食管鳞癌及其前驱病变9q基因杂合子缺失的研究  

Loss of Heterozygosity on Chromosome 9q in Esophageal Squamous Cell Carcinoma and its Precursor Lesion

作　　者：田云[1] 王全红[2] 王耀华[2] 

机构地区：[1]长治医学院组胚教研室,046000 [2]山西省肿瘤医院

出　　处：《长治医学院学报》2006年第3期165-168,共4页Journal of Changzhi Medical College

基　　金：太原市科技计划项目

摘　　要：目的:通过对食管黏膜高级别不典型和鳞状细胞癌中的等位基因杂合子缺失(LOH)的检测,以期发现9q上与食管鳞癌密切相关的抑癌基因。方法:应用显微切割、PCR扩增、凝胶电泳、AgNO3染色等技术,对照分析正常组织、高级别不典型增生和癌组织中的LOH的变化,并就各位点的杂合性丢失率与患者的临床病理参数分别进行单因素分析。结果:①在食管高级别不典型增生和癌组织中,3个微卫星位点的LOH率分别为D9S303(31%,38%)、D9S753(29%,43%)、D9S242(11%,17%)。②应用SPSS软件对3个微卫星序列的等位基因LOH率与患者的性别、组织学分化及是否有淋巴结转移进行单因素分析,差异均无显著性(P>0.05)。结论:①从正常鳞状上皮到不典型增生再到癌变的过程中存在基因的异常累积。②9q末端可能存在与食管鳞癌的发生发展相关的抑癌基因。Objective ：The aim of this study was to evaluate possible tumor suppressor genes（TSG） on chromosome 9q in the development and progression of ESCC, through detecting the loss of heterozygosity （LOH） in ESCC and its high - grade squamous dysplasia. Method： LOH was detected in normal esophageal mucosa, -grade squamous dysplasia and esophageal squamous cell carcinoma using microdissection, polymerase chain reaction, denaturing polyacrylamide gel electrophoresis and silver nitrate staining tecnology.The changes of LOH at three microsatellite markers and the relationship between LOH rate and clinicopathologic parameters were analyzed. Results：①In high grade squamous dysplasia and squamous cell carcinoma, LOH was detected as follows： D9S303 （31%, 38%）, D9S753 （29%, 43%）, D9S242 （11%, 17%）.②The frequency of LOH in the three microsatellite markers was found no associated with the sex, differentiation, and occurrence of lymph node metas- tasis （ P 〉 0.05）. Conclusions：①The progression from normal squamous epithelium to high - grade squamous dysplasia and subsequently to squamous cell carcinoma of the esophagus was associated with accumulation of genetic errors. ②Possible tumor suppressor genes related to the development of esophageal squamous cell carcinoma may exist near chromosome 9q.

关 键 词：食管鳞状细胞癌 高级别不典型增生 抑癌基因 杂合性缺失 

分 类 号：R361.2[医药卫生—病理学]