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Hormonal status of castration-resistant prostate cancer and cancer progression

Posted Sep 28 2008 5:40pm

According to a report in the June 1 issue of Cancer, researchers have uncovered new information about why metastatic prostate cancer may progress following failure of androgen-deprivation therapy (ADT).

ADT is designed to suppress circulating testosterone and other hormones that may promote prostate cancer growth. This is done by the use of surgical castration (orchiectomy) or medical castration with testosterone-blocking drugs such as LHRH agonists and antiandrogens, which can extend survival time for some patients, but do not offer a curative effect. Eventually, the prostate cancer will become “androgen resistant” and starts to grow again.

Dr. Elahe Mostaghel, a clinical research associate at the Fred Hutchinson Cancer Research Center in Seattle is quoted by HealthDay as stating, “We found that despite the suppression of circulating androgen levels to very low or castrate levels, metastatic prostate tumors are themselves able to maintain significant levels of testosterone, which fuels the growth of the cancer.”

Mostaghel and his colleagues discovered that testosterone levels in metastatic prostate tumors from men who had been castrated and had just died of prostate cancer were four times higher than testosterone levels in benign and cancerous prostate tissue in men with normal circulating androgen levels. They also demonstrated that metastatic prostate tumor tissue contains the genetic information needed to make the proteins that produce testosterone and other androgen hormones.

“We not only found that metastatic tumor tissues have high enough androgen levels within them to support continued growth of the tumor cells, but also a critically important reason behind why those androgens are there — the discovery that the gene pathways for synthesizing androgens from cholesterol appear to be present in the distant tumor sites. This finding will allow us to start honing in on the specific source of those androgens and how we can eliminate them,” Mostaghel said.

“As we develop new drug targets, we will need to focus on enzymes that seem to be active in the tumor itself. This offers a new way of looking at hormone suppression. In addition to systemic suppression, it suggests we also need to target hormone suppression much more specifically, inside the tumor itself.”

There has long been discussion about the precise nature of androgen-resistant prostate cancer because it has been clear that some forms of cancer are more androgen resistant than others. While this research may help to clarify the nature of androgen resistance in some patients, The “New” Prostate Cancer InfoLink is less sure that it will offer an absolute explanation for androgen resistance in all patients, and we should be cautious about over-interpretation of these data at this stage.

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