Molecular Pathology of Pancreatic Cancer: Implications for Molecular Targeting Therapy

被引：19
|
作者：
Furukawa, Toru [1 ]
机构：
[1] Tokyo Womens Med Univ, Int Res & Educ Inst Integrated Med Sci, Shinjuku Ku, Tokyo 1628666, Japan
来源：
CLINICAL GASTROENTEROLOGY AND HEPATOLOGY | 2009年 / 7卷 / 11期
关键词：
PAPILLARY-MUCINOUS NEOPLASMS; TUMOR-SUPPRESSIVE PATHWAY; MUTANT K-RAS; INTRAEPITHELIAL NEOPLASIA; DUCTAL ADENOCARCINOMA; PRECURSOR LESIONS; SONIC-HEDGEHOG; PROGRESSION; CELLS; MICE;
D O I：
10.1016/j.cgh.2009.07.035
中图分类号：
R57 [消化系及腹部疾病];
学科分类号：
摘要：
Pancreatic cancer develops through ductal dysplastic lesions or pancreatic intraepithelial neoplasia (PanIN). The origin of pancreatic cancer remains controversial. Some of the molecular origins of pancreatic cancer have been described. For example, KRAS, SHH, CDKN2A, TP53, SMAD4, and DUSP6 are crucial molecules in the development and progression of pancreatic cancer. Understanding the mechanisms of carcinogenesis could help researchers find the Achilles' heel of pancreatic cancer. Molecular targeting is a promising strategy for curing this devastating disease.
引用
收藏
页码：S35 / S39
页数：5
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