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9p23杂合性缺失定义了非小细胞肺癌中的一个新位点。

Loss of heterozygosity at 9p23 defines a novel locus in non-small cell lung cancer.

作者信息

Neville E M, Stewart M, Myskow M, Donnelly R J, Field J K

机构信息

Department of Clinical Dental Sciences, University of Liverpool, UK.

出版信息

Oncogene. 1995 Aug 3;11(3):581-5.

PMID:7630642
Abstract

Genetic studies have previously demonstrated cytogenetic deletions and allelic imbalance or loss of heterozygosity (LOH) on the p arm of chromosome 9, in a number of tumour types. We have analysed 45 Non-Small Cell Lung Cancers (NSCLC) with a panel of highly polymorphic microsatellite markers on chromosome 9. Our results indicate that loss on 9p is concentrated within the D9S156-D9S161 region with 44% (20/45) LOH, however the area with minimal loss in this set of lung tumours was found at D9S157 (9p23), with 30% LOH (10/33), whereas loss at the IFNA locus was only found in 6% (2/34) tumours. Five of the lung tumours in this study which demonstrated LOH at D9S157 retained heterozygosity at the adjacent informative markers lying centromeric and telomeric to D9S157. No correlations were found between any of the clinico-pathological parameters and LOH on 9p or at the D9S157 locus. The results of this study indicates the presence of a further putative tumour suppressor gene on 9p at the D9S157 locus (9p23) to be most likely involved in the pathogenesis of non-small cell lung cancer.

摘要

基因研究先前已证实在多种肿瘤类型中,9号染色体短臂存在细胞遗传学缺失以及等位基因失衡或杂合性缺失(LOH)。我们使用一组9号染色体上高度多态的微卫星标记分析了45例非小细胞肺癌(NSCLC)。我们的结果表明,9p缺失集中在D9S156 - D9S161区域,杂合性缺失率为44%(20/45),然而在这组肺肿瘤中缺失最少的区域位于D9S157(9p23),杂合性缺失率为30%(10/33),而IFNA基因座的缺失仅在6%(2/34)的肿瘤中发现。本研究中有5例肺肿瘤在D9S157处显示杂合性缺失,但在D9S157着丝粒和端粒方向相邻的信息性标记处保持杂合性。未发现任何临床病理参数与9p或D9S157基因座的杂合性缺失之间存在相关性。本研究结果表明,9p上D9S157基因座(9p23)很可能存在另一个推定的肿瘤抑制基因,其参与非小细胞肺癌的发病机制。

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