BALTIMORE, MD -- October 1, 2007 -- A popular prostate cancer treatment
called androgen deprivation therapy may encourage prostate cancer cells
to produce a protein that makes them more likely to spread throughout
the body, a new study by Johns Hopkins researchers suggests.

Although the finding could eventually lead to changes in this standard
treatment for a sometimes deadly disease, the Johns Hopkins researchers
caution that their discovery is far too preliminary for prostate cancer
patients or physicians to stop using it.

The therapy is effective at slowing tumor growth, they emphasized.

David Berman, an assistant professor of pathology, urology and oncology
at The Johns Hopkins University School of Medicine, and his colleagues
identified the unsuspected potential problem with treatments that
suppress testosterone after discovering that the gene that codes for the
protein, called nestin, was active in lab-grown human prostate cancer
cells.

Curious about whether prostate cancer cells in people also produce
nestin, the researchers looked for it in cells taken from men who had
surgery to remove locally confined cancers of their prostates and found
none. But when they looked for nestin in prostate cancer cells isolated
from patients who had died of metastatic prostate cancer - in which
cancer cells spread out from the prostate tumor - they found substantial
evidence that the nestin gene was active.

What was different, Berman speculated, is that androgen deprivation
therapy, a treatment that reduces testosterone in the body, is generally
given only when prostate cancers become aggressive and likely to
metastasize.

Because prostate cancer growth is typically stimulated by testosterone,
the treatment is thought to slow tumor growth and weaken the disease.
Patients who eventually die because their disease metastasizes are
almost certain to have received this type of therapy, he says.

Speculating that depriving cells of androgens might also, however,
affect nestin expression, the researchers experimented on a prostate
cancer cell line that depends on androgens to grow. When they removed
androgens from the chemical mixture that the cells live in, their
production of nestin increased.

Aware that the nestin gene has long been suggested to play some role in
cell growth and development, Berman and his colleagues used a bit of
laboratory sabotage called RNA interference to decrease the genetic
expression of nestin and found that these cells weren't able to move
around and through other cells nearly as well as cells with normal
nestin levels.

Prostate cancer cells with hampered nestin expression were also less
likely than normal prostate cancer cells to migrate to other parts of
the body when transplanted into mice. However, while nestin expression
seemed pivotal for metastasis in these experiments, it didn't seem to
make a difference in tumor growth.

"What all this suggests is that nestin levels increased when prostate
cancer cells are deprived of androgens and may encourage the cells to
metastasize," says Berman.

Besides Berman, other Johns Hopkins researchers involved in this study
were Wolfram Kleeberger, MD, G. Steven Bova, MD, Matthew E. Nielsen, MD,
Mehsati Herawi, MD, PhD, Ai-Ying Chuang, MD, and Jonathan I. Epstein,
MD.

The research, published in the Oct. 1 issue of Cancer Research, was
funded by grants from the National Institutes of Health, National Cancer
Institute, Evensen Family Foundation, and German Cancer Aid Foundation.

SOURCE: Johns Hopkins Medical Institutions

knowledge is power - growing old is mandatory - growing wise is optional    
"Many more men die with prostate cancer than of it. Growing old is
invariably fatal. Prostate cancer is only sometimes so."
http://community.webtv.net/PALMER_ENT/doc