THURSDAY, Jan. 19 (HealthDay News) -- Amid hints that statins -- cholesterol-lowering drugs -- might also play a role in preventing or treating certain types of cancer, new research sheds some light on how these drugs may help stop breast cancer in its tracks among certain women.
The p53 tumor suppressor gene stops the uncontrolled growth of cancer cells, but some women with breast cancer have mutant forms of this gene. In the new study, when the mutant p53 cells were treated in the laboratory with statins, the cells stopped their erratic growth, and even died in some cases.
It seems that the mutated p53 genes may activate the same pathway that the statins inhibit -- the mevalonate pathway, the study suggests. The mevalonate pathway is important in the body's production of cholesterol.
In the study, the effects of the statin drugs were erased when the mevalonate pathway was reactivated, supporting the potential mechanism. The new research is published in the Jan. 20 issue of the journal Cell.
Study author Dr. Carol Prives, chair of the department of biological sciences at Columbia University in New York City, is cautious in her enthusiasm about the results and their implications.
"The study is adding the possibility that there may be classes of breast cancer patients who will respond better to statins than others," she said, but noted that this research is far away from the bedside.
"By understanding better what sort of cells would respond to statins, one might have a better idea of whether or not to consider using them," she added. "The next step could be a trial of statins in women with breast cancer who have a mutated copy of the p53 gene."
Commenting on the study, cancer expert Marc Symons said, "This paper unravels a mechanism whereby p53, a frequently mutated cancer gene, promotes the aberrant behavior of cancer cells."
The mutated protein stimulates the mevalonate pathway, explained Symons, an investigator at the Center for Oncology and Cell Biology at the Feinstein Institute for Medical Research in Manhasset, N.Y.
"Statins, drugs that are widely used to lower cholesterol levels, block a key step in the mevalonate pathway," Symons said. "The new results may well give new momentum to the use of statins as anti-cancer agents."
Dr. Stephanie Bernik, chief of surgical oncology at Lenox Hill Hospital in New York City, is also intrigued by the potential of the new findings.
"This paper addresses a possible new target for therapeutic agents based on a well-known tumor suppressor gene that is common in many cancers," Bernik said. "Identifying novel pathways that lead to tumor formation is the first step to developing new drugs that can specifically target some of the complex mechanisms that contribute to the development of cancer," she pointed out.
"This work and other projects like this raise the hope that we will one day be able to cure cancers on a molecular level," Bernik said.
Learn more about how breast cancer is treated at the U.S. National Cancer Institute.
SOURCES: Carol Prives, Ph.D., DaCosta Professor of Biology and chair, department of biological sciences at Columbia University, New York City; Marc Symons, Ph.D., investigator, Center for Oncology and Cell Biology, Feinstein Institute of Medical Research, Manhasset, N.Y.; Stephanie Bernik, M.D., chief, surgical oncology, Lenox Hill Hospital, New York City; Jan. 20, 2012, Cell
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