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Pancreatic Cancer Study Reveals Mechanism Initiating Disease, In Mice
Date:3/11/2010

the mutated KRAS blocked the action of a protein know as beta catenin. They also showed that beta catenin was required for efficient acinar regeneration. Most notably, they showed that when beta-catenin’s signaling pathways were forcibly maintained in the context of the KRAS mutation, acinar cells did not become PDA precursors.

“These results indicate that beta-catenin is essential for acinar regeneration,” says Hebrok, a member of the UCSF Helen Diller Comprehensive Cancer Center. “They also demonstrate that beta-catenin signaling must be blocked in order for mutant Kras to exploit the plasticity of cell fate that arises during pancreatic damage and to force these de-differentiated cells to become PDA precursors.”

In the absence of injury, he says, “a mutation in Kras in an acinar cell likely would not cause the cell to undergo changes leading toward cancer, or it might cause these changes at a very slow rate. But if there is a mutation in Kras in a cell that has become de-differentiated in response to acute or chronic pancreatitis, this progression toward cancer would occur relatively quickly.”

The finding, he says, illuminates the fine line between regeneration and carcinogenesis in the body’s cells. “Cellular plasticity is necessary to allow damaged cells to activate their embryonic programs and temporarily activate embryonic signaling pathways to regenerate themselves,” says Hebrok. “But cells also need to be able to turn off these signaling pathways.”

“Our study underlines the likelihood that not only must mutations be acquired in a specific sequence in order to develop PDA, but levels of developmental signaling pathways must be tightly regulated to alter normal cellular plasticity and drive neoplastic cell fates.”

The finding also reveals a new role of beta catenin in cancer. While the beta catenin and KRAS proteins appear to oppos
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