YAP1 and TAZ Control Pancreatic Cancer Initiation in Mice by Direct Upregulation of JAK–STAT3 Signaling

Pancreatitis is the most important risk factor for pancreatic ductal adenocarcinoma (PDAC). Pancreatitis predisposes to PDAC because it induces a process of acinar cell reprogramming known as acinar-to-duct metaplasia (ADM)—a precursor of pancreatic intra-epithelial neoplasia lesions that can progress to PDAC. Mutations in KRAS are found at the earliest stages of pancreatic tumorigenesis, and it appears to be a gatekeeper to cancer progression. We investigated how mutations in KRAS cooperate with pancreatitis to promote pancreatic cancer progression in mice.

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