Coincident involvement of flvi-2, c-myc, and novel env genes in natural and experimental lymphosarcomas induced by feline leukemia virus.
Coincident involvement of flvi-2, c-myc, and novel env genes in natural and experimental lymphosarcomas induced by feline leukemia virus.
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flvi-2、c-myc 和新型 env 基因同时参与猫白血病病毒诱导的自然和实验性淋巴肉瘤。
DOI：
10.1006/viro.1993.1553
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发表时间：
1993
期刊：
影响因子：
3.7
通讯作者：
Roy-Burman,P
中科院分区：
文献类型：
--
作者：
Levy,LS;Lobelle-Rich,PA;Overbaugh,J;Abkowitz,JL;Fulton,R;Roy-Burman,P
Flvi-2基因是猫白血病病毒(FeLV)诱导的胸腺淋巴肉瘤插入突变的靶点。flvi-2编码基因bmi-1，其产物与B细胞和T细胞淋巴瘤的发生密切相关。我们已经研究了自然和实验诱导的FeLV阳性猫淋巴肉瘤的参与情况，这些肿瘤在解剖来源、地理来源和所涉及的FeLV毒株上是不同的。我们进一步将这些发现与之前关于同一肿瘤中新的FeLVenv基因的报道进行了比较。结果表明，在不同来源的自然和实验性猫胸腺淋巴肉瘤中，atflvi-2的前病毒插入普遍存在[52%]，c-myc的改变通常伴随着插入突变flvi-2[54%]。然而，46%的有flvi-2插入的肿瘤明显缺乏c-myc的参与。这些观察结果支持这样的假设，即LVI-2的中断可能是多步级联中的早期事件，完成该级联的一种可能性是c-myc的激活。在消化性或多中心来源的非胸腺淋巴肉瘤中未观察到LVI-2的阻断，尽管c-myc可能参与其中。先前已经证明，胸腺和非胸腺肿瘤中都含有带有重组或突变基因的FeLV前病毒。我们的发现强烈地表明，在FeLV介导的淋巴瘤发生中，尤其是在胸腺淋巴肉瘤的诱导过程中，LVI-2的插入突变、c-myc的激活以及新基因的出现都是可能的。数据显示，这些事件可能会重叠，但不一定同时发生。
Theflvi-2 locus is a target of insertional mutagenesis in thymic lymphosarcomas induced by feline leukemia virus (FeLV).flvi-2 encodes the genebmi-1, whose product is implicated as amyc-collaborator in the induction of B- and T-cell lymphoma. We have examined the involvement offlvi-2 andmycin natural and experimentally induced FeLV-positive feline lymphosarcomas which are heterogeneous in anatomical origin, geographic origin, and strain of FeLV involved. We further compared these findings with previous reports of novel FeLVenvgenes in the same tumors. The results show that proviral insertion atflvi-2 occurs commonly in natural and experimental feline thymic lymphosarcomas of diverse origins [52% overall], and that alterations in c-myccommonly accompany insertional mutagenesis offlvi-2 [54% overall]. However, 46% of tumors withflvi-2 insertions apparently lack involvement of c-myc. These observations support the hypothesis that interruption offlvi-2 may be an early event in a multistep cascade, one possibility for completion of which is activation of c-myc. Interruption offlvi-2 was not observed in nonthymic lymphosarcomas of alimentary or multicentric origin, although c-mycmay be involved. A proportion of both thymic and nonthymic tumors have been shown previously to contain FeLV proviruses with recombinant or mutantenvgenes. Our findings strongly implicate the insertional mutagenesis offlvi-2, the activation of c-myc, and the emergence of novelenvgenes in FeLV-mediated lymphomagenesis, particularly in the induction of thymic lymphosarcoma. The data show that these events may overlap, but do not necessarily occur concurrently.