Custom-Fit Treatments for Prostate Cancer

hopeful and optimistic

http://online.wsj.com/news/article_email/SB10001424052702303819704579318943273912098-lMyQjAxMTA0MDEwMzExNDMyWj

VascodaGama

Interesting article indeed

Ira

Thanks for bringing about this article of the Wall Street Journal. This is not new to us but newbies will benefit in knowing that diagnosis based on genetics will be important in their decisions of a treatment and subsequent follow-ups. We have discussed in this forum before about the relationship between genetics and PCa, and this article summarizes our thoughts and confirm the way we will be seeing the medical community in dealing with PCa, in the future.

Ron Winslow, the writer/editor at WSJ, has some glitches in his writings. He may have miss interpreted the comments from the doctors he has consulted, but overall the article is well described and focus on his main subject of “Custom-Fit Treatments for Prostate Cancer”.

According to the article, researchers at MSKCC identified the reason for the higher rates of success of RT when administered in combination with HT. They say that HT “immobilizes” the action of the androgens receptors (AR) of cancer cells inhibiting the cells capability for repairing the damage cause by radiation (RT) at the DNA of the cancer. This corresponds to the 35% improvement in combo treatment over radiation alone, we know from other studies.
What impressed me was the comment about the type of some Pca cells that have low AR activity. These may also reflect in those patients in whom HT as prime therapy does not work as well as it does in some others.

If I am correct in judging the facts, the matter could also resume to that recurrences from combo treatments may not be tackled with a sequential therapy of typical HT (ADT) because the “leftovers PCa” from the combo are made of cells with insignificant ARs. By other words, these tumors are made up of cancer cells that do not dependent on testosterone for survival. They may be the cells that produce their own intratumoral androgens (food) that can only be tackled with the second-line drugs such as Zytiga and Ketoconazole (CYP17A1 enzyme inhibitor).

The overall spectrum of the above study will surely “modify” the way some treatments are administerd today. An example we may see as modified is to have LHRH agonist (such as Lupron) suppressed from protocols using Zytiga. We may as well see HRPC patients that lost the benefit of the AAWR phenomenon (androgen withdrawing response) to stop taking agonist or antagonists.

Interesting article indeed.

Best wishes for 2014.

VGama 

 

richardlvance

VascodaGama said:

Interesting article indeed

Ira

Thanks for bringing about this article of the Wall Street Journal. This is not new to us but newbies will benefit in knowing that diagnosis based on genetics will be important in their decisions of a treatment and subsequent follow-ups. We have discussed in this forum before about the relationship between genetics and PCa, and this article summarizes our thoughts and confirm the way we will be seeing the medical community in dealing with PCa, in the future.

Ron Winslow, the writer/editor at WSJ, has some glitches in his writings. He may have miss interpreted the comments from the doctors he has consulted, but overall the article is well described and focus on his main subject of “Custom-Fit Treatments for Prostate Cancer”.

According to the article, researchers at MSKCC identified the reason for the higher rates of success of RT when administered in combination with HT. They say that HT “immobilizes” the action of the androgens receptors (AR) of cancer cells inhibiting the cells capability for repairing the damage cause by radiation (RT) at the DNA of the cancer. This corresponds to the 35% improvement in combo treatment over radiation alone, we know from other studies.
What impressed me was the comment about the type of some Pca cells that have low AR activity. These may also reflect in those patients in whom HT as prime therapy does not work as well as it does in some others.

If I am correct in judging the facts, the matter could also resume to that recurrences from combo treatments may not be tackled with a sequential therapy of typical HT (ADT) because the “leftovers PCa” from the combo are made of cells with insignificant ARs. By other words, these tumors are made up of cancer cells that do not dependent on testosterone for survival. They may be the cells that produce their own intratumoral androgens (food) that can only be tackled with the second-line drugs such as Zytiga and Ketoconazole (CYP17A1 enzyme inhibitor).

The overall spectrum of the above study will surely “modify” the way some treatments are administerd today. An example we may see as modified is to have LHRH agonist (such as Lupron) suppressed from protocols using Zytiga. We may as well see HRPC patients that lost the benefit of the AAWR phenomenon (androgen withdrawing response) to stop taking agonist or antagonists.

Interesting article indeed.

Best wishes for 2014.

VGama 

 

HT+RT

I believe this course of treatment was especially good for intermediate risk.

And they are talking now about putting low risk PC men on Casodex for life

to prevent the need for any additional treatment.