Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE, USA.
Cancer Biomark. 2010;9(1-6):421-40. doi: 10.3233/CBM-2011-0168.
We describe the pathology of early pancreatic cancer and present an overview of known molecular alterations that occur in these lesions. There are three defined precursor lesions in current models of pancreatic cancer: pancreatic intraepithelial neoplasia (PanIN), mucinous cystic neoplasms (MCN), and intraductal papillary mucinous neoplasms (IPMN). Molecular alterations detected in these lesions include: telomeres, K-ras and downstream targets, p16/CDKN2A, p53, SMAD4/DPC4, microRNAs, mucins and their post-translational processing, inflammatory cytokines, CEACAM, and epigenetic alterations. We summarize previous analyses of these markers as diagnostic markers of disease, and suggest areas of future study.
我们描述了早期胰腺癌的病理学，并概述了这些病变中已知的分子改变。在当前的胰腺癌模型中，有三种明确的前体病变：胰腺上皮内瘤变（PanIN）、黏液性囊腺瘤（MCN）和导管内乳头状黏液性肿瘤（IPMN）。在这些病变中检测到的分子改变包括：端粒、K-ras 及其下游靶标、p16/CDKN2A、p53、SMAD4/DPC4、microRNAs、粘蛋白及其翻译后加工、炎症细胞因子、CEACAM 和表观遗传改变。我们总结了以前对这些标志物作为疾病诊断标志物的分析，并提出了未来研究的方向。
