Castration resistance in human prostate cancer is conferred by a frequently occurring androgen receptor splice variant.
By Shihua Sun, C. Sprenger, R. Vessella, K. Haugk, Kathryn R. Soriano, E. Mostaghel, S. Page, Ilsa M Coleman, Holly M. Nguyen, Huiying Sun and 2 more. Journal of Clinical Investigation, 2010
749 citations recorded by the source corpus.
Subfields: Endocrinology, Diabetes and Metabolism, Genetics, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/7f24e48760a5cec09510a000f8d9fa3b1150cf6c
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In Pulmonary and Respiratory Medicine
Citations in the corpus
- 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).”
- Constitutively active androgen receptor splice variants expressed in castration-resistant prostate cancer require full-length androgen receptor (2010, neutral): “PSA expression was increased in LNCaP/mAR-V4, consistent with similar findings recently reported for LNCaP cells expressingAR (13).”
- Androgen receptor splice variants mediate enzalutamide resistance in castration-resistant prostate cancer cell lines (2012, background): “[3] Freedland SJ, Moul JW.”