Researchers from the Massachusetts General Hospital have discovered that metformin, the most commonly prescribed diabetes drug, reduces inflammation and fibrosis characteristics of the most common form of pancreatic cancer. Those who benefit the most from the unintended effect of the drug are overweight and obese patients.

The discovery of the novel mechanism behind metformin’s ability to inhibit progression of pancreatic cancer adds to the growing list of metformin’s potential beyond diabetes. There is an ongoing human clinical trial in the US on the use of metformin as an anti-ageing medication which could possibly prolong life up to an average of 120 years. The drug could also treat pre-eclampsia and breast cancer too.

In the Massachusetts study, half of the pancreatic cancer patients are overweight or obese and up to 80 percent have type 2 diabetes or insulin-resistant. Diabetics taking the drug have lower risk of developing pancreatic cancer and for those who develop tumour, reduced risk of death, reports Thehansindia.

In tumour samples from overweight or obese patients, levels of hyaluronan, a component of the extracellular matrix, were 30 percent lower for those who took metformin. When the drug was given to obese animal model of pancreatic cancer, it reduced expression of both hyaluronan and collagen-1. The animals also had fewer activated pancreatic stellate cells.

Obese mouse models treated with metformin cut metastasis-associated changes in epithelial, a cellular characteristic, to mesenchymial transition and overall level of metastasis. Those effects on tumour are independent of metformin’s effect on metabolic pathways involved in glucose metabolism and body weight.

“Understanding the mechanism behind metformin’s effects on pancreatic and other cancers may help up identify biomarkers – such as patent body weight and increase tumor fibrosis – that can identify the patients for whom metformin treatment would be most beneficial,” says Rakesh Jainn, co-senior author of the study, published in PLOS.