有哪些信誉好的足球投注网站acute pancreatitis accelerates initiation and progression to pancreatic cancer in mice expressing oncogenic kras in the nestin cell lineage急性胰腺炎小鼠胰腺癌的发生和发展加速致癌喀斯特表达巢蛋白的细胞谱系.pdfVIP
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acute pancreatitis accelerates initiation and progression to pancreatic cancer in mice expressing oncogenic kras in the nestin cell lineage急性胰腺炎小鼠胰腺癌的发生和发展加速致癌喀斯特表达巢蛋白的细胞谱系
Acute Pancreatitis Accelerates Initiation and Progression
to Pancreatic Cancer in Mice Expressing Oncogenic Kras
in the Nestin Cell Lineage
` 1,4 1 1 2 1,3,4
Catherine Carriere *, Alison L. Young , Jason R. Gunn , Daniel S. Longnecker , Murray Korc
1 Department of Medicine, Dartmouth Medical School, Hanover, New Hampshire, United States of America, 2 Department of Pathology, Dartmouth Medical School,
Hanover, New Hampshire, United States of America, 3 Department of Pharmacology and Toxicology, Dartmouth Medical School, Hanover, New Hampshire, United States
of America, 4 Norris Cotton Cancer Center, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire, United States of America
Abstract
Targeting of oncogenic Kras to the pancreatic Nestin-expressing embryonic progenitor cells and subsequently to the adult
acinar compartment and Nestin-expressing cells is sufficient for the development of low grade pancreatic intraepithelial
neoplasia (PanIN) between 2 and 4 months. The mice die around 6 month-old of unrelated causes, and it is therefore not
possible to assess whether the lesions will progress to carcinoma. We now report that two brief episodes of caerulein-
induced acute pancreatitis in 2 month-old mice causes rapid PanIN progression and pancreatic ductal adenocarcinoma
(PDAC) development by 4 months of age. These events occur with similar frequency as observed in animals where the
oncogene is targeted during embryogenesis to all pancreatic cell types. Thus, these data show that oncogenic Kras-driven
PanIN originating in a non-ductal compartment can rapidly progress to PDAC when subjected to a brief inflammatory insult.
`
Citation: Carriere C,
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