摘要
目的研究幽门螺杆菌(Hp)感染胃癌患者增殖细胞核抗原、抑癌基因P53基因突变情况,以探讨Hp可能的致癌机制.方法应用免疫组化法检测PCNA蛋白表达情况,PCR/SSCP方法观察P53基因第5~8外显子突变情况,快速尿素酶法和HE染色检测Hp感染情况.结果胃癌组Hp感染21例(21/30,70%).从浅表性胃炎到胃癌PCNA指数呈递增趋势,各组间均有显著性差异(P<0.05).浅表性胃炎和萎缩性胃炎组中Hp阳性患者与Hp阴性者的PCNA LI相比有显著性差异(P<0.05),其余各组间Hp阳性和Hp阴性病例间的PCNA LI无显著性差异(P>0.05).异型增生P53基因第8外显子突变1例(1/30,3.33%),为Hp阳性者.胃癌组织P53第5~8外显子突变17例(17/30、56.67%),Hp阳性胃癌组的突变率与Hp阴性组相比有显著性差异(P<0.05).结论Hp感染者具有更多肿瘤生物学行为,可以引起PCNA蛋白表达增强、抑癌基因P53突变,Hp可能为促癌剂在胃癌的发生发展中起一定作用.
Objective To investigate the potential role of infection with Helicobacter pylori (H.pylori) in the development of gastric cancer with increased expression of proliferating cell nuclear antigen (PCNA) and P 53. Methods Immunohistochemical staining was used to detect the expression of PCNA in 30 cases of gastric cancer, 18 dyspasia, 12 intestinal metaplasia, 24 atrophicgastritis, and 16 superficial gastritis. Exon 5~8 mutations were detected by PCR-SSCP. H.pylori was assessed by using rapid unease test combined with HE stain. Results PCNA LI was gradually increased from superficial gastritis to gastric cancer. There was significant difference among five groups. (P < 0.05). There was significant difference for PCNA LI in chronic gastritis between H. pylori positive and negative group (P < 0.05). Exon 5~8 mutation was 17 cases in gastric cancet. There was significant difference in exon 5~8 mutation between H.pyloric positive and negative group(P < 0.05) . Conclusion H. pyloric infections may increase expression of PCNA and exon5~8 mutation, therefore that acts as an oncogenic agent in occurrence and development of gastric cancer. 〔
出处
《深圳中西医结合杂志》
2004年第5期264-266,271,共4页
Shenzhen Journal of Integrated Traditional Chinese and Western Medicine
关键词
幽门螺杆菌
胃肿瘤
癌前病变
增殖细胞核抗原
基因
P53
Helicobacter pylori
Gastric tumour
Precancerous lesion
Proliferating cell nuclear antigen
Gene
P53