肿瘤的恶性转移至少需要两种遗传变化。其中一种可能是癌基因的活化。另一种可能是我们已在体细胞杂交株中检验的“抑制肿瘤发生”基因的丧失。我们用RFLP标记与核型分析方法,辨认一些染色体的亲本细胞来源,这些染色体在最初不发生肿瘤的体细胞杂交株(NT)中分离,伴随着重新表现出发生肿瘤(TG)的表型。这些正常人细胞与癌衍生细胞融合产生的杂交株用来在裸鼠中检验致癌性。结果指出,正常No.11染色体带有一个(或几个)基因,当它在细胞中以双考贝形式存在时可以抑制恶性转移表型,而Hela—衍生D98细胞的No.11染色体是纯合的(二倍体的)或至少在我们所用的探针之间的短臂片断是纯合的。所检测 Malignant metastases of tumors require at least two genetic changes. One of these may be the activation of oncogenes. Another possibility is the loss of the “inhibition of tumorigenesis” gene that we have tested in somatic cell hybrids. Using RFLP markers and karyotyping methods, we identified the origin of the parental cells of some chromosomes. These chromosomes were isolated in a somatic cell hybrid (NT) that did not initially develop a tumor, with a reappearance of the phenotype of the tumor (TG). Hybrids produced by fusion of these normal human cells with cancer-derived cells were used to test for carcinogenicity in nude mice. The results indicate that the normal No. 11 chromosome carries one (or several) genes and that it inhibits the malignant metastatic phenotype when it is present in cells in the form of the dipstick, whereas the No. 11 chromosome of Hela-derived D98 cells is pure. The homozygous (diploid) or at least the short arm fragment between the probes we use is homozygous. Detected