Tahara E, Nakatani H, Yoshida K, Yokozaki H
Dept. of Pathology, Hiroshima University School of Medicine.
Gan To Kagaku Ryoho. 1988 Apr;15(4 Pt 2-2):1236-40.
Recent in vivo and in vitro evidence suggests that EGF-related growth factors and TGF beta derived from tumor cells mutually act not only on tumor cells themselves but also on fibroblasts surrounding the tumor, resulting in extensive progression and fibrosis of gastric scirrhous carcinoma. There are two mechanisms involved in such extensive fibrosis. One is collagen production by fibroblasts upon stimulation by tumor-derived growth factors, and the other is collagen synthesis by the tumor cells themselves. However, the expressions of the EGF-related growth factors, TGF beta and procollagen, in tumor cells are not specific for gastric scirrhous carcinoma. Future elucidation of the function and structure of the sam gene may shed light on the developmental mechanism of gastric scirrhous carcinoma.
最近的体内和体外证据表明，肿瘤细胞衍生的表皮生长因子（EGF）相关生长因子和转化生长因子β（TGFβ）不仅相互作用于肿瘤细胞本身，还作用于肿瘤周围的成纤维细胞，导致胃硬癌广泛进展和纤维化。这种广泛纤维化涉及两种机制。一种是肿瘤衍生生长因子刺激后成纤维细胞产生胶原蛋白，另一种是肿瘤细胞自身合成胶原蛋白。然而，EGF相关生长因子、TGFβ和前胶原蛋白在肿瘤细胞中的表达并非胃硬癌所特有。未来对sam基因功能和结构的阐明可能会揭示胃硬癌的发生机制。
