A bright future for protein kinase D1 as a drug target to prevent or treat pancreatic cancer. (2nd January 2016)

• Record Type: Journal Article
• Authors: Liou, Geou-Yarh; Storz, Peter; Leitges, Michael
• Is Part Of: Molecular & cellular oncology. Volume 3:Number 1(2016)
• Publication Date: 2016-01-02
• Subjects: Acinar-to-ductal metaplasia -- mechanisms of oncogenesis and tumor progression -- mouse model -- oncogenic Kras -- pancreatic cancer -- protein kinase D1; Tumors -- Periodicals; Neoplasms; Periodicals; 616.99
• DOI: 10.1080/23723556.2015.1035477
• Languages: English
• ISSNs: 2372-3556

Abstract

Abstract: Pancreatic ductal adenocarcinoma originates from acinar cells that undergo acinar-to-ductal metaplasia (ADM). ADM is initiated in response to growth factors, inflammation, and oncogene activation and leads to a de-differentiated, duct-like phenotype. Our recent publication demonstrated a transforming growth factor α-Kras G12D -protein kinase D1-Notch1 signaling axis driving the induction of ADM and further progression to pancreatic intraepithelial neoplasia. This suggests that protein kinase D1 might be an early marker for tumor development and a potential target for drug development.