Canonical Wnt signaling in Pancreatic Ductal
Adenomacarcinoma

Abstract

Cancer is one of the major diseases causing worldwide death of human, related to some different epigenetic dysregulation. Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal cancer due to its rapid clinical progression and resistance to therapies. Recently, PDAC incidences have risen, while 5-year overall survival is about 6%. A primary complicating factor is the remarkable genetic & epigenetic heterogeneity of pancreatic cancer. Vividly, these highly variable alterations also define a core set of twelve signaling pathways along with cellular processes in most of PDAC tumors, including Wnt signaling also. One of the major dysregulation is overexpression of Wnt Proteins. There are 19 set of Wnt proteins found. In this project, novel IWP-2 inhibitor will focus a new light on cancer therapy. The findings indicate that WNT7B can serve as a primary determinant of differential Wnt/B-catenin activation in PDAC. Thereby, disrupting the interaction between Wnt ligands and their receptors may be suitable approach for therapeutic modulation of Wnt/B-catenin signaling in PDAC and other cancer contexts where the Wnt activation is mediated through ligand expression rather than mutations in members of canonical pathway