Researchers from Massachusetts General Hospital report the discovery of a mechanism of action by which the common diabetes drug metformin is able to inhibit the spread pf pancreatic cancer. The team found that metformin decreases the inflammation and fibrosis that characterizes most pancreatic cancers, although the degree of this suppression may be most prevalent in obese patients. The study focused on pancreatic ductal adenocarcinoma, the most common form of pancreatic cancer, and the cause of almost 40,000 cancer deaths in the US annually. It has been previously noted that diabetic patients taking metformin exhibit a lower risk for developing ductal adenocarcinoma, but this is the first research to clarify the mechanism of action. The results of this study of animal and cellular models are published in the journal PLOS One.
Study coauthor Dai Fukumura, MD, PhD, at the Steele Laboratory of Tumor Biology in the MGH Department of Radiation Oncology, said "We found that metformin alleviates desmoplasia—an accumulation of dense connective tissue and tumor-associated immune cells that is a hallmark of pancreatic cancer—by inhibiting the activation of the pancreatic stellate cells that produce the extracellular matrix and by reprogramming immune cells to reduce inflammation." Coauthor Rakesh K. Jain, PhD, director of the Steele Laboratory, added that this understanding should aid in the identification of biomarkers that will point to the most promising patient candidates for metformin treatment.
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Read a press release on the study findings here.
The full journal article may be read here.