by only a few residues. For example, the sequences of cytochrome c in humans are identical to that of chimpanzees (our closest relatives) illustrated here below quite comprehensively as follows:
  • Class I includes the lowspin soluble cytochrome c of mitochondria and bacteria. It has the heme- attachment site towards the N terminus of histidine and the sixth ligand provided by a methionine residue towards the C terminus.
  • Class II includes the highspin cytochrome c'. It has the heme-attachment site closed to the N terminus of histidine.
  • Class III comprises the low redox potential multiple heme cytochromes.
  • the heme c groups are structurally and functionally nonequivalent and present different redox potentials in the range 0 to -400 mV.
  • Class IV was originally created to hold the complex proteins that have other prosthetic groups as well as heme c.
  • Cytochrome C is suspected to be the functional complex in so called LLLT: Low-level laser therapy.
  • LLLT Low-level laser therapy.
  • red light and some near infra-red wavelengths penetrate tissue in order to increase cellular regeneration.
  • Light of this wavelength appears capable of increasing activity of cytochrome C, thus increasing metabolic activity and freeing up more energy for the cells to repair the tissue.
  • Cytochrome C is also an intermediate in apoptosis, a controlled form of cell death used to kill cells in the process of development or in response to infection or DNA damage. Cytochrome C binds to cardiolipin in the inner mitochondrial membrane, thus anchoring its presence and keeping it from releasing out of the mitochondria and initiating apoptosis. While the initial attraction between cardiolipin and cytochrome C is electrostatic due to the extreme positive charge on cytochrome C, the final interaction is hydrophobic, where a hydrophobic tail from cardiolipin inserts itself into the hydrophobic portion of cytochrome C.
  • mitochondrial ROS production is stimulated, and cardiolipin is oxidized by a peroxidase function of cardiolipin-cytochrome C complex.
  • the hemoprotein is detached from mitochondrial inner membrane and can be extruded into the soluble cytoplasm via pores in outer membrane.
  • the invention presents a process for initiating apoptosis in a cancer cell comprising:
  • the cell cycle arresting drug is selected from the group consisting of: gemcytabine, cisplatin, carboplatin, cyclophosphamide, topoisomerase inhibitor, etoposide, 5-fluorouracil, doxorubicin, Methotrexate, hydroxyurea, and 3 '-azido-3'-deoxy thymidine, wherein the mechanical vibrational energy is ultrasound energy having a frequency of about 50 megahertz to about 2 gigahertz, wherein the exposure to mechanical vibrational energy is repeated or sustained over a period of at least one typical cell cycle, wherein the step of contacting the cell with mechanical vibrational energy is repeated or sustained over a period of at least one typical cell division.
  • step of synchronizing tubulin assembly in the cell, wherein the step of synchronizing tubulin assembly is effected by exposing the cell to a microtubule stabilizing agent and/or radiation, and the step is performed prior to contacting the cell with mechanical vibrational energy, wherein the microtubule stabilizing agent is selected from the group consisting of taxanes, coumarins, and combinations thereof.
  • the disease or condition should be responsive to intracellular hyperthermia treatment
  • Weight should be within 45% (+/-) of ideal body weight and patients must weigh at least 35 kg;
  • Pretreatment evaluation should include a complete medical history and physical examination focused on the selection criteria listed above.
  • Laboratory evaluation should include pulmonary function tests- if indicated, full hematological survey with hemostatic profile, EKG, liver function tests, serum biochemical profile, thyroid panel, serum creatinine, calcium, phosphate, and stress-EKG or exercise-multigated radionucleotide ejection scan on patients whose cardiac ejection fraction is suspect not to be greater than 45% with probable deterioration on exercise.
  • the DNP may be administered by intravenous infusion.
  • the route of administration may also be orally, rectally or topically.
  • the frequency and optimal time interval between administrations is individualized and determined by measuring V0 2 , as well as other parameters. For example, various laboratories, x-ray, CAT scan, MRI, PET scan, HIV load, CD4+ lymphocyte counts, HSP expression, prostatic specific antigen (PSA) and other surrogate markers of clinical outcome can establish the V0 2 , frequency and duration of therapy.
