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Drug tricks cancer, stops growth

By ED SUSMAN, UPI Science News

SAN FRANCISCO, April 9 (UPI) -- Scientists said Tuesday they have figured out a way to trick a cancerous tumor into thinking it is starving and has to shut down -- even when plenty of nutrients are available.

Faced with a perceived wasteland instead of an actual cornucopia, the cancer cells go into starvation mode and stop growing, preventing spread of the disease, researchers said.

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"Basically we fool the tumor cells into thinking that there are no nutrients around," said Tim Clackson, vice president for gene therapy and genomics at ARIAD Pharmaceuticals of Cambridge, Mass., during a news briefing at the annual meeting of the American Association for Cancer Research in San Francisco, Calif.

Clackson explained ARIAD scientists developed a drug -- a first cousin of rapamycin, a drug used to prevent organ rejection in transplant patients -- that attacks "an emerging target of anti-cancer therapy," a protein called mTOR.

He said mTOR coordinates the uptake of nutrients in cells needed for cell growth and cell division.

"The reaction between mTOR and rapamycin has been known for some time," said Frank Rauscher, professor and chairman of molecular genetics at The Wistar Institute, Philadelphia. "It is very important for nutrient balance."

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He said the rapamycin analog, called AP23573, is an example of drugs being developed for fighting cancer through understanding the structure of the molecular target and then modeling a compound to block the activity.

Clackson and colleagues administered AP23573 to groups of 10 mice that had been implanted with human brain cancers and received either the active drug or no drug. The mice that received intermittent treatment with AP23573 showed about a 46 percent shrinkage in the size of the tumors. If the mice did not receive the drug, their tumors grew an average of 150 percent.

Clarkson said the shrinkage could have been caused by two actions -- cells that are not growing tend to be small in size and it is possible that some died through a process known as apoptosis.

Clackson told United Press International the experimental mice had a denuded immune system so the tumors were not shrinking because of the natural defenses of the animal. However, he said human immune system interactions might also be able to attack the static tumor cell.

"The intermittent schedule is important," Clackson said, "because in that way we can prevent buildup of AP23573 in the blood and keep it from functioning as an immunosuppressant."

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To prevent organ rejection in patients receiving donor organ transplants, a high level of rapamycin in the blood has to be maintained. Immunosuppression in a patient with cancer would be counter-productive since the patient's immune system is being called upon to get rid of cancers.

Clackson said the drug has been formulated to be taken orally or through injections.

He said the company will begin recruiting patients to begin safety and toxicity studies of AP23573 later this year.

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