C-myc activation in an unusual retrovirus-induced avian T-lymphoma resembling Marek's disease: proviral insertion 5' of exon one enhances the expression of an intron promoter.
C-myc activation in an unusual retrovirus-induced avian T-lymphoma resembling Marek's disease: proviral insertion 5' of exon one enhances the expression of an intron promoter.
复制标题
C-myc 在一种罕见的逆转录病毒诱导的类似于马立克氏病的禽 T 淋巴瘤中激活:前病毒插入外显子 1 的 5 增强了内含子启动子的表达。
DOI:
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发表时间:
1987
期刊:
影响因子:
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通讯作者:
H. Kung
中科院分区:
文献类型:
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作者:
R. Isfort;R. Witter;H. Kung
Characterization of nonacute retrovirus-induced neoplasms have greatly facilitated our understanding of the mechanisms by which host protooncogenes are activated. Here we report the molecular characterization of a newly identified chicken lymphoma, which does not involve the bursa of Fabricius. This lymphoma, specifically induced by reticuloendotheliosis virus (REV), is similar in tumor location and T-cell origin to Marek's disease, a herpesvirus-induced T-lymphoma. We show the c-myc is the specific target locus for REV insertion. Integrated proviruses are all located upstream of the c-myc coding exons, and 60% are 5' to the first noncoding exon. One-half of the proviruses are oriented in the opposite transcriptional direction as the c-myc gene. This insertion pattern is in contrast to the pattern in B-lymphomas induced by the same virus. While some of the proviruses in these T-lymphomas used the 3' LTR promoter to transcribe the downstream c-myc gene, others apparently activated a common, cryptic promoter located in the first intron. To our knowledge, this is the first molecular description of an avian T-lymphoma induced by a nonacute retrovirus.