Targeting chromatin binding regulation of constitutively active AR variants to overcome prostate cancer resistance to endocrine-based therapies
about
Emerging data on androgen receptor splice variants in prostate cancerTruncation and constitutive activation of the androgen receptor by diverse genomic rearrangements in prostate cancer.Androgen receptor splice variants and prostate cancer: From bench to bedside.Exploiting Epigenetic Alterations in Prostate Cancer.Lessons from tissue compartment-specific analysis of androgen receptor alterations in prostate cancer.Androgen Receptor-Dependent and -Independent Mechanisms Involved in Prostate Cancer Therapy Resistance.The Bromodomain BET Inhibitor JQ1 Suppresses Tumor Angiogenesis in Models of Childhood SarcomaPROTAC-induced BET protein degradation as a therapy for castration-resistant prostate cancer.Targeting the N-Terminal Domain of the Androgen Receptor: A New Approach for the Treatment of Advanced Prostate Cancer.Androgen receptor-dependent and -independent mechanisms driving prostate cancer progression: Opportunities for therapeutic targeting from multiple angles.Multidisciplinary intervention of early, lethal metastatic prostate cancer: Report from the 2015 Coffey-Holden Prostate Cancer Academy Meeting.Intrinsic BET inhibitor resistance in SPOP-mutated prostate cancer is mediated by BET protein stabilization and AKT-mTORC1 activation.A novel nonsense mutation in androgen receptor confers resistance to CYP17 inhibitor treatment in prostate cancerRole of steroid receptor and coregulator mutations in hormone-dependent cancers.Epigenetic blockade of neoplastic transformation by bromodomain and extra-terminal (BET) domain protein inhibitor JQ-1.Combination of carmustine and selenite effectively inhibits tumor growth by targeting androgen receptor, androgen receptor-variants, and Akt in preclinical models: New hope for patients with castration resistant prostate cancer.Second-Generation HSP90 Inhibitor Onalespib Blocks mRNA Splicing of Androgen Receptor Variant 7 in Prostate Cancer Cells.Novel mechanism-based therapeutics for androgen axis blockade in castration-resistant prostate cancer.BET Bromodomain Inhibitors Enhance Efficacy and Disrupt Resistance to AR Antagonists in the Treatment of Prostate Cancer.Development of AR-V7 as a putative treatment selection marker for metastatic castration-resistant prostate cancer.Androgen receptor variant-driven prostate cancer: clinical implications and therapeutic targeting.Analytic Validation of RNA In Situ Hybridization (RISH) for AR and AR-V7 Expression in Human Prostate Cancer.Bromodomain inhibitors and cancer therapy: From structures to applications.Androgen Signaling in Prostate Cancer.Rationale for the development of alternative forms of androgen deprivation therapy.Analytical Validation and Clinical Qualification of a New Immunohistochemical Assay for Androgen Receptor Splice Variant-7 Protein Expression in Metastatic Castration-resistant Prostate Cancer.Lipid catabolism inhibition sensitizes prostate cancer cells to antiandrogen blockade.Regulation of the glucocorticoid receptor via a BET-dependent enhancer drives antiandrogen resistance in prostate cancer.STAT5 deletion in macrophages alters ductal elongation and branching during mammary gland development.Targeting constitutively active androgen receptor splice variants in castration resistant prostate cancerClinical relevance of androgen receptor alterations in prostate cancer.Dual effects of constitutively active androgen receptor and full-length androgen receptor for N-cadherin regulation in prostate cancer.Androgen Receptor Variant AR-V9 Is Coexpressed with AR-V7 in Prostate Cancer Metastases and Predicts Abiraterone Resistance.Androgen Receptor Variants Mediate DNA Repair after Prostate Cancer Irradiation.Androgen receptor splice variants bind to constitutively open chromatin and promote abiraterone-resistant growth of prostate cancer.Role of Androgen Receptor Variants in Prostate Cancer: Report from the 2017 Mission Androgen Receptor Variants Meeting.BET inhibitors in metastatic prostate cancer: therapeutic implications and rational drug combinations.Novel Selective Agents for the Degradation of Androgen Receptor Variants to Treat Castration-Resistant Prostate Cancer.DNA Sequence Constraints Define Functionally Active Steroid Nuclear Receptor Binding Sites in Chromatin.Reactivation of androgen receptor-regulated lipid biosynthesis drives the progression of castration-resistant prostate cancer.
P2860
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P2860
Targeting chromatin binding regulation of constitutively active AR variants to overcome prostate cancer resistance to endocrine-based therapies
description
2015 nî lūn-bûn
@nan
2015年の論文
@ja
2015年論文
@yue
2015年論文
@zh-hant
2015年論文
@zh-hk
2015年論文
@zh-mo
2015年論文
@zh-tw
2015年论文
@wuu
2015年论文
@zh
2015年论文
@zh-cn
name
Targeting chromatin binding re ...... e to endocrine-based therapies
@ast
Targeting chromatin binding re ...... e to endocrine-based therapies
@en
type
label
Targeting chromatin binding re ...... e to endocrine-based therapies
@ast
Targeting chromatin binding re ...... e to endocrine-based therapies
@en
prefLabel
Targeting chromatin binding re ...... e to endocrine-based therapies
@ast
Targeting chromatin binding re ...... e to endocrine-based therapies
@en
P2093
P2860
P356
P1476
Targeting chromatin binding re ...... e to endocrine-based therapies
@en
P2093
Ganesh V Raj
James E Bradner
Michael D Nyquist
Scott M Dehm
Siu Chiu Chan
Yingming Li
P2860
P304
P356
10.1093/NAR/GKV262
P407
P577
2015-04-23T00:00:00Z