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首页> 外文期刊>Journal of Nanjing Medical University >Chromosome 6q deletion mapping in human ovarian tumor: a common deletion region between D6S1649 and D6S311
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Chromosome 6q deletion mapping in human ovarian tumor: a common deletion region between D6S1649 and D6S311

机译:人卵巢肿瘤中的染色体6q缺失定位:D6S1649和D6S311之间的常见缺失区域

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Objective: To explore the loss of heterozygosity(LOH) on chromosome 6q in ovarian cancer, and localize a minimum area in deletion region. Methods: 93 ovarian tumors were analyzed for LOH studies with 10 microsatellite markers spanning chromosome 6q. To further localize a minimum area in deletion region. Nineteen microsatellite markers were used to refined a minimum area. Results: Forty three tumors (46% ) were demonstrated allelic losses, which spanned less than two megabase areas, franked by a distal marker D6S311 and a proximal marker D6S1649, and likely harbored ovarian tumor suppressor gene (s). With analysis of density of LOH, increased DNA copy number at loci of 6q was demonstrated between D6S1649 and D6S311. Conclusion: It is possible that duplication after the allelic loss might be a main mechanism that leads to carcinogenesis in ovarian tumor. The refinement of these candidate tumor suppressor genes loci might facilitate future loss of het-erozygosity studies and enable the isolation of candidate genes from this region.
机译:目的:探讨卵巢癌6q染色体上杂合性(LOH)的丢失,并定位缺失区域的最小区域。方法:使用10个跨6q染色体的微卫星标记物分析了93个卵巢肿瘤的LOH研究。为了进一步定位删除区域中的最小区域。 19个微卫星标记用于细化最小区域。结果:证实有43个肿瘤(占46%)等位基因缺失,覆盖不到两个兆碱基的区域,由远端标志物D6S311和近端标志物D6S1649盖章,并且可能带有卵巢肿瘤抑制基因。通过分析LOH的密度,证实了D6S1649和D6S311之间在6q位点的DNA拷贝数增加。结论:等位基因缺失后重复可能是导致卵巢癌致癌的主要机制。这些候选肿瘤抑制基因基因座的完善可能会促进未来的半纯合性研究的丧失,并能够从该区域分离候选基因。

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