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作 者:孙丽萍[1] 张晔[1] 柳云恩[1] 陈威[1] 袁媛[1]
机构地区:[1]中国医科大学附属第一医院肿瘤研究所,沈阳110001
出 处:《中华肿瘤杂志》2008年第9期644-648,共5页Chinese Journal of Oncology
基 金:国家自然科学基金资助项目(30572131)
摘 要:目的探讨胃癌发生发展过程中,胃蛋白酶原C(PGC)基因插入一缺失多态与幽门螺杆菌(Hp)及其不同基因亚型菌株感染的交互作用。方法1:1频数配伍,选择基本正常(NOR)、胃糜烂溃疡(GU)、萎缩性胃炎(AG)和胃癌(GC)各141例,分析PGC基因多态和Hp感染的交互作用。同时选择177例Hp感染阳性者,分析PGC基因多态与不同基因亚型Hp感染的交互作用。以聚合酶链反应(PCR)检测PGC基因多态型及Hp基因亚型。以酶联免疫吸附实验(FLISA)检测血清Hp-IgG抗体。结果PGC基因多态与Hp感染两因素交互作用,PGC等位基因1纯合型、Hp-IgG阳性者罹患GU、AG和GC的OR值分别为8.69、11.16和10.61(P值分别为0.049、0.02和0.03),交互作用指数分别为5.40、6.48和4.34,归因比分别为0.721、0.770和0.697。PGC基因多态与不同基因亚型Hp感染对于AG和GC患病均无交互作用。结论GC发生发展过程中,PGC基因多态与Hp感染存在正交互作用。而与不同基因亚型Hp菌株感染无交互作用。Objective This study was designed to investigate the interaction between pepsinogen C (PC, C) insertion/deletion polymorphism and Helicobacter trylori (Hp) infection, together with its different subtype strains, in the development of gastric cancer (GC). Methods PGC Genotypes were determined by polymerase chain reaction (PCR) assay in 564 subjects with superficial gastritis ( NOR ), gastric ulcer (GU), atrophic gastritis (AG) and GC, who were frequency-matched as 1:1. Serum Hp-IgG antibodies were determined by an enzyme linked immtmoadsorbent assay (ELISA). Hp genetic subtypes in 171 patients with Hp infection were determined by PCR methods. Results In GU, AG and GC, the OR of interaction was 8.69 (P=0.049), 11.16 (P=0.02), and 10.61 (P=0.03), respectively; the interaction index of PGC homozygous allele 1 genotype and Hp infection was 5.40, 6.48 or 4.34, respectively; the atributable proportions were 0. 721, 0. 770 and 0. 697, respectively. In AG and GC, no significant interactions were observed between PGC polymorphism and Hp genetic subtypes. Conclusion The findings of this study suggest that PGC insertion/deletion polymorphism and Hp infection seem to present a positive interaction in the development of gastric cancer. While no interactions may be present between PGC polymorphism and Hp genetic subtypes.
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