GENETIC ASPECTS OF VIRAL ONCOGENESIS IN WILD MOUSE SPECIES

不同的小鼠染色体基因改变了小鼠对 逆转录病毒引起的肿瘤疾病。这些基因包括内源 逆转录病毒序列以及小鼠细胞基因 限制病毒复制。我们发现了一种新的常见病毒 整合区与B型白血病致癌相关 逆转录病毒。这种病毒与小鼠乳腺肿瘤病毒有关，但 诱发T细胞胸腺淋巴瘤。一种新的病毒整合位点是 在筛查的20%的肿瘤中发现，表明存在 参与肿瘤诱导的功能基因。该基因被定位到一种 X染色体上未知的含有原癌基因的位置 序列。其他实验是为了跟踪基因连锁而设计的 负责自身MLSF反应性T细胞克隆性删除的基因座。 这些调查的结果表明，至少有三种已知的MMTV PRORUS、MTV-8、-9和-11负责此删除。

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.