  • PSA prostatic specific antigen
  • the HIV relationships between viral load, CD4 + lymphocyte counts, presence of opportunistic infections and clinical status of the patient can be used to develop more optimal regimes of DNP administration.
  • Applicants' studies have revealed that the methods of the present invention can be effective in the diagnosis and treatment of a wide range of disease states and conditions in which uncoupler induced hypermetabolism, hyperthermia, oxidative stress and their sequela, play a beneficial role.
  • DNP may also be administered with other compounds used to treat infectious, malignant or other diseases.
  • agents include antifungal, antibacterial, antiviral or antineoplastic drugs, cell differentiating agents, and, various biologic response modifiers.
  • anti-fungal agents include Amphotericin B, Griseofulvin, Fluconazole (Diflucan), Intraconazole, 5 fluoro-cytosine (Flutocytosine, 5-FC), Ketatoconazole and Miconazole.
  • anti-bacterial agents include antibiotics, such as those represented from the following classifications: beta lactam rings (penicillins), macrocyclic lactone rings (macrolides), polycyclic derivatives of naphthacenecarboxamide (tetracyclines), amino sugars in glycosidic linkages (aminoglycosides), peptides (bacitracin, gramicedin, polymixins, etc.), nitrobenzene derivatives of dichloroacedic acid, large ring compounds with conjugated double bond systems (polyenes), various sulfa drugs including those derived from sulfanilamide (sulfonamides, S-nitro-2-furanyl compounds (nitrofurans), quinolone carboxylic acids (nalidixic acid), fluorinated quinilones (ciprofloxan, enoxacin, ofloxacin, etc.), nitroimidazoles (metroindazole) and numerous others.
  • antibiotics such as those represented from the following classifications:
  • antibiotic groups are examples of preferred antibiotics, and examples within such groups include: peptide antibiotics, such as: Bacitracin, bleomycin, cactinomycin, capreomycin, colistin, dactinomycin, gramicidin A, enduracitin, amphomycin, gramicidin J, mikamycins, polymyxins, stendomycin, actinomycin; aminoglycosides represented by streptomycin, neomycin, paromycin, gentamycin ribostamycin, tobramycin, amikacin; lividomycin beta lactams represented by benzylpenicillin, methicillin, oxacillin, hetacillin, piperacillin, amoxicillin and carbenacillin; lincosaminides represented by clindamycin, lincomycin, celesticetin, desalicetin; chloramphenicol; macrolides represented by erythromycins, lankamycin,
  • Antiviral agents that can be used with DNP include: interferons ⁇ , ⁇ and ⁇ , amantadine, rimantadine, arildone, ribaviran, acyclovir, abacavir, vidarabine (ARA-A) 9-l-3-dihydroxy-2-propoxy methylguanine (DHPG), ganciclovir, enviroxime, foscarnet, ampligen, podophyllotoxin, 2,3-dideoxytidine (ddC), iododeoxyuridine (IDU), trifluorothymidine (TFT), dideoxyinosine (ddi), d4T, 3TC, Zidovudine, efavirenz, protease inhbt, such as indinavir, saquinavir, ritonavir, nelfinavir, amprenavir &specific antiviral antibodies.
  • ARA-A 9-l-3-dihydroxy-2
  • Anti-cancer drugs that can be used with DNP include, but are not limited to, various cell cycle-specific agents represented by structural analogs or antimetabolites of methotrexate, mercaptopurine, fluorouracil, cytarabine, thioguanine, azacitidine; bleomycin peptide antibiotics, such as podophyllin alkaloids including etoposide (VP- 16) and teniposide (VM- 26); and various plant alkaloids such as vincristine, vinblastine, and paclitaxel.
  • various cell cycle-specific agents represented by structural analogs or antimetabolites of methotrexate, mercaptopurine, fluorouracil, cytarabine, thioguanine, azacitidine
  • bleomycin peptide antibiotics such as podophyllin alkaloids including etoposide (VP- 16) and teniposide (VM- 26)
  • various plant alkaloids such as vincristine,
  • Anti-neoplastic cell cycle- nonspecific agents such as various alkylating compounds such as busulfan, cyclophosphamide, mechlorethamine, melphalan, altretamine, ifosfamide, cisplatin, dacarbazine, procarbazine, lomustine, carmustine, lomustine, semustine, chlorambucil, thiotepa and carboplatin.
