Molecular pathogenesis of precursor lesions of pancreatic ductal adenocarcinoma

被引:42
作者
Biankin, AV
Kench, JG
Dijkman, FP
Biankin, SA
Henshall, SM
机构
[1] St Vincents Hosp, Garvan Inst Med Res, Canc Res Program, Darlinghurst, NSW 2010, Australia
[2] Div Surg, Darlinghurst, NSW, Australia
[3] Westmead Hosp, Inst Clin Pathol & Med Res, Westmead, NSW 2145, Australia
基金
英国医学研究理事会;
关键词
PanIN; IPMT; pancreas; cancer; genetics; DPC4;
D O I
10.1080/003130202201472
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Precursor lesions are assuming greater importance in the study of pancreatic ductal adenocarcinoma. As pancreatic cancer is almost universally fatal due to late clinical presentation and biological aggressiveness, characterisation of its precursor lesions may create scope for early diagnosis and improved outcome with conventional therapies as well as the development of novel therapeutic and preventative strategies. Pancreatic intraepithelial neoplasia (PanIN) and intraductal papillary mucinous tumours (IPMTs) are thought to be precursor lesions of ductal adenocarcinoma of the pancreas. Recent work has focused on the molecular aberrations associated with these lesions leading to the formulation of a progression model for pancreatic cancer. Progressive histopathological changes along the progression model are associated with aberrations of cell cycle regulatory and growth factor signalling molecules that occur in pancreatic cancer at high frequency and are common to many cancers. Characterisation of these molecular aberrations provides scope for the development of novel diagnostic and treatment strategies that will ultimately impact on the outcome for people who develop pancreatic cancer.
引用
收藏
页码:14 / 24
页数:11
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