Nilsen T W, Maroney P A, Goodwin R G, Rottman F M, Crittenden L B, Raines M A, Kung H J
Cell. 1985 Jul;41(3):719-26. doi: 10.1016/s0092-8674(85)80052-0.
ALV-induced erythroblastosis results from the specific interruption of the host oncogene, c-erbB, by the insertion of an intact provirus. Integrated proviruses are oriented in the same transcriptional direction as c-erbB, and expression of truncated c-erbB transcripts is observed. Evidence, including sequence analysis of cDNA clones, indicates that transcription of truncated c-erbB mRNA is initiated in the 5' LTR of the integrated provirus. This transcript is processed through a series of remarkable splicing reactions to yield viral gag and env sequences fused to erbB sequences. These results establish a novel pathway of promoter insertion oncogenesis that stands in contrast to the pathways used in the activation of c-myc in B lymphomas.
禽白血病病毒(ALV)诱导的成红细胞增多症是由于完整的前病毒插入宿主癌基因c-erbB导致其特异性中断所致。整合的前病毒与c-erbB的转录方向相同,并观察到截短的c-erbB转录本的表达。包括cDNA克隆序列分析在内的证据表明,截短的c-erbB mRNA的转录起始于整合前病毒的5'长末端重复序列(LTR)。该转录本通过一系列显著的剪接反应进行加工,产生与erbB序列融合的病毒gag和env序列。这些结果建立了一种新的启动子插入致癌途径,这与B淋巴瘤中c-myc激活所使用的途径形成对比。