Constitutively active androgen receptor splice variants expressed in castration-resistant prostate cancer require full-length androgen receptor

By Philip A Watson, Yinan F. Chen, M. Balbas, John Wongvipat, Nicholas D. Socci, A. Viale, Kwanghee Kim, C. Sawyers. Proceedings of the National Academy of Sciences of the United States of America, 2010

650 citations recorded by the source corpus.

Subfields: Endocrinology, Diabetes and Metabolism, Genetics, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/389c569d24d6f475e45912d43b9879891a785c46

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Genetics

1. Hui Shen
2. Chip Stewart
3. P. Park
4. Christopher Sander
5. Peter W. Laird
6. Mark Gerstein
7. Marco A. Marra
8. Gad Getz

In Pulmonary and Respiratory Medicine

1. Mark A. Rubin
2. S. Lippman
3. Marc Ladanyi
4. R. Vessella

Citations in the corpus

• The molecular taxonomy of primary prostate cancer (2015, background): “…output is a proxy for ligand-driven AR activity in many tumors, AR transcript variants have been described that encode truncated AR proteins that lack the ligand-binding domain and hence are capable of activating AR target genes in the absence of androgens (Dehm et al., 2008, Watson et al., 2010).”
• Resistance to CYP17A1 inhibition with abiraterone in castration resistant prostate cancer: Induction of steroidogenesis and androgen receptor splice variants (2011, positive): “These AR splice variants have ligand-independent activity, and AR can also function by enhancing the response of AR to low ligand concentrations (10, 13).”
• Androgen receptor splice variants mediate enzalutamide resistance in castration-resistant prostate cancer cell lines (2012, background): “However, despite being able to induce a CRPC growth phenotype, ectopically expressed AR-Vs were shown to remain dependent on activity of endogenous full-length AR (11).”
• Association of AR-V7 on Circulating Tumor Cells as a Treatment-Specific Biomarker With Outcomes and Survival in Castration-Resistant Prostate Cancer (2016, neutral): “Blood age, median (range), h 25 (2-78) 27 (1-51) .”
• PROTAC-induced BET protein degradation as a therapy for castration-resistant prostate cancer (2016, background): “Accumulating evidence in the literature suggests that AR splice variants may mediate castration resistance, in part by heterodimerization with FL-AR and activation of the latter in an androgenindependent manner (15, 16, 37).”