Researchers investigating how inflammation is associated with the development of pancreatic cancer have published new findings which clarify the link.

The new study found that while pancreatic cells show an adaptive response to repeat inflammation which protects against tissue damage initially, this process can support the formation of tumours in the presence of mutant KRAS, which is found in roughly 95% of all pancreatic cancers.

While the link between inflammation and tumour development in a number of cancers is well-known, the team from the University of Texas MD Anderson Cancer Center set out to investigate the effect of pancreatitis – inflammation in the pancreas linked to a greater risk of pancreatic cancer – on pancreatic epithelial cells.

Corresponding author Dr Andrea Viale, assistant professor of Genomic Medicine, said: “We discovered that a single transient inflammatory event induced long-term transcriptomic and epigenetic reprogramming of epithelial cells that cooperated with oncogenic KRAS to promote pancreatic tumours long after the inflammation was resolved.

“In the setting of repeated pancreatitis, KRAS mutations can be acquired early on to limit tissue damage, suggesting the existence of a strong evolutionary pressure to select mutated cells and providing a possible explanation for the nearly universal presence of mutant KRAS in pancreatic cancers.”

Modelling by the researchers suggested that inflammation promotes long-term changes in epithelial cells that work with mutant KRAS to promote cancer development. Researchers identified cellular reprogramming of epithelial cells following a single inflammatory event, which continued long after recovery of the tissue damage – a process described by researchers as ‘epithelial memory’. This reprogramming prompted pathways relating to cell survival, proliferation, and embryonic development – similar to pathways seen during the development of cancer.

Co-first author I-Lin Ho, graduate student in the Viale Laboratory, said: “We are working to better understand how cells maintain the epithelial memory we observed, but our data suggest that KRAS initially has a beneficial role during pancreatitis. There may be similar phenomenon in other cancers with universal driver mutations, where there is a strong pressure to select those mutations based on some purpose unrelated to cancer development.”

The study has been published in Science.

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