Malik et al., 2015 - Google Patents
Targeting the MLL complex in castration-resistant prostate cancerMalik et al., 2015
View PDF- Document ID
- 18323296661843693270
- Author
- Malik R
- Khan A
- Asangani I
- Cieślik M
- Prensner J
- Wang X
- Iyer M
- Jiang X
- Borkin D
- Escara-Wilke J
- Stender R
- Wu Y
- Niknafs Y
- Jing X
- Qiao Y
- Palanisamy N
- Kunju L
- Krishnamurthy P
- Yocum A
- Mellacheruvu D
- Nesvizhskii A
- Cao X
- Dhanasekaran S
- Feng F
- Grembecka J
- Cierpicki T
- Chinnaiyan A
- Publication year
- Publication venue
- Nature medicine
External Links
Snippet
Resistance to androgen deprivation therapies and increased androgen receptor (AR) activity are major drivers of castration-resistant prostate cancer (CRPC). Although prior work has focused on targeting AR directly, co-activators of AR signaling, which may represent …
- 206010060862 Prostate cancer 0 title abstract description 61
Classifications
-
- C—CHEMISTRY; METALLURGY
- C12—BIOCHEMISTRY; BEER; SPIRITS; WINE; VINEGAR; MICROBIOLOGY; ENZYMOLOGY; MUTATION OR GENETIC ENGINEERING
- C12Q—MEASURING OR TESTING PROCESSES INVOLVING ENZYMES OR MICRO-ORGANISMS; COMPOSITIONS OR TEST PAPERS THEREFOR; PROCESSES OF PREPARING SUCH COMPOSITIONS; CONDITION RESPONSIVE CONTROL IN MICROBIOLOGICAL OR ENZYMOLOGICAL PROCESSES
- C12Q1/00—Measuring or testing processes involving enzymes, nucleic acids or micro-organisms; Compositions therefor; Processes of preparing such compositions
- C12Q1/68—Measuring or testing processes involving enzymes, nucleic acids or micro-organisms; Compositions therefor; Processes of preparing such compositions involving nucleic acids
- C12Q1/6876—Hybridisation probes
- C12Q1/6883—Hybridisation probes for diseases caused by alterations of genetic material
- C12Q1/6886—Hybridisation probes for diseases caused by alterations of genetic material for cancer
-
- G—PHYSICS
- G01—MEASURING; TESTING
- G01N—INVESTIGATING OR ANALYSING MATERIALS BY DETERMINING THEIR CHEMICAL OR PHYSICAL PROPERTIES
- G01N33/00—Investigating or analysing materials by specific methods not covered by the preceding groups
- G01N33/48—Investigating or analysing materials by specific methods not covered by the preceding groups biological material, e.g. blood, urine; Haemocytometers
- G01N33/50—Chemical analysis of biological material, e.g. blood, urine; Testing involving biospecific ligand binding methods; Immunological testing
- G01N33/53—Immunoassay; Biospecific binding assay
- G01N33/574—Immunoassay; Biospecific binding assay for cancer
- G01N33/57407—Specifically defined cancers
-
- G—PHYSICS
- G01—MEASURING; TESTING
- G01N—INVESTIGATING OR ANALYSING MATERIALS BY DETERMINING THEIR CHEMICAL OR PHYSICAL PROPERTIES
- G01N33/00—Investigating or analysing materials by specific methods not covered by the preceding groups
- G01N33/48—Investigating or analysing materials by specific methods not covered by the preceding groups biological material, e.g. blood, urine; Haemocytometers
- G01N33/50—Chemical analysis of biological material, e.g. blood, urine; Testing involving biospecific ligand binding methods; Immunological testing
- G01N33/5005—Chemical analysis of biological material, e.g. blood, urine; Testing involving biospecific ligand binding methods; Immunological testing involving human or animal cells
-
- C—CHEMISTRY; METALLURGY
- C12—BIOCHEMISTRY; BEER; SPIRITS; WINE; VINEGAR; MICROBIOLOGY; ENZYMOLOGY; MUTATION OR GENETIC ENGINEERING
- C12N—MICRO-ORGANISMS OR ENZYMES; COMPOSITIONS THEREOF; PROPAGATING, PRESERVING OR MAINTAINING MICRO-ORGANISMS; MUTATION OR GENETIC ENGINEERING; CULTURE MEDIA
- C12N2310/00—Structure or type of the nucleic acid
- C12N2310/10—Type of nucleic acid
- C12N2310/14—Type of nucleic acid interfering N.A.
