胰腺上皮内瘤变
癌症研究
胰腺癌
癌变
生物
胰腺
祖细胞
癌症
医学
胰腺导管腺癌
病理
干细胞
细胞生物学
内分泌学
遗传学
作者
Sunil R. Hingorani,Emanuel F. Petricoin,Anirban Maitra,Vinodh N. Rajapakse,Catrina E. King,Michael A. Jacobetz,Sally Ross,Thomas P. Conrads,Timothy D. Veenstra,Ben A. Hitt,Yoshiya Kawaguchi,Don Johann,Lance A. Liotta,Howard C. Crawford,Mary Putt,Tyler Jacks,Christopher V.E. Wright,Ralph H. Hruban,Andrew M. Lowy,David A. Tuveson
出处
期刊:Cancer Cell
[Elsevier]
日期:2003-12-01
卷期号:4 (6): 437-450
被引量:2311
标识
DOI:10.1016/s1535-6108(03)00309-x
摘要
To evaluate the role of oncogenic RAS mutations in pancreatic tumorigenesis, we directed endogenous expression of KRAS(G12D) to progenitor cells of the mouse pancreas. We find that physiological levels of Kras(G12D) induce ductal lesions that recapitulate the full spectrum of human pancreatic intraepithelial neoplasias (PanINs), putative precursors to invasive pancreatic cancer. The PanINs are highly proliferative, show evidence of histological progression, and activate signaling pathways normally quiescent in ductal epithelium, suggesting potential therapeutic and chemopreventive targets for the cognate human condition. At low frequency, these lesions also progress spontaneously to invasive and metastatic adenocarcinomas, establishing PanINs as definitive precursors to the invasive disease. Finally, mice with PanINs have an identifiable serum proteomic signature, suggesting a means of detecting the preinvasive state in patients.
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