Variations of serum testosterone levels in prostate cancer patients under luteinizing hormone-releasing hormone therapy: An open question - Abstract

The hypothesis of 'the lower the better castration levels of testosterone' is based on second line hormonal manipulation and its molecular basis on better oncological results for lower castration levels, including maximal androgen blockade.

The equivalence of surgical and different pharmacological castrations has been controversial and variations on chemical structure due to modified amino acid making analogues more potent than luteinizing hormone-releasing hormone (LH-RH) and also on the vehicle for delivering will impact bioavailability, potentially causing differences in androgen levels and in its final oncological efficacy. Add to this scenario a myriad of circumstances such as ethnic variations and co-morbidities impacting uniquely the pharmacological approach in a highly heterogeneous population of castration resistant prostate cancer (CRPC). Until now, the optimal serum testosterone level in patients under castration and the impact of its variations remain open questions and have been merged to patients' heterogeneity in which a broad multitude of spectra of patients has been identified, due to emphatically miscellaneous related mechanisms regarding response to treatment, influencing the biology of the relapsing tumor and the sensitivity to subsequent therapies in the individual patient. The universe far beyond (below) 20-50 ng/dl testosterone levels warrants further investigation once have recently rescued CRPC patients. Mainly in the current scenario of advancements measured in a few months and under high costs, not reachable for most of the world population compared to the benefits of hormonal manipulation that are measured in years, denoting huge potential for accessible and durable effect expansion and optimization, essentially for the current tendency of a progressively more individual approach.

Written by:
Reis LO. Are you the author?
Surgery (Urology), University of Campinas - Unicamp, Campinas, Brazil.

Reference: Endocr Relat Cancer. 2012 Mar 7. Epub ahead of print.
doi: 10.1530/ERC-12-0040

PubMed Abstract
PMID: 22399012

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