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Pancreatic Ductal Adenocarcinoma (PDAC) belongs to the most aggressive malignancies among solid tumors. The increasing incidence of PDAC and its dismal prognosis with a five-years overall survival rate of less than five percent characterize PDAC as one of the most clinically challenging diseases among all malignancies. In recent years, increasing knowledge about the molecular pathogenesis of PDAC has shown that mutational activation of oncogenic Kras represents the defining event in pancreatic cancer initiation, but full neoplastic pancreatic cancer progression requires dysregulation of additional pathways. In this review we summarize and discuss the impact of inflammation-induced transcription of the Nuclear Factor of Activates T-cell (NFAT)-family in pancreatic carcinogenesis.
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