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How anti-diabetic drug could help cut cancer risk: Study

In 2005, news first broke that researchers in Scotland found unexpectedly low rates of cancer among diabetics taking the drug, which is commonly prescribed to patients with Type II diabetes.

How anti-diabetic drug could help cut cancer risk: Study

In a new study, scientists have tried to solve the mystery surrounding how the anti-diabetic drug metformin could reduce the risk of developing cancer and what were the mechanisms involved.

In 2005, news first broke that researchers in Scotland found unexpectedly low rates of cancer among diabetics taking the drug, which is commonly prescribed to patients with Type II diabetes.

Many follow-up studies reported similar findings, some suggesting as much as a 50 percent reduction in risk.

Fr the current study, researchers from McGill University and the University of Montreal reported an unexpected finding " they learned that exposure to metformin reduces the cellular mutation rate and the accumulation of DNA damage.

It is well known that such mutations are directly involved in carcinogenesis, but lowering cancer risk by inhibiting the mutation rate has never been shown to be feasible.

“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 findings suggest that it reduces mutation rate in somatic cells, providing an additional mechanism by which it could prevent cancer,” Newswise quoted Michael Pollak, professor in McGill’s Departments of Medicine and Oncology, researcher at the Lady Davis Institute for Medical Research at the Jewish General Hospital and the study’s director.

The study, carried out in collaboration with the laboratory of Dr. Gerardo Ferbeyre at Universite de Montréal’s Department of Biochemistry, suggests that metformin reduces DNA damage by reducing levels of reactive oxygen species (ROS).

ROS are known to be DNA-damaging agents produced as by-products when cells generate energy from nutrients. This action appears to take place in mitochondria, the cellular organelles that produce energy in cells by “burning” nutrients.

Past studies have identified the mitochondria as a site of action for metformin related to its anti-diabetic function, but those studies had not considered that the drug also acted here to reduce ROS production, thereby reducing the rate at which DNA damage accumulates.

“We found that metformin did not act as a classic antioxidant,” Ferbeyre said.

“The drug seems to selectively prevent ROS production from altered mitochondria such as those found in cells with oncogenic mutations,” he added.

The study has been recently published in the journal Cancer Prevention Research.
 

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