Researchers say they’ve identified the first stages of how pancreatic cancer starts. This could be a lifesaving discovery given that the cancer is usually not discovered until it’s very advanced, meaning it has one of the lowest survival rates, with only 3% of people living for five years after diagnosis. (In the UK, it affects 9000 people a year.)
Cancer biologist Peter Storz and his team at the Mayo Clinic studied how acinar cells in the pancreas develop precancerous lesions that sometimes become cancerous. Acinar cells’ usual job in the pancreas is to release digestive enzymes, making it easier for us to absorb food. Over 95% of pancreatic cancers are linked to a mutation of the Kras protein, which regulates cell division.
The researchers found that Kras mutations in the acinar cells triggered a molecule called ICAM-1, which attracts macrophages, a type of immune cell that causes inflammation by encouraging the release of different proteins, some of which loosen cell structure, allowing acinar cells to mutate, thus producing the precancerous lesions.
‘We show a direct link between Kras mutations and the inflammatory environment that drives the initiation of pancreatic cancer,’ says Dr Storz. Even better, they’ve had some success at stopping this process in its tracks in the lab, finding that ICAM-1 can be shut down with an antibody designed to block it, or by reducing the number of macrophages. They’ll now work to find the best method of treating and preventing pancreatic cancer.
Image by Nephron via Wikimedia Commons.
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