Statins May Keep Breast Cancer at Bay

Breast cancer patients with mutant p53 genes may benefit from statin therapy

/ Author:  / Reviewed by: Joseph V. Madia, MD

(RxWiki News) Years ago, cholesterol-lowering statin medications were thought to possibly cause cancer, bur large clinical trials disproved that therapy. Now, it seems these drugs may actually do just the opposite.

New research suggests that statins may control breast cancer in some patients who have a mutant tumor suppressor gene - p53.

Looking for mutations in this gene may also help determine if patients will respond to statin therapy.

"Ask your oncologist if DNA testing is right for you."

Carol Prives, Ph.D., the DaCosta Professor of Biology and chair of the Department of Biological Sciences at Columbia University, led the study. She is an expert in p53 gene mutations, which are involved in more than half of  all human cancers.

The p53 gene is involved in a number of aspects of cell growth. Its main role is to halt uncontrolled growth. However, when this gene is corrupted, the damage goes beyond disrupting its ability to stop disorganized growth.

Mutations create new functions that promote cancer growth. Why and how this happens has been a large question mark in the cancer research world.

In an attempt to unravel this mystery, researchers conducted experiments studying the behavior of cancer cells grown in an artificial environment that resembles a human breast. They found that cells with the faulty p53 grow in a chaotic and invasive manner, much like breast cancers do.

When the levels of mutant p53 genes were lowered, the 3-D cell cultures grew in a more normal fashion.

Additional studies under the direction of Columbia M.D./Ph.D, William Freed-Pastor, found these changes were linked to a cholesterol-lowering pathway - the mevalonate pathway - that's treated with statins.

When the faulty p53 cells were given statins, their growth became less disorganized and invasive. In some cases the treated cells died.

Prives and Freed-Pastor, working with collaborators in Norway, examined and analyzed tissue taken from breast cancer patients. They found that mutations in p53 and increased activity in the mevalonate pathway tend to go together in human tumors.

Prives said in a news release reporting these early findings, "There are great implications, but nothing clinical yet. Perhaps one could do a clinical trial, and that may support these findings, or it may be more complicated."

dailyRx asked Contributing Expert, Stig E. Bojesen, M.D., Ph.D., of Herlev Hospital, Copenhagen University Hospital and the University of Copenhagen to comment on this work. "This study seems very important because it asks the right questions and comes up with answers with an almost direct clinical implication," said Dr. Bojesen, who was not involved in this research.

"However, before giving statins without discrimination to all cancer patients, further substantiation in patients is needed. The ultimate study would be a randomized controlled trial of statins vs. placebo in newly diagnosed cancer patients large enough to give definitive answers," he said.

Dr. Bojesen continued, "The drawback is that these studies are very expensive and difficult to set up as well as the long (but necessary) follow-up time needed. Meanwhile, more observational studies could try to substantiate the finding and hopefully pinpoint the cancer patients most likely to benefit from statin treatment."

This research was published in the January 20th issue of the journal Cell, a Cell Press publication.

Reviewed by: 
Review Date: 
January 19, 2012
Last Updated:
January 19, 2012