| Autor: |
Ram Makena M; Department of Physiology, Johns Hopkins School of Medicine, Baltimore, MD 21205, USA., Gatla H; Department of Pediatric Oncology, Johns Hopkins School of Medicine, Baltimore, MD 21287, USA., Verlekar D; Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA., Sukhavasi S; Center for Distance Learning, GITAM University, Visakhapatnam 530045, India., K Pandey M; Department of Biomedical Sciences, Cooper Medical School of Rowan University, Camden, NJ 08103, USA., C Pramanik K; Department of Basic Sciences, Kentucky College of Osteopathic Medicine, University of Pikeville, Pikeville, KY 41501, USA. kartickpramanik@upike.edu. |
| Abstrakt: |
Pancreatic ductal adenocarcinoma (PDAC) is responsible for 7.3% of all cancer deaths. Even though there is a steady increase in patient survival for most cancers over the decades, the patient survival rate for pancreatic cancer remains low with current therapeutic strategies. The Wnt/β-catenin pathway controls the maintenance of somatic stem cells in many tissues and organs and is implicated in pancreatic carcinogenesis by regulating cell cycle progression, apoptosis, epithelial-mesenchymal transition (EMT), angiogenesis, stemness, tumor immune microenvironment, etc. Further, dysregulated Wnt has been shown to cause drug resistance in pancreatic cancer. Although different Wnt antagonists are effective in pancreatic patients, limitations remain that must be overcome to increase the survival benefits associated with this emerging therapy. In this review, we have summarized the role of Wnt signaling in pancreatic cancer and suggested future directions to enhance the survival of pancreatic cancer patients. |
