Certain forms of breast cancer occur when a certain gene, the p53 tumour suppressor gene, that normally stops the growth of cancer cells, mutates. In the study, mutant p53 cells stopped erratic cell growth and even died in some cases after being treated in a laboratory with statins.

The study suggests that the mutant p53 gene activates the same cellular pathway ‘€”the mevalonate pathway’€”that statins stunt. The mevalonate pathway is important in the body’€™s production of cholesterol.

The study, published in the journal Cell, found that the effects of statins were erased when the mevalonate pathway was reactivated, supporting the potential mechanism.

According to a HealthDay News report, the study author Dr Carol Prives from Columbia University in the US, is cautious in her enthusiasm about the results and their implications. Dr Prives noted that the study only adds the possibility that there may be classes of breast cancer that will respond better to treatment with statins than others, and the research is still far away from the bedside.

“By understanding better what sort of cells would respond to statins, one might have a better idea of whether or not to consider using them,” Dr Prives commented in the HealthDay News report. “The next step could be a trial of statins in women with breast cancer who have a mutated copy of the p53 gene.”

 

Sources: HealthDay News

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