| Literature DB >> 27308552 |
Geou-Yarh Liou1, Peter Storz1, Michael Leitges2.
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.Entities:
Keywords: Acinar-to-ductal metaplasia; mechanisms of oncogenesis and tumor progression; mouse model; oncogenic Kras; pancreatic cancer; protein kinase D1
Year: 2015 PMID: 27308552 PMCID: PMC4845192 DOI: 10.1080/23723556.2015.1035477
Source DB: PubMed Journal: Mol Cell Oncol ISSN: 2372-3556