propecia x finasterida

Information is Power!

Mysterious p53 protein could be key to cancer cure

January 27, 2013 Pat Killingsworth No Comments

My good friend, fellow multiple myeloma (bone cancer) survivor, Barb Davis, sent me this link to a New York Times article a month ago.  I saved it to pass-along on a rainy day.

Not to rub-it-in, but it is bright, warm and sunny today in Weeki Wachee, Florida.  With no rain in sight, I wanted to share this excerpt with you now:

GENETIC GAMBLE

New Approaches to fighting cancer

Drugs Aim to Make Several Types of Cancer Self-Destruct

By Gina Kolata

Dr. Donald Bergstrom, cancer specialist at Sanofi

For the first time ever, three pharmaceutical companies are poised to test whether new drugs can work against a wide range of cancers independently of where they originated — breast, prostate, liver, lung. The drugs go after an aberration involving a cancer gene fundamental to tumor growth. Many scientists see this as the beginning of a new genetic age in cancer research.

Great uncertainties remain, but such drugs could mean new treatments for rare, neglected cancers, as well as common ones. Merck, Roche and Sanofi are racing to develop their own versions of a drug they hope will restore a mechanism that normally makes badly damaged cells self-destruct and could potentially be used against half of all cancers.

No pharmaceutical company has ever conducted a major clinical trial of a drug in patients who have many different kinds of cancer, researchers and federal regulators say. “This is a taste of the future in cancer drug development,” said Dr. Otis Webb Brawley, the chief medical and scientific officer of the American Cancer Society. “I expect the organ from which the cancer came from will be less important in the future and the molecular target more important,” he added.

And this has major implications for cancer philanthropy, experts say. Advocacy groups should shift from fund-raising for particular cancers to pushing for research aimed at many kinds of cancer at once, Dr. Brawley said. John Walter, the chief executive officer of the Leukemia and Lymphoma Society, concurred, saying that by pooling forces “our strength can be leveraged…”

The genetic alteration the drug targets has tantalized researchers for decades. Normal healthy cells have a mechanism that tells them to die if their DNA is too badly damaged to repair. Cancer cells have grotesquely damaged DNA, so ordinarily they would self-destruct. A protein known as p53 that Dr. Gary Gilliland of Merck calls the cell’s angel of death normally sets things in motion. But cancer cells disable p53, either directly, with a mutation, or indirectly, by attaching the p53 protein to another cellular protein that blocks it. The dream of cancer researchers has long been to reanimate p53 in cancer cells so they will die on their own.

The p53 story began in earnest about 20 years ago. Excitement ran so high that, in 1993, Science magazine anointed it Molecule of the Year and put it on the cover. An editorial held out the possibility of “a cure of a terrible killer in the not too distant future.”

Companies began chasing a drug to restore p53 in cells where it was disabled by mutations. But while scientists know how to block genes, they have not figured out how to add or restore them. Researchers tried gene therapy, adding good copies of the p53 gene to cancer cells. That did not work….

Roche was the first to start testing a p53 drug in patients. The company began, as required, with an attempt to establish a dose strong enough to be effective but not too toxic. It took a surprisingly long time — three years — because Roche was cautious, starting with a tiny dose and gradually escalating it.

Health authorities in the United States and Europe worried that the medicines might have unexpected effects.

“Drugs of this type had never been given to a human being,” Dr. Gwen Nichols of Roche said.

The studies looked only at safety, but Dr. Nichols said there were encouraging hints that the drugs might be working. In biopsies and scans, cancer cells appeared to be dying. Rigorous efficacy studies are next. If they are successful, they will be followed by clinical trials across cancer types.

More recently, Merck began its study to find a safe dose. It is enrolling only patients with acute myelogenous leukemia, a cancer in which p53 is almost always disabled by the blocking protein MDM2.

Once the company finds the best dose, it plans to give its drug to just 15 to 30 patients and look for efficacy. And if the drug fails to break apart the two huge proteins and enable the angel of death to do its job?

The article is so long I can’t reproduce it here.  Read more by clicking below:

http://www.nytimes.com/2012/12/23/health/new-drugs-aim-to-make-cells-destroy-cancer.html?_r=0

Aren’t researchers due for a blockbuster breakthrough like this one might be?  Keep your fingers crossed!

Feel good and keep smiling!  Pat

Be Sociable, Share!

p53, p53 protein, research collaboration Cancers, Research

Leave a Reply