  • alkylating compounds such as busulfan, cyclophosphamide, mechlorethamine, melphalan, altretamine, ifosfamide, cisplatin, dacarbazine, procarbazine, lomustine, carmustine, lomustine, semustine, chlorambucil, thiotepa and carboplatin.
  • Anticancer antibiotics and various natural products and miscellaneous agents that can be used with DNP include: dactinomycin, daunorubicin, doxorubicin, plicamycin, mitomycin, idarubicin, amsacrine, asparaginase, quinacrine, retinoic acid derivatives (etretinate), phenylacetate, suramin, taxotere, tenizolamide, gencytabine, amonafide, streptozocin, mitoxanthrone, mitotane, fludarabine, cytarabine, cladribine, paclitaxel (taxol), tamoxifen, and hydroxyurea, etc.DNP can also be administered with various hormones, hormone agonists and biologic response modifying agents which include, but are not limited to:
  • the aromatase inhibitor, amino glutethimide, the peptide hormone inhibitor octreotide and gonadotropin-releasing hormone agonists such as goserilin acetate and leuprolide can also be used with DNP.
  • Biologic response modifiers such as various cytokines, interferon alpha-2a, interferon alpha- 2b, interferon-gamma, interferon-beta, interleukin-1, interleukin-2, interleukin-4, interleukin-10, monoclonal antibodies (anti-HER-2/neu humanized antibody), tumor necrosis factor, granulocyte-macrophage colony- stimulating factor, macrophage-colony-stimulating factor, various prostaglandins, phenylacetates, retinoic acids, leukotrines, thromboxanes and other fatty acid derivatives can also be used with DNP.
  • cytokines interferon alpha-2a, interferon alpha- 2b, interferon-gamma, interferon-beta, interleukin-1, interleukin-2, interleukin-4, interleukin-10, monoclonal antibodies (anti-HER-2/neu humanized antibody), tumor necrosis factor,
  • Phosphoprotein p53 Ifosfamide, Mitomycin C, Carmustine, Psoralen, Adenovirus, Antigens, immunotoxins, Monoclonal Antibody, Interleukin, Epitope, Idiotypes, Allergen, Superantigen, Tolerogen, Immunoglobulin, Alpha-Lactalbumin, Quercetin, p53 tumour suppressor gene, BI811283 Small Molecule Inhibitor, BRCA1, BRCA2, Gene Suppressors, Oncogenes Suppressors, SSFD Programmable Nucleotide Sequence of Genomic DNA, SSFD Programmable chromosomes, SSFD Genomic De-amplification, SSFD Programmable Mitosis, Solamargine, Prostacyclin, Ruthenium, SSFD Genomic De-amplification, SSFD Re-programmable coding sequence, HPV, HBV, Sipuleucel-T (Provenge.
  • Retinoids Vinca Alkaloids.
  • Monoclonal antibody therapy drugs Provenge Vaccine, Immunomodulating drugs, Mitotic Inhibitors, Epothilones, Estramustine, Topoisomerase inhibitors, Antimetabolites, Anti-microtubule agents, Cytotoxic antibiotics, Topoisomerase inhibitors, Antibody-Drug Conjugates, SSF Infused Nanoparticles, Cytostatic Drugs, Alkylating Agents, Anthracyclines, Cytoskeletal Disruptors, Epothilones, Histone Deacetylase Inhibitors, Topoisomerase Inhibitors, Kinase Inhibitors, Nucleotide Analogs, Precursor Analogs, Peptide Antibiotics, Platinum-Based Agents, Retinoids, Vinca Alkaloids, opiate, insulin, Hydrochloride, Biologically Intensive Phototherapeutic Agents, Highly illuminating Biological Agents, Heat-borne Biological Agents, Anti-Heat Borne Biological Agents, HPV, HBV, Si
  • Electromagnetically Biochemical Signaling Communication Frequency is not the same as far as the electrochemical infusion of each individual pharmaceutical drug for the sole treatment of cancer and carcinogenic cells.
  • Electromagnetically Biochemical Signaling Communication Frequency is not the same as far as the electrochemical infusion of each individual pharmaceutical drug for the sole treatment of cancer and carcinogenic cells.
