The Androgen Axis in Recurrent Prostate Cancer
By J. Mohler, C. Gregory, O. H. Ford, Desok Kim, Catharina M. Weaver, P. Petrusz, E. Wilson, F. S. French. Clinical Cancer Research, 2004
701 citations recorded by the source corpus.
Subfields: Genetics, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/0ab42995a2cf736039f5eae4a2dd238c1ae86f51
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In Pulmonary and Respiratory Medicine
Citations in the corpus
- Increased expression of genes converting adrenal androgens to testosterone in androgen-independent prostate cancer. (2006, background): “The increased AKR1C3 expression in androgen-independent prostate cancer is consistent with (and provides a mechanism for) the substantial levels of androgens found in prostate biopsies from castrated men with androgen-independent prostate cancer compared with normal prostate or nonneoplastic prostat”
- Maintenance of intratumoral androgens in metastatic prostate cancer: a mechanism for castration-resistant tumor growth. (2008, background): “In contrast, this ratio was markedly reversed in metastatic tumors, which displayed a DHT/testosterone ratio of f0.25:1, consistent with a prior report evaluating locally recurrent, castration-resistant primary prostate tumors ( 7 ).”
- Androgen levels increase by intratumoral de novo steroidogenesis during progression of castration-resistant prostate cancer. (2008, background): “The latter has also been investigated, primarily with the suggestion that adrenal androgens provide a systemic source of androgens to be used by prostate cancer tumors (20, 23).”
- Resistance to CYP17A1 inhibition with abiraterone in castration resistant prostate cancer: Induction of steroidogenesis and androgen receptor splice variants (2011, neutral): “As shown inmultiple studies, suppression of serumandrogensdoesnot correlatewellwith suppression of tissue androgens in men undergoing androgen deprivation (4, 19, 20).”
- Serum Sex Steroids Depict a Nonlinear U-Shaped Association with High-Risk Prostate Cancer at Radical Prostatectomy (2012, background): “that the study lacks a measurement of either circulating or intraprostatic dihydrotestosterone (DHT), the 5a-reducedT product which binds androgen receptors with high affinity both at the normal and the prostate tumor tissue level (43, 44), eventually acting as a more active androgen than T (45).”