Androgen levels increase by intratumoral de novo steroidogenesis during progression of castration-resistant prostate cancer.

By J. Locke, E. Guns, A. Lubik, H. Adomat, S. Hendy, Catherine A. Wood, S. Ettinger, M. Gleave, C. Nelson. Cancer Research, 2008

801 citations recorded by the source corpus.

Subfields: Cancer Research, Endocrinology, Diabetes and Metabolism, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/7b97a48ded1219d9783bea11a47a18d4639b8f91

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Citations in the corpus

• Resistance to CYP17A1 inhibition with abiraterone in castration resistant prostate cancer: Induction of steroidogenesis and androgen receptor splice variants (2011, neutral): “Tissue androgens such as dihydrotestosterone (DHT) may be maintained via the "classical" pathway of steroidogenesis proceeding through dehydroepiandrosterone (DHEA), or through a "back-door" pathway using 5a-reduced steroid precursors as the primary source of DHT (6).”
• Molecular genetics of prostate cancer: new prospects for old challenges. (2010, background): “Finally, an unusual mechanism for increased AR signaling activity is the endogenous expression of androgen synthetic enzymes by tumor tissue, which can lead to de novo androgen synthesis or conversion of weaker adrenal androgens into testosterone and dihydrotestosterone (Titus et al. 2005; Stanbroug”