  • the urine test successfully identified cancerous cells in urine samples in patients with a history of the disease, with reported sensitivity of 84.4% and specificity of 82.7% for the study's primary endpoint.
  • the technology is being developed by Solar Sonic Laboratories as cancer diagnostics subsidiary, and allows an accurate diagnosis of cancerous and precancerous cells, based on a unique combination of color and morphology by utilizing a proprietary kit containing unique extract and dyes.
  • the blinded clinical study was conducted in nine medical centers in Africa, where urine samples from 360 subjects with a history of bladder cancer were tested.
  • the study population included 114 healthy subjects and about 246 patients currently suffering from the disease.
  • the results of the urine tests were compared with results from biopsy or cystoscopy, in cases where biopsies were not taken.
  • the results also indicated that the urine test's negative predictive value (NPV), defined as the probability that a patient having a negative result doesn't suffer from the disease, was 98.5%.
  • NPV negative predictive value
  • Solar Sonic technology allows an accurate diagnosis of cancerous and precancerous cells, based on unique combination of color and morphology. The technology may be implemented in screening tests and monitoring tests of disease recurrence in cancer patients after being treated. Solar Sonic Laboratories have proven the efficacy in diagnosing cervical cancer and bladder cancer in the framework of clinical trials, and estimates that the technology underlying the products may be implemented for use in additional cancer indications.
  • the cervical cancer detection screening diagnostic test kit is in the initial commercial stage and has recently completed a clinical trial to prove its ability to monitor bladder cancer recurrence, while the underlying Solar Sonic Technologies are also adapted for other types of cancer as well, after a long history of extensively vigorous clinical trials in Africa.
  • HgB hemoglobin
  • the hemoglobin (HgB) level measures the amount of the protein in RBCs that actually carries the oxygen. If the level of hemoglobin is low the body works much harder to deliver oxygen to tissues throughout the body.
  • Their HgB had range from 12.6 to 16.1 grams per deciliter. They had a normal range for platelet count, were approximately from 150,000 to 350,000 platelets per mcL. They had normal Neutrophils and their Absolute Neutrophil Count (ANC) had ranged from 2,500 to 6,000 neutrophils.
  • ANC Absolute Neutrophil Count
  • Glioblastoma had started as a single tumor and a few random symptoms at first. As the cancer progresses, a conglomeration of tumors had developed in different areas around the brain. More symptoms had cropped up, with some of them linked to a tumor in a particular part of the brain. The treatment was really focused on stopping the growth of the tumor and making the patient as comfortable as possible while attempting to prolong life through radiation &chemotherapy. Glioblastoma is always fatal, but we had insisted on fighting.
  • This invention should be under the strict direction of a qualified and specialized team to insure safety and effectiveness.
  • the treatment team remains with the patient throughout the procedure to insure that safe and controlled dosages of patient, which are being administered by monitoring real time changes in V0 2 , metabolic rate, temperature, respiratory rate, heart rate, urine output and clinical status of the patient.
  • This invention is practiced in controlled steps so as to attain a predetermined V0 2 and plateau of infusion time for a particular session of any given cancer condition.
  • the specialized team will periodically recheck V0 2 , heart rate, blood pressure, CAT scan, MRI, etc., and other laboratory and clinical parameters to insure continued safety and efficacy of SSQF Cancer Therapeutic Infusion Procedure. It is preferred that the specialized team undergo a training period in the use of this invention prior to its administration to human patients.
  • This SSQF Cancer Therapeutic Infusion Device has 46 Medical Characteristics, that are the administration of the technological capabilities and that must become a precisely collective training mission before any attempt to operate this Solar Sonic Multidimensional Superior group of Technologies, resonating within just one medical device.

