Inexpensive diabetes drug may reduce DNA damage, cancer risks
The diabetes drug metformin may reduce the risk of developing cancer by reducing the cellular mutation rate and the accumulation of DNA damage, according to a paper published in Cancer Prevention Research.
“It is remarkable that metformin, an inexpensive, off-patent, safe and widely used drug, has several biological actions that may result in reduced cancer risk–these latest finding suggest that it reduces mutation rate in somatic cells, providing an additional mechanism by which it could prevent cancer,” said Dr. Michael Pollak, professor in McGill University's Departments of Medicine and Oncology and the study's director.
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The study found that metformin reduces the levels of reactive oxygen species (ROS) that are known to damage DNA. Cells in mitochondria generate energy by burning nutrients, producing ROS as byproducts.
It's well established that the cellular mutation rate and the accumulation of DHA damage are directly involved in the development of cancer.
“We found that metformin did not act as a classic antioxidant,” said Dr. Gerardo Ferbeyre at the University of Montreal and co-author of the study. “The drug seems to selectively prevent ROS production from altered mitochondria such as those found in cells with oncogenic mutations.”
Past studies have shown that metformin works within the mitochondria to act against diabetes as well.
“This study opens an exciting new direction in cancer-prevention research,” said Pollak. “This doesn't imply, however, that metformin is now ready to be widely used for cancer prevention.”
According to Pollak, more research is needed about the efficacy of metformin as a cancer-fighting drug. For example, it's unknown what dosages are needed for metformin to accumulate in the right concentrations in breast or colon tissues that are at high risk for cancer. Also, the original studies that showed reduced cancer risk were performed on people with diabetes, so studies are required on people without diabetes.
“But the possibility of protecting DNA from oxidative damage by the use of a well-tolerated drug was not expected, and this topic now needs further study at many levels,” said Pollak.
Source: McGill University
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