IL-17 and Reg3β are emerging players in the microenvironment by promoting pancreatic cancer in chronic pancreatitis

Juan Iovanna

Abstract


Chronic pancreatitis is clearly linked to a significantly increased risk of pancreatic ductal adenocarcinoma (PDAC), but the mechanism of tumorigenesis involved in this process has not been completely defined. It is well known that precursor lesions PanIN can be induced by activation of KRAS but the progression to PDAC requires an additional challenge such as chronic inflammation. An unexpected dialogue was recently established between tumor stroma and epithelial pancreatic cells, which plays a major role in progression from chronic pancreatitis to PDAC. This pathway follows the axis IL-17-Reg3β-gp130-JAK-STAT, which contributes to PanIN progression, modulates the tumor-associated immune response and the response of the healthy tissue surrounding the tumor. This pathway is putatively targetable by chemical inhibitors or specific antibodies at different points and therefore, it should be considered as a novel strategy to prevent progression from chronic pancreatitis to PDAC.


Keywords


Reg-3beta, IL-17, chronic pancreatitis, pancreatic cancer

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References


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DOI: http://dx.doi.org/10.18103/imr.v0i4.88

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