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C-myc causes hormones to lose control in recurrent prostate cancer

Current treatment for progressed prostate cancer is withdrawal of the hormone androgen. While initially effective, this treatment is unable to completely and permanently eliminate all prostate cancer cells. It is not uncommon, that after a patient shows an initial response to treatment, there is a relapse as the cancer progresses to an androgen-independent stage.

A major goal of researchers has been to identify the molecular mechanisms involved in the progression of prostate cancer from androgen dependence to independence.

David Beach and colleagues from University College London studied the ability of c-myc to confer androgen-independent prostate cancer cell growth. In the December 4 issue of the Journal of Clinical Investigation these authors report that ectopic expression of c-myc allowed human androgen-dependent prostate cancer cells to grow without androgen stimulation and to keep their tumorigenic activity in androgen-depleted conditions.

Analysis of signaling pathways showed that c-myc is regulated by the androgen receptor, is required for androgen-dependent growth and, following ectopic expression, can induce androgen-independent growth.

In addition, c-myc downregulation slowed the growth of androgen-independent tumor cell lines. These results suggest a physiological role for c-myc in prostate cancer and a possible target for therapeutic intervention.


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Contact: Brooke Grindlinger
science_editor@the-jci.org
212-342-9006
Journal of Clinical Investigation
4-Dec-2003


Page: 1

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