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首页> 美国卫生研究院文献>Journal of Virology >Lack of ecotropic virus involvement in induction of lymphomas in DBA/2J mice by 7,12-dimethylbenz(a)anthracene.
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Lack of ecotropic virus involvement in induction of lymphomas in DBA/2J mice by 7,12-dimethylbenz(a)anthracene.

机译：缺乏嗜统病毒参与7,12-二甲基苯并（a）蒽诱导的DBA / 2J小鼠淋巴瘤的发病。

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DBA/2 mice carry a single endogenous ecotropic murine leukemia provirus, Emv-3, that is replication defective because of a single nucleotide substitution in codon 3 of p15gag. However, when weanling DBA/2 mice are treated percutaneously with 7,12-dimethylbenz(a)anthracene (DMBA), ecotropic virus replication is induced in almost all of the treated mice. Previous studies have shown that this induction results from DMBA-induced reverse mutations in codon 3 that allow efficient virus replication. In addition to ecotropic virus replication, DMBA also induces lymphomas in 100% of the treated mice. These results have raised the possibility that ecotropic virus replication is causally associated with the development of lymphomas in DBA/2 mice, perhaps via the insertional activation or mutation of cellular proto-oncogenes. To test this possibility, we compared lymphoma incidence after percutaneous DMBA treatment in DBA/2J-dv/dv mice, which carry two copies of Emv-3, with lymphoma incidence in DBA/2J-d+18J/d+18J mice, which lost both copies of Emv-3 by homologous recombination involving the long terminal repeat sequences. The results of this study conclusively demonstrated that Emv-3 is not causally associated with the development of DMBA-induced lymphomas in DBA/2J mice. Interestingly, histopathological and molecular analyses of the lymphomas indicated that the majority of the lymphomas in both strains of mice were of the B-cell lineage. This was unanticipated, since the majority of chemically induced lymphomas in other inbred strains are thymic lymphomas, presumably of the T-cell lineage. Thus, DBA/2 mice appear to present a unique model system for the investigation of chemically induced B-cell lymphomas in mice.
机译：DBA / 2小鼠携带单个内源性嗜生性小鼠白血病原病毒Emv-3，由于p15gag密码子3中的单个核苷酸取代，因此复制缺陷。但是，当用7,12-二甲基苯并（a）蒽（DMBA）经皮处理断奶的DBA / 2小鼠时，几乎所有处理过的小鼠均会诱发嗜性病毒复制。先前的研究表明，这种诱导是由DMBA诱导的密码子3反向突变导致的，该突变允许有效的病毒复制。除了亲病毒复制之外，DMBA还可以在100％的治疗小鼠中诱发淋巴瘤。这些结果增加了嗜性病毒复制可能与DBA / 2小鼠淋巴瘤的发生有因果关系的可能性，可能是通过细胞原癌基因的插入激活或突变引起的。为了检验这种可能性，我们比较了经DBA / 2J-dv / dv小鼠经皮DMBA处理后的淋巴瘤发生率，其中DBA / 2J-dv / dv小鼠携带了两个Emv-3拷贝，而将DBA / 2J-d + 18J / d + 18J小鼠淋巴瘤发生率进行了比较。通过涉及长末端重复序列的同源重组，Emv-3的两个拷贝都丢失了。这项研究的结果最终证明Emv-3与DBA / 2J小鼠中DMBA诱导的淋巴瘤的发生没有因果关系。有趣的是，对淋巴瘤的组织病理学和分子分析表明，两种小鼠品系中的大多数淋巴瘤都属于B细胞谱系。这是出乎意料的，因为其他近交系中大多数化学诱导的淋巴瘤是胸腺淋巴瘤，大概是T细胞谱系。因此，DBA / 2小鼠似乎提出了一个独特的模型系统，用于研究小鼠中化学诱导的B细胞淋巴瘤。

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