GENETIC ASPECTS OF VIRAL ONCOGENESIS IN WILD MOUSE SPECIES

各种小鼠染色体基因改变小鼠对 逆转录病毒引起的肿瘤性疾病。这些基因包括内源性 逆转录病毒序列以及促进或 限制病毒复制。 我们发现了一种新的常见病毒 与B型白血病细胞诱导肿瘤相关整合区 逆转录病毒 这种病毒与小鼠乳腺肿瘤病毒有关， 诱发T细胞胸腺淋巴瘤。 一个新的病毒整合位点， 在20%的筛查肿瘤中发现，这表明存在一种 参与肿瘤诱导的功能基因。 这个基因被定位到一个 X染色体上一个以前不知道含有原癌基因的位点 序列的 其他的实验被设计来追踪遗传连锁 自身Mlsf反应性T细胞克隆缺失的基因座。 这些调查的结果表明，至少有三个已知的MMTV 前病毒、Mtv-8、-9和-11负责这种缺失。

Various mouse chromosomal genes alter the susceptibility of mice to retrovirus-induced neoplastic disease. These genes include endogenous retroviral sequences as well as mouse cellular genes which facilitate or restrict virus replication. We have identified a novel common viral integration region associated with tumor induction by type-B leukemogenic retrovirus. This virus is related to mouse mammary tumor virus, but induces T-cell thymic lymphomas. A novel virus integration site was identified in 20% of the tumors screened, suggesting the presence of a functional gene involved in tumor induction. This gene was mapped to a site on the X chromosome not previously known to contain protooncogene sequences. Other experiments were designed to follow the genetic linkage of loci responsible for the clonal deletion of self-Mlsf reactive T cells. Results from these investigations indicated that at least three known MMTV proviruses, Mtv-8, -9, and -11 are responsible for this deletion.