GRP78 haploinsufficiency suppresses acinar-to-ductal metaplasia, signaling, and mutant Kras -driven pancreatic tumorigenesis in mice
Year: 2017
Type: article
Abstract: Significance KRAS is mutated in more than 90% of pancreatic adenocarcinoma (PDAC). Despite its well-known role in cancer, development of drugs directly targeting KRAS has been unfruitful, underscoring the critical need to identify novel therapeutic targets. This study provides evidence that haploinsufficiency of a single cellular protein, GRP78, although having no harmful effect on the normal pancreas, is sufficient to impede Kras -driven pancreatic tumorigenesis in a genetically engineered mouse model. This study also establishes a role of GRP78 in acinar-to-ductal metaplasia, which is regarded as a precursor to PDAC development.
Language: English
Subfield: Oncology
Field: Medicine
Domain: Health Sciences
Open Access status: green
Awards: Stress Induction of Glucose Regulated Protein GRP78/BiP, Targeting Cell Surface GRP78 as a Novel Therapy for Pancreatic Cancer, Role of the Mullerian Tract in Ovarian Cancer Development, USC Research Center for Liver Disease, University of Southern California Norris Comprehensive Cancer Center Support Grant (CCSG)
OpenAlex ID: W2610196269