Increased expression of genes converting adrenal androgens to testosterone in androgen-independent prostate cancer.
By Michael Stanbrough, G. Bubley, K. Ross, Todd R. Golub, Mark A. Rubin, Trevor M. Penning, P. Febbo, S. Balk. Cancer Research, 2006
1,118 citations recorded by the source corpus.
Subfields: Cell Biology, Endocrinology, Diabetes and Metabolism, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/a5d6c8149a2ed45d9cabd39b5395c19a226b9795
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Citations in the corpus
- Abiraterone and Increased Survival in Metastatic Prostate Cancer (2011, neutral): “Hypertension 77 (10) 10 (1) 0 31 (8) 1 (<1) 0”
- 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”
- Design and end points of clinical trials for patients with progressive prostate cancer and castrate levels of testosterone: recommendations of the Prostate Cancer Clinical Trials Working Group. (2008, background): “Sources include the adrenal glands or the tumor itself as a result of the upregulation of the genes involved in androgen synthesis.(15,16) Recognizing that some patients have higher testosterone levels despite continued androgen depletion with GnRH analog therapy, and that total testosterone levels ”
- Androgen Receptor Regulates a Distinct Transcription Program in Androgen-Independent Prostate Cancer (2009, methodology): “To identify genes that might account for the androgen-independent growth of abl compared with LNCaP, we examined gene expression profiles of abl cells in the absence of DHT and LNCaP cells in the absence and presence of DHT treatment for 4 hr (Figure S1B) using Affymetrix U133 plus 2.0 expression ar”
- Mammalian Krüppel-Like Factors in Health and Diseases (2010, background): “Expression of KLF6 is decreased in aggressive, androgen-independent, metastatic prostate tumors (402).”
- Integrative molecular concept modeling of prostate cancer progression (2007, result): “The marked decrease in androgen signaling concepts observed in hormone-refractory metastatic prostate cancer compared with localized cancer is consistent with a recent profiling stud”
- Maintenance of intratumoral androgens in metastatic prostate cancer: a mechanism for castration-resistant tumor growth. (2008, background): “Furthermore, the specific steroidogenic genes altered in our data confirm and extend previous studies of gene expression in castration-resistant bone marrow metastases ( 10 ) to include upregulated expression of CYP17A1, a critical enzyme mediating sequential steps in the production of adrenal andro”
- Androgen levels increase by intratumoral de novo steroidogenesis during progression of castration-resistant prostate cancer. (2008, background): “be up-regulated leading to the potential reactivation of AR (23).”
- Cancer cell metabolism: Warburg and beyond. (2008, background): “Androgen-independent prostate cancer cells still express the androgen receptor and may be capable of autonomously synthesizing their own androgens (Stanbrough et al., 2006).”
- Resistance to CYP17A1 inhibition with abiraterone in castration resistant prostate cancer: Induction of steroidogenesis and androgen receptor splice variants (2011, neutral): “Upregulated androgen receptor (AR) expression and autonomous synthesis of androgens by neoplastic prostate epithelium (either de novo from cholesterol or through metabolism of adrenal precursors) are important contributors to castration resistant prostate cancer (CRPC) growth (2-5).”