-
- A—HUMAN NECESSITIES
- A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
- A61K—PREPARATIONS FOR MEDICAL, DENTAL, OR TOILET PURPOSES
- A61K31/00—Medicinal preparations containing organic active ingredients
- A61K31/33—Heterocyclic compounds
- A61K31/395—Heterocyclic compounds having nitrogen as a ring hetero atom, e.g. guanethidine, rifamycins
Similar Documents
| Publication | Publication Date | Title |
|---|---|---|
| Malik et al. | Targeting the MLL complex in castration-resistant prostate cancer | |
| Adachi et al. | Scribble mis-localization induces adaptive resistance to KRAS G12C inhibitors through feedback activation of MAPK signaling mediated by YAP-induced MRAS | |
| Zhang et al. | Intrinsic BET inhibitor resistance in SPOP-mutated prostate cancer is mediated by BET protein stabilization and AKT–mTORC1 activation | |
| Lou et al. | Circular RNA CDR1as disrupts the p53/MDM2 complex to inhibit Gliomagenesis | |
| Kurppa et al. | Treatment-induced tumor dormancy through YAP-mediated transcriptional reprogramming of the apoptotic pathway | |
| Lv et al. | NAD+ metabolism maintains inducible PD-L1 expression to drive tumor immune evasion | |
| Leucci et al. | Melanoma addiction to the long non-coding RNA SAMMSON | |
| Zhu et al. | Impaired autophagic degradation of lncRNA ARHGAP5-AS1 promotes chemoresistance in gastric cancer | |
| Wong et al. | Targeting wild-type KRAS-amplified gastroesophageal cancer through combined MEK and SHP2 inhibition | |
| Wong et al. | JMJD6 is a tumorigenic factor and therapeutic target in neuroblastoma | |
| Edwards et al. | The receptor tyrosine kinase EphA2 promotes glutamine metabolism in tumors by activating the transcriptional coactivators YAP and TAZ | |
| Zhang et al. | Analysis of the androgen receptor–regulated lncRNA landscape identifies a role for ARLNC1 in prostate cancer progression | |
| Atwood et al. | GLI activation by atypical protein kinase C ι/λ regulates the growth of basal cell carcinomas | |
| Asangani et al. | Therapeutic targeting of BET bromodomain proteins in castration-resistant prostate cancer | |
| Zhu et al. | lnc-β-Catm elicits EZH2-dependent β-catenin stabilization and sustains liver CSC self-renewal | |
| Hussong et al. | The bromodomain protein BRD4 regulates the KEAP1/NRF2-dependent oxidative stress response | |
| Deblois et al. | ERRα mediates metabolic adaptations driving lapatinib resistance in breast cancer | |
| Switzer et al. | Targeting SET/I2PP2A oncoprotein functions as a multi-pathway strategy for cancer therapy | |
| Bott et al. | The nuclear deubiquitinase BAP1 is commonly inactivated by somatic mutations and 3p21. 1 losses in malignant pleural mesothelioma | |
| Chiou et al. | Musashi-1 promotes a cancer stem cell lineage and chemoresistance in colorectal cancer cells | |
| Wang et al. | HNF1B-mediated repression of SLUG is suppressed by EZH2 in aggressive prostate cancer | |
| Ramachandran et al. | Hypoxia-induced SETX links replication stress with the unfolded protein response | |
| Yin et al. | TFE3 fusions escape from controlling of mTOR signaling pathway and accumulate in the nucleus promoting genes expression in Xp11. 2 translocation renal cell carcinomas | |
| Zhai et al. | A negative regulation loop of long noncoding RNA HOTAIR and p53 in non-small-cell lung cancer | |
| Chu et al. | Induction of senescence-associated secretory phenotype underlies the therapeutic efficacy of PRC2 inhibition in cancer |