Dofuku R, Matsuzawa A
Anticancer Res. 1983 Jan-Feb;3(1):17-34.
The chromosome analysis of mammary tumors of mice by the Giemsa banding procedures yielded the following results: (1) Mammary tumors induced by urethan displayed the same chromosome aberration of trisomy of chromosome 13 as spontaneous mammary tumors; (2) By analyzing tumor cells with translocated chromosomes, genes assumed to be involved in mammary tumor development were mapped in the proximal region of chromosome 13; (3) Polyploid tumor cells manifested heteromorphism among homologous chromosomes which segregated regularly. The analysis of its segregation indicated that trisomy of chromosome 13 was derived from endomitosis and loss of a chromosome. The possible mechanisms of the genesis of the endomitosis were put forth based on a probable role of replicator played by a long terminal repeat of the viral mammary tumor genome integrated into chromosome 13.
通过吉姆萨显带程序对小鼠乳腺肿瘤进行染色体分析,得出以下结果:(1) 由氨基甲酸乙酯诱导的乳腺肿瘤显示出与自发性乳腺肿瘤相同的13号染色体三体性染色体畸变;(2) 通过分析具有易位染色体的肿瘤细胞,假定参与乳腺肿瘤发生发展的基因被定位在13号染色体的近端区域;(3) 多倍体肿瘤细胞在同源染色体间表现出异态性,且这些同源染色体能规则分离。对其分离情况的分析表明,13号染色体三体性源自核内有丝分裂和一条染色体的丢失。基于整合到13号染色体上的病毒性乳腺肿瘤基因组的长末端重复序列可能发挥的复制子作用,提出了核内有丝分裂发生的可能机制。