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Full-Text Articles in Medicine and Health Sciences
Deletion Of Rb Accelerates Pancreatic Carcinogenesis By Oncogenic Kras And Impairs Senescence In Pre-Malignant Lesions, Catherine Carrière, A. Jesse Gore, Alixanna M. Norris, Jason R. Gunn, Alison Young, Daniel Longnecker, Murray Korc
Deletion Of Rb Accelerates Pancreatic Carcinogenesis By Oncogenic Kras And Impairs Senescence In Pre-Malignant Lesions, Catherine Carrière, A. Jesse Gore, Alixanna M. Norris, Jason R. Gunn, Alison Young, Daniel Longnecker, Murray Korc
Dartmouth Scholarship
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.
Ras Activity Levels Control The Development Of Pancreatic Diseases, Baoan Ji, Lilian Tsou, Huamin Wang, Sebastian Gaiser, David Chang, Jaroslaw Daniluk, Yan Bi, Tobias Grote, Daniel Longnecker, Craig Logsdon
Ras Activity Levels Control The Development Of Pancreatic Diseases, Baoan Ji, Lilian Tsou, Huamin Wang, Sebastian Gaiser, David Chang, Jaroslaw Daniluk, Yan Bi, Tobias Grote, Daniel Longnecker, Craig Logsdon
Dartmouth Scholarship
Differentiated pancreatic acinar cells expressing endogenous levels of mutant K-Ras do not spontaneously develop pancreatic ductal adenocarcinoma (PDAC). However, we hypothesized that acinar cells would develop PDAC in the presence of Ras activity levels mimicking those of human tumor cells.We measured Ras activity in PDAC cells from mice and humans using a Raf pull-down assay. We compared the effects of acinar cell expression of mutant K-Ras at endogenous and elevated levels on Ras activity and on the development of PDAC.
Ccr5 Mediates Specific Migration Of Toxoplasma Gondii—Primed Cd8+ Lymphocytes To Inflammatory Intestinal Epithelial Cells, Souphalone Luangsay, Lloyd H. Kasper, Nicolas Rachinel, Laurie A. Minns
Ccr5 Mediates Specific Migration Of Toxoplasma Gondii—Primed Cd8+ Lymphocytes To Inflammatory Intestinal Epithelial Cells, Souphalone Luangsay, Lloyd H. Kasper, Nicolas Rachinel, Laurie A. Minns
Dartmouth Scholarship
Toxoplasma gondii, an obligate intracellular parasite, can invade intestinal epithelial cells and elicit a robust Th1 immune response. In this model of intestinal inflammation, CD8+ intraepithelial lymphocytes (IELs) secrete transforming growth factor (TGF)-β, which appears necessary for the maintenance of homeostasis in the intestine. However, the mechanism responsible for the IEL migration to the inflamed intestine is still unclear.An in vitro coculture cell system was used to quantify the IEL attraction by an infected intestinal epithelial cell line (m-ICcl2). We used CCR5-deficient mice to determine which chemokine receptor—chemokine interaction could be responsible for the recruitment of …