摘要
胰腺癌是常见的消化道恶性肿瘤，病因至今不明。分子肿瘤学的进展在 DNA水平阐述了胰腺癌的多种遗传学改变，发现肿瘤组织中的 p16基因座几乎都有变异。该抑癌基因位于染色体 9p21，编码一个蛋白质，参与细胞周期调节。胰腺癌发生过程中的 p16基因改变涉及不同的分子学机制，包括缺失、突变或甲基化。最近，针对胰腺癌聚集在某些家庭的轶闻病例报道，运用分子遗传学技术研究了胰腺癌聚集家系的遗传模式，发现 p16基因种系突变易患胰腺癌。另外，将外源性 p16基因导入胰腺癌细胞系则显示出抗肿瘤作用。目前尚不能确定 p16基因能否为临床提供预后信息。大多数胰腺癌在一个或多个位点有微卫星不稳定性，但有错配修复缺陷的胰腺癌可能预后良好。
Pancreatic cancer is a common malignant neoplasm in digestive tract, which is of unknown etiology as yet. Recent advances in molecular oncology have provided explanations at the DNA level that multiple genetic changes contribute to pancreatic cancer development, in which the p16 locus of tumor tissue is nearly always altered. This tumor suppressor gene, located on chromosome 9p21, encodes for a protein that is involved in cell cycle regulation. Alterations of the p16 gene for the carcinogenesis in the pancreas involve different molecular mechanisms, including deletion, mutation or methylation. As recent anecdotal case reports that pancreatic cancer aggregates in some families, the patterns of inheritance of pancreatic cancer were studied utilizing molecular genetic techniques for some kindreds which exhibit aggregation of the cancer, and germline mutation in p16 gene have been demonstrated to predispose to pancreatic cancer. In addition, the anticancer effects of exogenous p16 gene have been shown by introduction of it into human pancreatic tumor cell lines. At the present time it is uncertain whether the p16 gene provides clinically prognostic information. Microsatellite instability was observed at one or more loci in a number of pancreatic cancers, but pancreatic cancers with mismatch repair deficiency may have an improved prognosis.
出处
《中国医学科学院学报》
CAS
CSCD
北大核心
2000年第5期491-493,共3页
Acta Academiae Medicinae Sinicae
关键词
胰腺癌
P16基因
基因变异
基因缺失
pancreatic neoplasms； p16 gene； cell cycle； gene deletion； mutation
