In a new study from the University of Texas, researchers clarified the long-established connection between inflammation and pancreatic cancer development.
They found pancreatic cells display an adaptive response to repeated inflammatory episodes that initially protects against tissue damage but can promote tumor formation in the presence of mutant KRAS.
The team demonstrated that mutant KRAS—which is found in roughly 95% of all pancreatic cancers—supports this adaptive response, leading to selective pressure to maintain the cancer-causing mutation.
Inflammation has long been linked to tumor development in several cancer types, but the specific reasons behind this connection were previously unclear.
In the study, the team sought to examine the effect of pancreatitis—a condition of inflammation in the pancreas linked with a higher risk of pancreatic cancer—on pancreatic epithelial cells.
The researchers stimulated transient inflammation in a model system of inducible KRAS-driven pancreatic cancer. Inflammation caused immediate pathological changes in pancreatic cells, but they resolved within one week.
However, activation of KRAS even months following the resolution of inflammation resulted in accelerated tumor formation compared with controls.
This suggests that inflammation drives long-term changes in epithelial cells that cooperate with mutant KRAS to promote cancer development.
Researchers suggest that KRAS initially has a beneficial role during pancreatitis. There may be a 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 research team now is working to develop new treatments for pancreatitis that could also prevent pancreatic cancer development.
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The study is published in Science. One author of the study is Andrea Viale, M.D.
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