And now … “the key to hormone-resistant prostate tumors”
Posted Mar 11 2010 12:00am
According to a new report from HealthDay , “scientists” have made yet another discovery in a mouse model that “may someday save men’s lives,” which may well be true, but is hardly “the key” promised in the article’s headline!
This report is based on a letter to the editor by Ammirante et al. in today’s issue of Nature. According to that study, there is a significant association between certain types of response to chronic inflammation in patients with hormone-sensitive prostate cancer that may actually be caused by hormone therapy. In other words, risk for development of castration-resistant prostate cancer may be a consequence of the body’s gradual response to inflammation initially induced by hormone therapy.
In the HeathDay report, what it actually states is that, “Doctors might be able to delay the onset of hormone-resistant tumors by two to three years if subsequent research finds a way to control the effects of inflammation.” (The bold italic type has been added for emphasis.) As usual, we are rapidly collecting a lot of ifs and mays in talking about this study which started out with such a categorical headline.
Things don’t get much better as the HealthDay article progresses:
“Don’t expect anything useful for humans anytime soon,” the article states. “Researchers will have to first make sure that human prostate cancer responds in the same way that the cancer did in mice.” And then it quotes Dr. Durado Brooks of the American Cancer Society:
‘ “There’s going to have to be a lot more work done to clarify that the mechanisms in humans are the same as those they have identified in mouse prostate cancer,” Brooks said. “It’s going to be quite a while before this mouse model moves to the bedside and actual clinical practice, if it ever does.” ‘
“What’s the bottom line to all of this?” you might well ask.
The bottom line is that Ammirante et al. have come up with an interesting scientific idea. That idea is that prostate cancer progression from androgen-sensitive to castration-resistant disease may be associated with”inflammatory infiltration” and activation of an enzyme called IKK-α, and that IKK-α then stimulates metastasis (at least in their mouse model). They also have shown (in their model) that “androgen ablation causes infiltration of regressing androgen-dependent tumors with leukocytes,” leading to the activation of IKK-α and another enzyme called STAT3 in prostate cancer cells, which enhance hormone-free survival.
It is certainly possible that an understanding of this biochemical pathway may have some significant impact on our ability to develop drugs that can prevent or delay the transition from hormone-sensitive to castration-resistant prostate cancer in some patients. It is also possible that we will never be able to replicate this effect in man.
While the hypothesis proposed by Ammirante et al. is interesting, it is far from justifying the media headlines. And we won’t be holding our breath in hope of a clinically effective therapeutic agent based on this research any time soon.