Mitsuru Sakitani*
Intraductal papillary neoplasm of the pancreas (IPMN) is a frequently found, pancreatic cystic neoplasm. IPMN has relatively high malignant potential, and its therapeutic strategy is limited to surgical resection. It is well known that mutations of GNAS and KRAS play important roles in its malignant progression, but its molecular mechanisms have not been well elucidated. In this review, clinical features and molecular alterations of IPMN were summarized. Then, crosstalk between KRAS signaling and phosphatidylinositol 3-kinase (PI3K) signaling was clarified. Finally, it was indicated that the final effector of KRAS mutant IPMN could be carbon anhydrase IX (CA9), and the possibility of molecular targeted therapy against IPMN by means of CA9 inhibitors was discussed.
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