论文部分内容阅读
目的:探讨胃癌组织中抑癌基因FHIT外显子5.8纯合性缺失及突变情况。方法:采用外显子特异聚合酶链反应(PCR)及聚合酶链反应-单链构象多态性分析(PCR-SSCP)-银染方法对30例胃癌和18例正常组织中FHIT基因外显子5,8的纯合性缺失和点突变显示检测和比较。结果:胃癌组织中FHIT基因外显子5、8总纯合性缺失率为23.3%,正常组织无一例缺失(P=0.011);外显子5、8纯合性缺失率分别为16.67%和13.33%(P>0.05);FHIT基因外显子5、8纯合性缺失与胃癌的分化程度、病理分期及淋巴结转移无显著性相关(P>0.05)。所有胃癌组织标本均未检测到外显子5,8的点突变。结论:提示FHIT基因外显子5、8纯合性缺失可能在胃癌的发生中起重要作用。而点突变不是FHIT基因失活的主要方式。
Objective: To investigate the homozygous deletion and mutation of exon 5.8 of tumor suppressor gene FHIT in gastric cancer. Methods: Exon-specific polymerase chain reaction (PCR) and polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) -silver staining were used to detect the expression of FHIT gene in 30 cases of gastric carcinoma and 18 cases of normal tissues Homozygous deletions and point mutations in sub-5,8 show detection and comparison. Results: The overall homozygous deletion rate of exon 5 and exon 8 of gastric cancer tissue was 23.3% and none of the normal tissues was missing (P = 0.011). The loss rate of exon 5 and 8 homozygote was 16.67% and 13.33% (P> 0.05). The homozygous deletion of exon 5 and 8 of FHIT gene had no significant correlation with the degree of differentiation, pathological stage and lymph node metastasis (P> 0.05). All gastric cancer tissue specimens did not detect exon 5,8 point mutation. Conclusion: It is suggested that the homozygous deletion of FHIT exon 5,8 may play an important role in the carcinogenesis of gastric cancer. Point mutation is not the main way of FHIT gene inactivation.