Avilès D, Jami J, Rousset J P, Ritz E
J Natl Cancer Inst. 1977 May;58(5):1391-9. doi: 10.1093/jnci/58.5.1391.
We investigated whether the malignancy of hybrids between normal and malignant cells could be correlated with the loss of specific genes borne by specific chromosomes from the normal parent cells. Tumors produced in mice by the inoculation of Cl.1D cells (an L cell derivative) contained tumor x host cell hybrids. Hybrid cell populations isolated from 14 tumors were injected into 123 mice, of which 108 (87%) developed tumors. Metaphases of growing hybrid cell tumors were analyzed by use of a trypsin-Giemsa banding technique. The chromosomes contributed by the host (normal) parent cell could be distinguished from Cl.1D chromosomes, since the latter exhibited morphologic differences due to rearrangements. In the 14 hybrid tumors analyzed, we found that any one of the chromosomes of the host cell might be present, which indicated that none of the chromosomes from the normal cell bore genetic information capable of suppressing the malignancy of Cl.1D cells. Absence of complimentation in the hybrids suggested that, even if the accumulation of several mutations were necessary for malignant tumor growth of Cl.D1 cells, none of these mutations is recessive.
我们研究了正常细胞与恶性细胞之间的杂交细胞的恶性程度是否与正常亲代细胞特定染色体所携带的特定基因的缺失相关。通过接种Cl.1D细胞(一种L细胞衍生物)在小鼠体内产生的肿瘤含有肿瘤x宿主细胞杂交体。从14个肿瘤中分离出的杂交细胞群体被注射到123只小鼠体内,其中108只(87%)长出了肿瘤。使用胰蛋白酶-吉姆萨显带技术分析生长中的杂交细胞瘤的中期相。宿主(正常)亲代细胞贡献的染色体可以与Cl.1D染色体区分开来,因为后者由于重排而表现出形态学差异。在分析的14个杂交肿瘤中,我们发现宿主细胞的任何一条染色体都可能存在,这表明正常细胞的染色体中没有携带能够抑制Cl.1D细胞恶性程度的遗传信息。杂交体中缺乏互补作用表明,即使Cl.D1细胞的恶性肿瘤生长需要积累几个突变,这些突变中也没有一个是隐性的。