Maintenance of intratumoral androgens in metastatic prostate cancer: a mechanism for castration-resistant tumor growth.

By R. Montgomery, E. Mostaghel, R. Vessella, D. Hess, T. Kalhorn, Celestia S. Higano, L. True, P. Nelson. Cancer Research, 2008

1,429 citations recorded by the source corpus.

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

View Paper: https://www.semanticscholar.org/paper/0315a7f70a265847aae49d2074c7ff7a96690ecc

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In Endocrinology, Diabetes and Metabolism

In Pulmonary and Respiratory Medicine

R. Vessella

Citations in the corpus

Obesity and Diabetes: The Increased Risk of Cancer and Cancer-Related Mortality. (2015, background): “In human prostate cancers, it has been demonstrated that the enzymes necessary for testosterone and dihydrotestosterone synthesis are expressed, suggesting that prostate cancers are capable of synthesizing androgens from cholesterol (138, 154) and therefore could promote their own growth through and”
Resistance to CYP17A1 inhibition with abiraterone in castration resistant prostate cancer: Induction of steroidogenesis and androgen receptor splice variants (2011, neutral): “RNA was isolated and prepared for quantitative PCR (qRT-PCR) as previously described (5).”
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”
Ligand-independent Androgen Receptor Variants Derived from Splicing of Cryptic Exons Signify Hormone Refractory Prostate Cancer (2009, neutral): “Furthermore, sufficient levels of local androgens continue to be present in patients treated with combined androgen blockade (19).”
Androgen Receptor Pathway-Independent Prostate Cancer Is Sustained through FGF Signaling (2017, background): “A substantial body of evidence has documented that essentially the entire AR cistrome is re-expressed in most CRPCs, and several mechanisms capable of maintaining AR activity have been established (Carver et al., 2011; Montgomery et al., 2008; Nelson et al., 2002; Taylor et al., 2010).”