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Cell pathway on overdrive prevents cancer response to dietary restriction
Date:3/11/2009

ne in which the PTEN gene could be switched on or off, Kalaany tested whether a change in the PTEN gene alone could affect a tumor's sensitivity to DR. When the PTEN gene was turned off, the cancer cells were not affected by dietary restriction, and tumor size increased similarly in control and DR mice. But when PTEN was turned on, thereby restoring normal function to the PI3K pathway, the cells became sensitized to dietary restriction and tumor size was smaller in the DR group.

This research was confirmed in two mouse models of cancer, one with prostate cancer caused by PTEN deletion and one with lung cancer and a functioning PTEN gene. Again, the mice without the PTEN gene did not respond to dietary restriction, but the mice with a functioning PTEN gene were sensitive to dietary restriction.

Sabatini says that Kalaany's results could lead to cancer treatments tailored to the characteristics of an individual patient's tumor cells.

"Her findings suggest that if we have therapies that mimic dietary restriction, we could better predict which tumors would respond to those dietary restriction-mimicking drugs and which ones would not," says Sabatini.

Sabatini is also intrigued by the inverse relationship between too much food and an increase in tumors. "We already know that the United States has an epidemic of obesity and that obesity is probably the biggest contributor to cancer in the U.S., even more so than smoking. Does this research have anything to do with that correlation between obesity and cancer, that if we make animals really obese, that this pathway is also involved in determining their sensitivity to cancer? Answering that question is the next step."


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Contact: Nicole Giese
giese@wi.mit.edu
617-258-6851
Whitehead Institute for Biomedical Research
Source:Eurekalert

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