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Abstract

Le cancer est la cause de décès la plus courante après les maladies coronariennes. Les progrès réalisés dans le diagnostic et le traitement ont un effet significatif sur la survie pour certains cancers, mais les cancers les plus courants tels que ceux du poumon et du côlon restent les plus réfractaires. Cette étude concerne un traitement efficace du cancer à l'aide d'une substance chimique électromagnétique sonique solaire accessible par perfusion et codée de façon exhaustive pour une variété d'états cancéreux. Tous les composants toxiques cancéreux sont soumis à une forme d'ingénierie physiologique/génétique/inverse. Toutes les toxicités pharmacologiques potentielles sont reformulées chimiquement et recondensées pour pénétrer spécifiquement des cellules cancérogènes et conduire à leur éradication progressive sans affecter les cellules saines, les composants sanguins ou autres organes internes. La présente invention concerne un dispositif médical spécialement conçu pour traiter le cancer par le biais d'un mécanisme de promotion de la cytostase, de perturbation de la mitose, d'infusion de la protéine C du cytochrome et de la programmation des lymphocytes T/cellules T, ainsi que des lymphocytes B/cellules B, du thymus et d'induction de l'apoptose ; toutes ces opérations étant effectuées simultanément avec un médicament choisi parmi une composition thérapeutique pharmaceutique perfusée fortement propriétaire et des agents immunothérapeutiques, des immunomodulateurs, et des agents antigéniques, des inhibiteurs de l'angiogenèse, des agents d'étanchéification vasculaire, des agents de thérapie génique, des agents de modification résistant aux antibiotiques et des agents de thérapie photodynamique. Ledit dispositif médical avec la totalité de la composition de perfusion thérapeutique qui l'accompagne et diverses autres capacités de soutien peut être utilisé en oncologie pour le traitement de tumeurs primaires et métastatiques.
PCT/IB2015/000426 2014-12-16 2015-05-20 Traitement du cancer par perfusion chimique électronique, à l'aide d'un nouveau langage adaptatif de communication cellulaire par biosignalement Ceased WO2016097831A1 (fr)

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US11013100B2 (en) 2016-10-10 2021-05-18 University Of Strathclyde Plasma accelerator
CN113041255A (zh) * 2021-04-13 2021-06-29 上海中医药大学 一种新发现miRNA–mRNA调控轴介导肺腺癌NCI-H1299细胞焦亡的方法
WO2021134010A1 (fr) * 2019-12-26 2021-07-01 The Board Of Trustees Of The Leland Stanford Junior University Procédés de normalisation du métabolisme glycolytique aberrant dans des cellules cancéreuses
WO2023069094A1 (fr) * 2021-10-20 2023-04-27 Castor Trevor P Procédé et appareil pour inactiver des pathogènes dans des unités de sang complet à l'aide de nanoparticules superparamagnétiques revêtues de réactifs de chimioluminescence et d'agents thérapeutiques antiviraux à large spectre
TWI906491B (zh) 2021-03-23 2025-12-01 瑞士商諾沃庫勒有限責任公司 用於向受試者身體遞送腫瘤治療場之傳感器設備

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Cited By (7)

* Cited by examiner, † Cited by third party
Publication number Priority date Publication date Assignee Title
US11013100B2 (en) 2016-10-10 2021-05-18 University Of Strathclyde Plasma accelerator
WO2021134010A1 (fr) * 2019-12-26 2021-07-01 The Board Of Trustees Of The Leland Stanford Junior University Procédés de normalisation du métabolisme glycolytique aberrant dans des cellules cancéreuses
CN115243720A (zh) * 2019-12-26 2022-10-25 利兰·斯坦福青年大学托管委员会 使癌细胞中异常糖酵解代谢正常化的方法
TWI906491B (zh) 2021-03-23 2025-12-01 瑞士商諾沃庫勒有限責任公司 用於向受試者身體遞送腫瘤治療場之傳感器設備
CN113041255A (zh) * 2021-04-13 2021-06-29 上海中医药大学 一种新发现miRNA–mRNA调控轴介导肺腺癌NCI-H1299细胞焦亡的方法
CN113041255B (zh) * 2021-04-13 2022-10-11 上海中医药大学 一种新发现miRNA–mRNA调控轴介导肺腺癌NCI-H1299细胞焦亡的方法
WO2023069094A1 (fr) * 2021-10-20 2023-04-27 Castor Trevor P Procédé et appareil pour inactiver des pathogènes dans des unités de sang complet à l'aide de nanoparticules superparamagnétiques revêtues de réactifs de chimioluminescence et d'agents thérapeutiques antiviraux à large spectre

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