Loss of heterozygosity in DNA mismatch repair genes in human atherosclerotic plaques
Loss of heterozygosity in DNA mismatch repair genes in human atherosclerotic plaques
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DOI：
10.1006/mcbr.2000.0255
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发表时间：
2000-07-01
期刊：
影响因子：
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通讯作者：
Spandidos, Demetrios A.
中科院分区：
文献类型：
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作者：
Flouris, George A.;Arvanitis, Demetrios A.;Spandidos, Demetrios A.
为检测动脉粥样硬化中DNA错配修复基因（MMR）杂合性丢失（洛）的发生率，应用19个微卫星标记，采用3个单标记和4个四标记对50例动脉粥样硬化尸检病例进行了洛检测。所使用的标记位于MMR基因上或附近。14例（28%）至少在一个位点上表现出等位基因不平衡。位点hMSH 2（2p22.3-p16.1）、hPMS 1（2q24.1-q32.1）和hMLH 1（3p21.32-p21.1）表现出洛缺失（分别为10%、10%和12%）。我们发现hMSH 2、hPMS 1和hMLH 1的杂合性缺失发生在动脉粥样硬化中。这种基因组改变的发生可能代表动脉粥样硬化发展中的重要事件。
To detect the incidence of loss of heterozygosity (LOH) in DNA mismatch repair genes (MMR) occurring in atherosclerosis, fifty human autopsy cases of atherosclerosis were examined for LOH using 19 microsatellite markers, in three single and four tetraplex microsatellite assays. The markers used are located on or close to MMR genes. Fourteen specimens (28%) showed allelic imbalance in at least one locus. Loci hMSH2 (2p22.3-p16.1), hPMS1 (2q24.1-q32.1), and hMLH1 (3p21.32-p21.1) exhibited LOH (10, 10, and 12% respectively). We found that loss of heterozygosity on hMSH2, hPMS1, and hMLH1, occurs in atherosclerosis. The occurrence of such genomic alterations may represent important events in the development of atherosclerosis.