胰腺癌的分子发病机制

Molecular pathogenesis of pancreatic cancer.

作者信息

Maitra Anirban, Kern Scott E, Hruban Ralph H

机构信息

Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, The Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA.

出版信息

Best Pract Res Clin Gastroenterol. 2006 Apr;20(2):211-26. doi: 10.1016/j.bpg.2005.10.002.

DOI:10.1016/j.bpg.2005.10.002

PMID:16549325

Abstract

Pancreatic cancer is fundamentally a disease of inherited and acquired mutations in cancer-related genes. The genes targeted in pancreatic cancer include tumor-suppressor genes (p16/CDKN2A, TP53 and SMAD4), oncogenes (KRAS, BRAF, AKT2, MYB, and AIB1), and genome-maintenance genes (MLH1, MSH2, BRAC2 and other Fanconi anemia genes). An understanding of the cancer-related genes that are altered in pancreatic cancer has a number of clinical applications including genetic counseling for individuals with a family history of cancer, early detection of pancreatic neoplasia, and mechanism-based therapies for patients with advanced disease. This chapter will provide an overview of the molecular pathogenesis of pancreatic cancer with emphasis on clinical applications.

摘要

胰腺癌本质上是一种由癌症相关基因的遗传和获得性突变引起的疾病。胰腺癌中靶向的基因包括肿瘤抑制基因（p16/CDKN2A、TP53和SMAD4）、癌基因（KRAS、BRAF、AKT2、MYB和AIB1）以及基因组维持基因（MLH1、MSH2、BRAC2和其他范可尼贫血基因）。了解胰腺癌中发生改变的癌症相关基因具有许多临床应用，包括为有癌症家族史的个体提供遗传咨询、早期检测胰腺肿瘤以及为晚期疾病患者提供基于机制的治疗。本章将概述胰腺癌的分子发病机制，并重点介绍临床应用。