Baltimore, MD (3/4/99)- Progress in the war against prostate cancer,
in the form of a newly discovered genetic switch present in 90% of tumors,
should lead to improved diagnostic tests and treatment approaches with the
potential to cure the disease, say researchers.
Researchers at Johns Hopkins University report that a majority of prostate
cancers involve a hitherto unsuspected but common genetic process called "gene
switching". The process, also seen in many other malignancies including
breast cancer, occurs when some members of a family of genes are switched
on while others in the family shut down.
"It's a process common during embryonic development. We believe this is the
first time anyone's definitively linked gene switching within a family of
genes, with cancer," says Shrihari S. Kadkol, M.D., Ph.D., a molecular pathologist
at Johns Hopkins School of Medicine.
The
research began as an attempt to resolve a paradox. Previous studies had shown
that a powerful tumor suppressor gene called pp32 was actually overexpressed
in 90% of prostate cancers. A comparison of healthy prostate tissue and adjacent
cancerous tissue from patients revealed that the malignant tissue expresses
variants of pp32 (pp32r1 and pp32r2) that are cancer-causing,
rather than the tumor-suppressing pp32.
Photo- Prostate
Cancer Cells Lit Up with the "Bad" Form of pp32
The research raises the possibility of therapeutic manipulation of this genetic
expression pattern to either stop or reverse the progression from the benign
to the malignant state, says molecular pathologist Gary R. Pasternack, M.D.,
Ph.D., who led the Hopkins research team. "Most important is that someday,
it's likely we can reverse switching with drugs. This means one of the commonest
cancers in men has the potential of being corrected without using typical
gene therapy." If all goes well, new candidate drugs can be identified and
studied in clinical trials within two years, he added.
The new research may also lead to improved diagnosis of prostate cancer,
helping to identify patients at greatest risk of disease progression. Clinical
studies on this front are in the early stages.
HERCEPTIN FOR PROSTATE CANCER?
In related research, investigators at the University of California, Los Angeles
report a discovery suggesting that Herceptin, a new antibody therapy approved
for the treatment of advanced breast cancer, may also prove useful in the
treatment of prostate cancer.
Because prostate cancers are androgen-sensitive, conventional treatment often
involves chemical or surgical castration, which removes circulating androgens
that stimulate cancer growth. Unfortunately, some of these tumors convert
from being androgen-sensitive to being androgen-independent, leading to disease
progression. The UCLA team showed that androgen-independent tumors can be
generated in mice by stimulating HER-2/neu receptors of the androgen receptor
pathway. If this is also found to be the case with humans, Herceptin, which
blocks HER-2/neu receptors, would be a logical treatment to evaluate.
"If the HER-2/neu gene is indeed involved in making prostate cancer
cells androgen-independent, 'we may see a new treatment modality sooner than
we thought,'' noted Dr. Tapio Visakorpi, of the Laboratory of Cancer Genetics
at the University of Tampere, Finland.
Prostate cancer is the second-leading cancer killer of men, behind lung
cancer. The disease kills more than 41,000 men each year in the US and accounts
for nearly one-quarter of all newly diagnosed cancer cases annually. According
to the American Cancer Society, more than 210,000 American men are diagnosed
with prostate cancer each year.
Both studies appear in the March 1999 issue of Nature Medicine
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