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Sep 04, 2014 - 12:17 pm
This was posted over on the HW PCa forum today by Profman and it's pretty interesting:
http://www.healingwell.com/community/default.aspx?f=35&m=3174673
"The September 4 issue of the New England Journal of Medicine has an article "AR-V7 and Resistance to Enzalutamide and Abiraterone in Prostate Cancer" in which a variant of the androgen receptor has been identified which produces a receptor which is active in the absence of androgen. This variant receptor was expressed in all men with androgen-resistant prostate cancer, although the sample size was small (31 men). If these results hold up it would provide for a molecular marker to identify men for whom testosterone lowering therapy would not work, and for whom other treatments would be required. There is also an op-ed piece on this article in the same issue of the journal."
http://www.nejm.org/doi/full/10.1056/NEJMoa1315815
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Joined: Nov 2010
Extended HRPC in intratumoral therapies
Interesting article but I am not so sure if the patients in the study were castrate resistant. Last January Ira (http://csn.cancer.org/node/265961) also provided a link related to a similar theme with regards to cell’s AR (androgen receptors) via genetics in PCa (Custom-Fit Treatments for Prostate Cancer). The link informs about the work of researchers at Memorial Sloan-Kettering who identified the reason behind the benefits of combo therapies (HT+RT). The researcher (a radiation oncologist) say this “….androgen's role in prostate cancer goes beyond providing fuel for the tumor's growth; the male sex hormone also activates androgen receptors that turn on genes which repair damaged DNA….” This could be due to the power our cells (or genes) have as demonstrated in the Darwin’s principle, the mechanism of natural selection (survival of the fittest). Here is the link;
http://online.wsj.com/news/articles/SB10001424052702303819704579318943273912098
The study of your thread (AR-V7 and Resistance to Enzalutamide and Abiraterone in Prostate Cancer ) involves many famous researchers one of them the head of oncology Dr. Mario Eisenberger in Johns Hopkins.(my commandant till 2006). Their findings in HRPC patients could mean that this AR-V7 (RNA) was already existent in cells before start taking the intratumoral HT drugs (Zytiga or Xtandi) that later was found not to work at a number of patients, as a natural environment of our genes codes. But it could be that cells created such AR variant once threatened with the possibility of dying, as much as it is known that the same cell got the power to start producing its own androgens. All these theories justify Darwin’s evolutionary principle. I believe that our scientists are in the good track to find that silver bullet via DNA. At this time we may use it to get the best in treatments till the day we manage to alter the RNA sequence to live for good or, if such is impossible, then to live to the age we most prefer.
http://www.sciencedaily.com/releases/2014/08/140826091051.htm
Regards,
VG
Joined: Apr 2010
AR-V7 Variant in CRPC