KRAS, Hedgehog, Wnt and the twisted developmental biology of pancreatic ductal adenocarcinoma

被引:447
作者
Morris, John P. [1 ]
Wang, Sam C. [1 ]
Hebrok, Matthias [1 ]
机构
[1] Univ Calif San Francisco, Ctr Diabet, San Francisco, CA 94143 USA
基金
美国国家卫生研究院;
关键词
ACINAR-CELL TRANSDIFFERENTIATION; SMALL-MOLECULE INHIBITOR; GROWTH-FACTOR-BETA; COLLAGEN TYPE-I; SONIC HEDGEHOG; INTRAEPITHELIAL NEOPLASIA; MOUSE MODEL; ONCOGENIC KRAS; E-CADHERIN; PROGRESSION MODEL;
D O I
10.1038/nrc2899
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Pancreatic ductal adenocarcinoma (PDAC) is characterized by near-universal mutations in KRAS and frequent deregulation of crucial embryonic signalling pathways, including the Hedgehog (Hh) and Wnt-beta-catenin cascades. The creation of mouse models that closely resemble the human disease has provided a platform to better understand when and in which cell types these pathways are misregulated during PDAC development. Here we examine the central part that KRAS plays in the biology of PDAC, and how the timing and location of Hh and Wnt-beta-catenin signalling dictate the specification and oncogenic properties of PDAC.
引用
收藏
页码:683 / 695
页数:13
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