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Testosterone Replacement, Low T, HCG, & Beyond
Prostate Related Issues
Testosterone paradox of advanced prostate cancer
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<blockquote data-quote="madman" data-source="post: 241126" data-attributes="member: 13851"><p><strong>Key points </strong></p><p><strong></strong></p><p><strong><em>• Androgens can drive prostate cancer growth providing the rationale for using deprivation of androgens as a first line of treatment for prostate cancer. Unfortunately, prostate cancer cells adapt to low androgen levels and eventually progress to a castration-resistant state </em></strong></p><p><strong><em></em></strong></p><p><strong><em>• Results of several studies have indicated a paradoxical decrease in tumor growth in prostate cancer models upon treatment with supraphysiological levels of testosterone. Evidence indicates several complementary mechanisms, including cell death and cytostasis, which might be responsible for paradoxical growth inhibition by supraphysiological testosterone </em></strong></p><p><strong><em></em></strong></p><p><strong><em>• Adaptive reliance on androgen signaling by castration-resistant prostate cancer cells becomes a therapeutic liability that can be exploited clinically through the administration of supraphysiological testosterone, an approach termed ‘bipolar androgen therapy’ (BAT). <u>The term bipolar is used to emphasize that, with this strategy, rapid cycling occurs between two extremes</u>: from supraphysiological back to near-castration testosterone levels over a 4-week cycle </em></strong></p><p></p><p><em><strong>• Understanding how BAT works at the molecular and cellular levels might help to develop biomarkers for patient stratification and to rationally combine BAT with other agents to achieve increased efficacy</strong></em></p></blockquote><p></p>
[QUOTE="madman, post: 241126, member: 13851"] [B]Key points [I]• Androgens can drive prostate cancer growth providing the rationale for using deprivation of androgens as a first line of treatment for prostate cancer. Unfortunately, prostate cancer cells adapt to low androgen levels and eventually progress to a castration-resistant state • Results of several studies have indicated a paradoxical decrease in tumor growth in prostate cancer models upon treatment with supraphysiological levels of testosterone. Evidence indicates several complementary mechanisms, including cell death and cytostasis, which might be responsible for paradoxical growth inhibition by supraphysiological testosterone • Adaptive reliance on androgen signaling by castration-resistant prostate cancer cells becomes a therapeutic liability that can be exploited clinically through the administration of supraphysiological testosterone, an approach termed ‘bipolar androgen therapy’ (BAT). [U]The term bipolar is used to emphasize that, with this strategy, rapid cycling occurs between two extremes[/U]: from supraphysiological back to near-castration testosterone levels over a 4-week cycle [/I][/B] [I][B]• Understanding how BAT works at the molecular and cellular levels might help to develop biomarkers for patient stratification and to rationally combine BAT with other agents to achieve increased efficacy[/B][/I] [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Prostate Related Issues
Testosterone paradox of advanced prostate cancer
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