Tidmarsh G F, Dailey M O, Weissman I L
J Exp Med. 1986 Oct 1;164(4):1356-61. doi: 10.1084/jem.164.4.1356.
Mice genetically susceptible or genetically resistant to the leukemogenic effects of A-MuLV(Mo) were tested for their expression of the B-lineage neoplastic transformation-associated antigen, 6C3Ag. Genetically resistant inbred strains and recombinant inbred lines developed neither cells expressing high levels of 6C3Ag (6C3Aghi) in their hematolymphoid tissues nor Abelson leukemias. Genetically susceptible inbred strains and recombinant inbred lines developed high percentages of 6C3Aghi hematolymphoid cells concomitant with development of Abelson leukemias and lymphomas. Thus the genetically-determined resistance to A-MuLV(Mo) leukemogenesis appears to act at some step(s) after virus infection but before the stage of malignant progression, which is marked by 6C3Ag expression.
对在基因上对A-MuLV(Mo)致白血病作用敏感或有抗性的小鼠,检测其B系肿瘤转化相关抗原6C3Ag的表达情况。具有基因抗性的近交系和重组近交系在其血液淋巴组织中既未产生表达高水平6C3Ag(6C3Aghi)的细胞,也未发生Abelson白血病。具有基因易感性的近交系和重组近交系在出现Abelson白血病和淋巴瘤的同时,产生了高比例的6C3Aghi血液淋巴细胞。因此,基因决定的对A-MuLV(Mo)白血病发生的抗性似乎在病毒感染后的某些步骤起作用,但在以6C3Ag表达为标志的恶性进展阶段之前。