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Standard
treatment for Prostate Cancer may encourage
spread of disease
Newswise — 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, M.D., G.
Steven Bova, M.D., Matthew E. Nielsen, M.D.,
Mehsati Herawi, M.D., Ph.D., Ai-Ying Chuang,
M.D., and Jonathan I. Epstein, M.D.
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