Title of article :
Castration-resistant prostate cancer: Targeting androgen metabolic pathways in recurrent disease
Author/Authors :
Mostaghel، نويسنده , , Elahe A. and Montgomery، نويسنده , , Bruce and Nelson، نويسنده , , Peter S.، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2009
Pages :
7
From page :
251
To page :
257
Abstract :
Emerging evidence suggests that despite testicular androgen ablation, residual androgens, likely of adrenal—though potentially of prostatic—origin, play a critical role in the progression of prostate cancer to recurrent “castration-resistant” disease. Thus, a reassessment of the concept of total androgen deprivation is warranted. Current treatment strategies may not only lack optimal efficacy, but may actually contribute to the selection of neoplastic clones adapted to exist and proliferate in a low (but not zero) androgen environment. Moreover, the adequacy of androgen receptor (AR) pathway inhibition cannot be surmised from serum or plasma androgen levels, but must be ascertained at the tissue and molecular level prior to drawing conclusions regarding clinical efficacy or failure. Recent studies by our group and others indicate that prostate cancers undergo an adaptive response to castration that is associated with the up-regulation of transcripts encoding enzymes involved in the biosynthesis of androgens. Targeting these metabolic enzymes either individually or using combinations of agents to inhibit testicular, adrenal, and intracrine sources may provide enhanced clinical responses in the setting of both localized and metastatic disease.
Keywords :
prostate cancer , Castration resistant , Hormone therapy , Metastatic , Intracrinology , androgen metabolism , Steroidogenesis
Journal title :
Urologic Oncology
Serial Year :
2009
Journal title :
Urologic Oncology
Record number :
1889263
Link To Document :
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