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作 者:房殿春[1] 罗元辉[1] 柳风轩[1] 梁智勇[1] 刘为纹[1]
出 处:《中华消化杂志》1997年第5期254-256,共3页Chinese Journal of Digestion
摘 要:目的:研究MCC、DCC基因和YNZ22位点杂合性丢失(LOH)与大肠癌发生发展的关系。方法:应用多聚酶链反应技术对41例大肠癌MCC、DCC基因和YNZ22位点的数量可变的重复序列(VNTR)区进行了分析。结果:大肠癌MCC基因LOH率为34.8%;DCC基因为36.0%,YNZ22位点为43.3%;若将以上基因综合分析,大肠癌的LOH率则为56.1%。分析LOH与临床病理参数间的关系发现,大肠癌DukesC、D期DCC基因的LOH率(53.3%)显著高于A、B期组(10.0%)(P<0.05),其它各组间的LOH率则无显著差别。结论:MCC、DCC基因和YNZ22位点的LOH与大肠癌发生、发展有关,DCC基因LOH多为大肠癌的晚期改变。Objective: To investigate the relationship between the loss of heterozygosity(LOH) of MCC, DCC or YNZ22 loci and the development and progression of colorectal carcinoma. Materials and methods: Polymorphic analysis of MCC, DCC and YNZ22 loci that contain a variable number of tandem repeat(VNTR) was performed in 41 surgical specimens of colorectal carcinoma by the polymerase chain reaction(PCR). Results It was found that loss of heterozygosity(LOH) at MCC,LOH of DCC and LOH of YNZ22 loci were detected in 34.8%,36.0%and 43.3% of informative cases,respectively. The overall rate of LOH at MCC, DCC and YNZ22 loci was 56.1%. The incidence ofLoH at DCC genetic locus in tumor staging of Duke C and D (53.3%) was significantly higher thanthat in Duke A and B(10.0%)(P<0.05). No significant difference was seen between the other two groups (P>0.05). Conclusion: The findings indicate that LOH at MCC, DCC and YNZ22 loci may beinvolved in carcinogenesis of colorectal cancer, and LOH of DCC is frequently a late event intumor progression.
分 类 号:R735.340.2[医药卫生—肿瘤]
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