Document Type
Article
Publication Date
9-2011
Publication Title
BioMed Central Gastroenterology
Department
Geisel School of Medicine
Abstract
Rb1 encodes a cell-cycle regulator that is functionally disrupted in most human cancers. Pancreatic ductal adenocarcinomas (PDACs) have a high frequency of mutations in KRAS and INK4A/CDKN2A that might allow cells to bypass the regulatory actions of retinoblastoma (RB). To determine the role of loss of RB function in PDAC progression, we investigated the effects of Rb disruption during pancreatic malignant transformation initiated by oncogenic Kras.We generated mice with pancreas-specific disruption of Rb, in the absence or presence of oncogenic Kras, to examine the role of RB in pancreatic carcinogenesis.
DOI
10.1053/j.gastro.2011.05.041
Original Citation
Carrière C, Gore AJ, Norris AM, Gunn JR, Young AL, Longnecker DS, Korc M. Deletion of Rb accelerates pancreatic carcinogenesis by oncogenic Kras and impairs senescence in premalignant lesions. Gastroenterology. 2011 Sep;141(3):1091-101. doi: 10.1053/j.gastro.2011.05.041. Epub 2011 May 27. PMID: 21699781; PMCID: PMC3163782.
Dartmouth Digital Commons Citation
Carrière, Catherine; Gore, A. Jesse; Norris, Alixanna M.; Gunn, Jason R.; Young, Alison; Longnecker, Daniel; and Korc, Murray, "Deletion of Rb Accelerates Pancreatic Carcinogenesis by Oncogenic Kras and Impairs Senescence in Pre-Malignant Lesions" (2011). Dartmouth Scholarship. 590.
https://digitalcommons.dartmouth.edu/facoa/590