BioMed Central Gastroenterology
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.
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). Open Dartmouth: Faculty Open Access Articles. 590.