Modeling variation in tumors in vivo.
Modeling variation in tumors in vivo.
复制标题
体内肿瘤变异建模。
DOI：
10.1073/pnas.0401340102
复制
发表时间：
2005
影响因子：
11.1
通讯作者：
Stringer,SaundraL
中科院分区：
文献类型：
--
作者：
Stringer,JamesR;Larson,JonS;Fischer,JaredM;Medvedovic,Mario;Hersh,MeganN;Boivin,GregoryP;Stringer,SaundraL
转基因小鼠允许突变细胞原位可视化，用于研究肿瘤的变异。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，通过在编码区插入一段G：C碱基对引起的移码而不能产生其酶产物。自发删除一个G：C碱基对从这一束恢复基因功能，和细胞与PLAP活性可以检测到组织化学。为了研究肿瘤，将G11 PLAP转基因导入多瘤病毒中T抗原乳腺肿瘤模型。这些小鼠中的肿瘤表现出比正常组织多300倍的PLAP+细胞。PLAP+细胞遍布每个肿瘤。许多PLAP+细胞是单线态，但簇也很常见，其中一个簇含有> 30，000个细胞。将这些数据与计算机模型产生的模拟进行比较表明，在肿瘤中产生突变细胞涉及多种因素。虽然遗传不稳定性似乎发生在大多数肿瘤中，但大集群比仅基于不稳定性的预期更常见。
Transgenic mice that allow mutant cells to be visualizedin situwere 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 frameshift 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.
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检查 HeLa x 成纤维细胞杂交体中肿瘤相关抗原、肠碱性磷酸酶的致癌潜力。
影响因子：
11.2
作者：
Latham,KM;Stanbridge,EJ
通讯作者：
Stanbridge,EJ
切尔诺贝利事故清理者后代的突变率非常高
DOI：
--
发表时间：
2001
期刊：
Proceedings of the Royal Society of London. Series B: Biological Sciences
影响因子：
--
作者：
H. M. Sh;Abraham B. Korol;V. Kirzhner;Aaron Avivi;T. Fahima;Eviatar Nevo;Stuart C. Shapiro;Gad Rennert;O. Piatak;E. Stepanova;E. Skvarskaja
通讯作者：
E. Skvarskaja
p53 缺陷不会影响转基因靶标中点突变的积累。
DOI：
10.1073/pnas.92.18.8517
发表时间：
1995
影响因子：
11.1
作者：
Sands,AT;Suraokar,MB;Sanchez,A;Marth,JE;Donehower,LA;Bradley,A
通讯作者：
Bradley,A
影响因子：
11.4
作者：
S. Dilworth;H. Hansson;C. Darnfors;G. Bjursell;C. Streuli;B. Griffin
通讯作者：
B. Griffin
携带含微卫星转基因的正常小鼠和错配修复缺陷小鼠组织中镶嵌现象的可视化。
DOI：
10.1016/s0027-5107(02)00120-3
发表时间：
2002
期刊：
Mutation research
影响因子：
--
作者：
Hersh,MeganN;Stambrook,PeterJ;Stringer,JamesR
通讯作者：
Stringer,JamesR