Tahara E, Kuniyasu H, Nakayama H, Yasui W, Yokozaki H
Dept. of Pathology I, Hiroshima University School of Medicine.
Gan To Kagaku Ryoho. 1993 Feb;20(3):326-31.
Alterations in multiple oncogenes and multiple tumor suppressor genes are observed in human gastro-intestinal cancer. Among them, the most frequently implicated in malignancy and metastasis of esophageal carcinoma may be amplification and overexpression of the human cyclin D gene. In gastric carcinoma, amplification and abnormal expression of the c-met gene encoding receptor for hepatocyte growth factor (HGF) may contribute to the tumor progression and metastasis. Interaction between cadherin in c-met overexpressed tumor cells and HGF from fibroblast may play an important role in morphogenesis of two histological types of stomach cancer. During stomach carcinogenesis the clone having critical p53 mutations may expand selectively to make up a finally advanced stage of malignancy and show metastasis. In colorectal cancer, loss of heterozygosity of the RB, p53 and DCC genes is frequently associated with liver metastasis. Overexpression of nm23 may participate in carcinogenesis and the reduction in nm23 expression is involved in metastasis in gastric and colorectal cancers.
在人类胃肠道癌症中观察到多个癌基因和多个肿瘤抑制基因的改变。其中，与食管癌恶性肿瘤和转移最常相关的可能是人类细胞周期蛋白D基因的扩增和过表达。在胃癌中，编码肝细胞生长因子（HGF）受体的c-met基因的扩增和异常表达可能促进肿瘤进展和转移。c-met过表达肿瘤细胞中的钙黏蛋白与成纤维细胞中的HGF之间的相互作用可能在两种组织学类型的胃癌形态发生中起重要作用。在胃癌发生过程中，具有关键p53突变的克隆可能选择性扩增，构成最终的晚期恶性肿瘤并显示转移。在结直肠癌中，RB、p53和DCC基因的杂合性缺失常与肝转移相关。nm23的过表达可能参与致癌作用，而nm23表达的降低与胃癌和结直肠癌的转移有关。
