Re: Research Yields Clues to Recurrent Prostate Cancer

[Guest guest]

Actually the determination of the presence of Stat5 existed when the

cancer was first diagnosed (see second paragraph below), and it was

that presence that could determine the likelihood of disease

recurrence despite various treatment options. From my

interpretation, this early Stat5 presence appears to then be an

impetus to aggressive cancer in recurrence leading to androgen

independent prostate cancer (AIPC) despite androgen deprivation

therapy. The commentary makes note that patients whose recurrence

eventually led to AIPC followed their having been treated with

androgen deprivation therapy. However, it doesn't appear to me that

ADT is the culprit, but rather the presence of Stat5 that causes ADT

failure and development to AIPC; particularly since the " findings "

also make particular note " in a form of prostate cancer for which

there are no effective therapies. "

Here is part of the same study as reported in Science Daily:

http://www.sciencedaily.com:80/releases/2007/12/071231091452.htm

" These findings validate Stat5 as a potential drug target in prostate

cancer, and in particular, in a form of prostate cancer for which

there are no effective therapies, " Dr. Nevalainen says.

Men with primary prostate cancer usually have either surgery or

radiation, whereas subsequent disease is frequently treated by

hormone therapy. But if the cancer recurs again, years later, it can

be more aggressive and typically fails to respond to hormone

treatment. In previous work, the researchers showed that when Stat5

is turned on in primary prostate cancer, men are more likely to have

recurrent disease.

In the current study, the team examined human prostate cancer cells

of 198 patients with prostate cancer recurrence. They found that

Stat5 was active in 74 percent of all recurrent prostate cancers. Of

these patients, 127 had been treated with androgen deprivation

therapy. The researchers found Stat5 was active in 95 percent of

these hormone resistant tumors, meaning it was more likely to be

active if the patient had been treated with hormone deprivation

therapy.

Dr. Nevalainen shows that Stat5 interacts with the androgen receptors

and keeps them " transcriptionally active. " Next, the scientists would

like to conduct tests in animal models to see if this synergy

promotes androgen-independent prostate tumor growth, and whether or

not Stat5 synergizes with androgen receptors activated by adrenal

androgens, which are present in the absence of testicular androgens

during the hormone therapy of prostate cancer in patients. "

It should be noted that research is already in progress to inhibit

the effects of Stat5:

http://otl.georgetown.edu/industry/inventions/nema432801.html

http://www.ncbi.nlm.nih.gov/sites/entrez?

db=pubmed & uid=16158916 & cmd=showdetailview & indexed=google

http://www.wi.mit.edu/research/summaries/lodish.html

(Chuck) Maack

Prostate Cancer Advocate

Wichita, Kansas Chapter, Us TOO

Bio: http://www.ustoowichita.org/leaders.cfm?content=bio & id=1

Email: maack1@...

>

> From US News and World

>

Report<http://health.usnews.com/usnews/health/healthday/080102/researc

h-yields-clues-to-recurrent-prostate-cancer.htm>

>

>

> " According to the researchers, Stat5 is more likely to be active if

patients

> are treated with androgen deprivation therapy. The protein

interacts with

> the hormone receptors and keeps them active.

>

> The researchers plan to test the dynamic between Stat5 and androgen

> receptors using animal models to find out if the relationship

produces

> androgen-independent prostate tumor growth. "

>

>

> --

>

> Emerson

> www.flhw.org

>