Schäfer R, Klemenz R
Abteilung für Krebsforschung, Universität Zürich.
Verh Dtsch Ges Pathol. 1990;74:328-34.
Two lines of evidence have suggested that the loss of tumor suppressor gene function contributes to the multi-step process of tumorigenesis. Tumorigenicity and transformed phenotypes are frequently suppressed in somatic cell hybrids of tumor and normal cells. Consistent chromosomal aberrations indicating gene losses and mutations have been found in hereditary and sporadic human tumors. Tumor suppressor genes can be molecularly cloned, even if the encoded protein products have not been characterized biochemically. Here we describe a functional assay based on DNA transfection permitting the molecular identification of candidate human tumor suppressor genes (R. SCHAFER et al., Proc. Natl. Acad. Sci. USA 85, 1590-1594, 1988). A molecular clone has been identified capable of suppressing the neoplastic phenotype induced by an oncogene belonging to the family of ras genes, whose activation is frequently found in tumors.
有两条证据表明肿瘤抑制基因功能的丧失参与了肿瘤发生的多步骤过程。在肿瘤细胞与正常细胞的体细胞杂交体中，致瘤性和转化表型常常受到抑制。在遗传性和散发性人类肿瘤中已发现一致的染色体畸变，表明存在基因缺失和突变。即使编码的蛋白质产物尚未进行生化特性鉴定，肿瘤抑制基因也能够进行分子克隆。在此，我们描述了一种基于DNA转染的功能测定方法，该方法可用于分子鉴定候选人类肿瘤抑制基因（R. 舍费尔等人，《美国国家科学院院刊》85，1590 - 1594，1988年）。已鉴定出一个分子克隆，它能够抑制由属于ras基因家族的致癌基因诱导的肿瘤表型，该致癌基因的激活在肿瘤中经常出现。
