论文部分内容阅读
为明确ｐ５３基因突变、缺失，ＡＰＣ基因缺失在胃癌发病机制中的作用，应用ＰＣＲ－ＳＳＣＰ方法对抑癌基因ｐ５３第４、５、６、７、８外显子、第６内含子在８７例胃癌及癌前病变中的突变规律以及ＰＣＲ－ＲＦＬＰ方法对ｐ５３基因第４外显子、第６内含子、ＡＰＣ基因在２５对胃癌及癌旁组织中的杂合缺失规律进行了探讨。结果发现，ｐ５３突变率在肠化、不典型增生、胃癌分别为３７．５％ （３／８），４２．１％（８／１９），５３．３％（１６／３０）。正常组织、浅表胃炎未发现ｐ５３突变。肠化、不典型增生、胃癌与正常对照组、浅表胃炎组相比均存在显著差异（Ｐ＜０．０５，Ｐ＜０．０１，Ｐ＜０．０１）。在肠化、不典型增生病变中未发现Ｅｘｏｎ８的突变，而在胃癌组Ｅｘｏｎ８的突变为４例（４／３０），提示Ｅｘｏｎ８的突变主要发生在晚期。在各病变组未发现Ｅｘｏｎ４、Ｉｎｔｒｏｎ６的突变。对Ｅｘｏｎ４、Ｉｎｔｒｏｎ６、ＡＰＣ基因的杂合缺失研究表明，２５对胃癌标本中有１９对Ｅｘｏｎ４杂合子，杂合率为７６．０％，９对有杂合缺失，ＬＯＨ为４７．４％，２３对Ｉｎｔｒｏｎ６杂合子，杂合率为９２．０％，其中２对为杂合缺失，ＬＯＨ为８．７％，１８对ＡＰＣ杂合子（１８／２５
In order to clarify the role of deletion and deletion of p53 gene in the pathogenesis of gastric cancer, PCR-SSCP method was used to analyze the exons 4、5、6、7、8 and 6 introns of tumor suppressor gene p53. The mutation patterns of gastric cancer and precancerous lesions and PCR-RFLP method were used to investigate the heterozygous deletion of p53 gene exon 4, exon 6 and APC gene in 25 pairs of gastric cancer and adjacent tissues. The results showed that the mutation rate of p53 was 37.5% (3/8), 42.1% (8/19), and 53.3% (16/30) respectively in intestinal metaplasia, atypical hyperplasia, and gastric cancer. P53 mutations were not found in normal tissues and superficial gastritis. There were significant differences in intestinal metaplasia, atypical hyperplasia, and gastric cancer compared with normal controls and superficial gastritis (P<0.05, P<0.01, P<0.01). No mutations in Exon8 were found in the lesions of intestinal metaplasia and dysplasia, but 4 mutations (4/30) were detected in Exon8 in gastric cancer. This suggests that Exon8 mutations mainly occur at late stage. No mutations in Exon4 and Intron6 were found in each lesion group. The study of the heterozygous deletion of Exon4, Intron6 and APC genes showed that among the 25 pairs of gastric cancer specimens, there were 19 pairs of Exon4 heterozygotes, the heterozygosity was 76.0%, there were 9 heterozygous deletions, and the LOH was 47.4%. 23 For Intron6 heterozygotes, the heterozygosity was 92.0%, of which 2 pairs were heterozygous deletions, LOH was 8.7%, and 18 pairs of APC heterozygotes (18/25)