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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Modeling variation in tumors in vivo
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Modeling variation in tumors in vivo

机译：体内肿瘤建模变化

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摘要

Transgenic mice that allow mutant cells to be visualized in situ were used to study variation in tumors. These mice carry the G11 placental alkaline phosphatase (PLAP) transgene, a mutant allele rendered incapable of producing its enzyme product by a frame-shift caused by insertion of a tract of G:C base pairs in a coding region. Spontaneous deletion of one G:C base pair from this tract restores gene function, and cells with PLAP activity can be detected histochemically. To study tumors, the G11 PLAP transgene was introduced into the polyoma virus middle T antigen mammary tumor model. Tumors in these mice exhibited up to 300 times more PLAP~+ cells than normal tissues. PLAP~+ cells were located throughout each tumor. Many of the PLAP~+ cells were singlets, but clusters also were common, with one cluster containing > 30,000 cells. Comparison of these data to simulations produced by computer models suggested that multiple factors were involved in generating mutant cells in tumors. Although genetic instability appeared to have occurred in most tumors, large clusters were much more common than expected based on instability alone.
机译：使用允许突变细胞在原位可视化的转基因小鼠来研究肿瘤的变异。这些小鼠携带G11胎盘碱性磷酸酶（PLAP）转基因，这是一种突变等位基因，由于在编码区域插入G：C碱基对而导致移码而无法产生其酶产物。从该管道中自发删除一个G：C碱基对可恢复基因功能，并且可以通过组织化学方法检测具有PLAP活性的细胞。为了研究肿瘤，将G11 PLAP转基因引入多瘤病毒中T抗原乳腺肿瘤模型中。这些小鼠的肿瘤中PLAP +细胞的数量最多是正常组织的300倍。 PLAP +细胞遍布整个肿瘤。许多PLAP〜+细胞是单线态，但簇也很常见，其中一个簇包含> 30,000个细胞。这些数据与计算机模型产生的模拟结果的比较表明，多种因素参与了肿瘤突变细胞的产生。尽管似乎大多数肿瘤都出现了遗传不稳定性，但仅基于不稳定性，大的簇比预期的要普遍得多。

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