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目的：通过分析胃癌组织幽门螺杆菌（Hp）感染与微卫星DNA不稳定性（MSI）的关系，探讨幽门螺杆菌在胃癌发生中的作用。方法：采用PCR为基础的方法对49例胃癌组织中Hp尿素酶A（HpA）和B（HpB）基因以及6个微卫星位点（D17s261，D17s799，TCF-2，D18s34，D5s409和D5s82）进行检测，对Hp感染与微卫星不稳定性间的关系进行分析。结果：胃癌组织HpDNA的检出率为40．8％（20/49），其D17s261，D17s799，TCF－2，D18s34，D5s409和D5s82位点MSI的检出率分别为22．4％（11／49），22．4％（11／49），18.4％（9／49），28．6％（14／49），14.3％（7／49）和20．4％（10／49）。Hp阳性组各位点MSI检出率与Hp阴性组比较无显著差异（P＞0．05）。结论：Hp感染与MSI无显著相关，在胃癌的发生中可能不起直接作用。
Objective: To explore the role of Helicobacter pylori in the development of gastric cancer by analyzing the relationship between Helicobacter pylori (Hp) infection and microsatellite DNA instability (MSI) in gastric cancer. Methods: Hp urease A (HpA) and B (HpB) genes and six microsatellite loci (D17s261, D17s799, TCF-2, D18s34, D5s409, and D5s82) were performed in 49 cases of gastric cancer using a PCR-based method. Detection, analysis of the relationship between Hp infection and microsatellite instability. Results: The detection rate of HpDNA in gastric cancer was 40.8% (20/49), and the detection rates of D17s261, D17s799, TCF-2, D18s34, D5s409 and D5s82 were respectively 22.4% (11/ 49), 22.4% (11/49), 18.4% (9/49), 28.6% (14/49), 14.3% (7/49) and 20.4% (10/49). There was no significant difference in the detection rate of MSI between the Hp-positive group and the Hp-negative group (P>0.05). CONCLUSIONS: Hp infection is not significantly associated with MSI and may not play a direct role in the development of gastric cancer.