Here's the New York Times article on it:
September 2, 1998
A Protein Is Said to Predict Prostate Cancer's Virulence
By JANE E. BRODY
NEW YORK -- Researchers at Memorial Sloan-Kettering Cancer Center here
have found that a protein seems to predict which prostate cancers are
likely to be deadly and warrant aggressive treatment and which can be
controlled with less treatment or perhaps none at all.
The new findings, published this week in The Journal of the National
Cancer Institute, also support the current understanding that benign
enlargement of the prostate, which occurs in many men as they age,
is an entirely separate development from prostate cancer and does not
lead to it.
The studies involve a protein called p27, which other research
suggests plays an important role in controlling the growth of many
cancers that arise in lining tissues throughout the body. Studies in
Boston, Seattle, Toronto and England have linked abnormally low levels
of the p27 protein to aggressive cancers of the breast, the colon, the
lung and the esophagus.
"This protein represents a common mechanism that helps to control and
regulate cell growth," explained Dr. Howard Scher, who directs
genitourinary oncology at Memorial Sloan-Kettering. "It may help us
predict who will be cured and who won't, and help determine who may
need additional treatment to improve the chance of cure."
Dr. Carlos Cordon-Cardo, director of molecular pathology at
Sloan-Kettering, said p27 acted like a brake that kept cell growth in
check. When levels of this protein are low or absent, cells are likely
to proliferate rapidly. Rapid cell growth can increase the chances of
genetic mutations that may allow a cancer to develop and grow
uncontrolled.
Cordon-Cardo explained that men with prostate cancer have a normal
gene that regulates the production of the p27 protein. But in those
with an aggressive prostate cancer that is most likely to spread and
be fatal, the tumor seems to have "a professional blender" that chews
up the protein. In men with less aggressive tumors that may be curable
without extensive treatment, p27 levels are much higher, he said.
"Two tumors may look alike under the microscope," Cordon-Cardo said,
and "yet one patient may go on for years without the cancer spreading,
and the other may die of his cancer in two years. If we can
prognosticate at the time of diagnosis, we can determine who should be
treated more aggressively."
In treatment of prostate cancer, the choices include radical surgery,
radiation therapy, radioactive implants, hormonal control and
chemotherapy, all of which involve varying degrees of both short-term
and long-lasting side effects.
The emerging understanding of p27's role in cancer grows out of
previous work by Dr. Joan Massague and Dr. Andrew Koff, molecular
biologists at Sloan-Kettering who first isolated and cloned the
protein. Koff showed that mice without the p27 gene developed
overgrowth of the prostate gland, similar to the growth that occurs in
men with benign prostatic hyperplasia.
In men with this benign condition, the p27 gene is inactive, and
little or no p27 protein is produced. In men with prostate cancer, on
the other hand, the gene is active, but in some cases the tumor has
the ability to chew up the protein that the gene produces.
The degradation of p27 protein by cancers of the colon was first
described last year by Dr. Massimo Loda of the Dana-Farber Cancer
Institute in Boston and Dr. Miguele Pagano of New York University.
Loda said that in colon cancer patients who initially had high levels
of the protein but whose tumors spread years later, the protein was
lost in the process of metastasis. "We also found that p27 protein was
involved in lung cancers and breast cancers," Loda said.
Scher, of Sloan-Kettering, suggested that in the future it might be
possible to identify a switch that would enable the p27 protein to
remain active and slow the growth of tumor cells. |
