Gastric cancers are the third leading cause of cancer mortality in the world. Helicobacter pylori causes over 60 % of all stomach cancers. Colonization of the gastric mucosa by H. pylori results in increased DNA damage. Repair of DNA damage may also be reduced by H. pylori infection. Reduced DNA repair in combination with increased DNA damage can cause carcinogenic mutations. During progression to gastric cancer, gastric epithelium goes through stages of increasing pathology. Determining the levels of DNA repair enzymes during progression to gastric cancer could illuminate treatment approaches. Our aim is to determine the level of gastric expression of DNA repair proteins ERCC1 (a nucleotide excision repair enzyme) and PMS2 (a mismatch repair enzyme) in the presence of H. pylori infection at successive stages of gastric pathology and in gastric cancers. We analyzed gastric tissues of 300 individuals, including 30 without dyspepsia, 200 with dyspepsia and 70 with gastric cancers. The presence of H. pylori, gastric pathology and expression of DNA repair proteins ERCC1 and PMS2 were evaluated. Infection by H. pylori carrying the common cagA gene reduced median nuclear expression of ERCC1 and PMS2 to less than 20 % and 15 % of normal, respectively, in all pathologic stages preceding cancer. ERCC1 and PMS2 nuclear expression was 0-5 % of normal in gastric cancers. H. pylori can cause deficiency of ERCC1 and PMS2 protein expression. These deficiencies are associated with gastric pathology and cancer. This reduction in DNA repair likely causes carcinogenic mutations. Substantially reduced ERCC1 and PMS2 expression appears to be an early step in progression to H. pylori-induced gastric cancer.

中文翻译：

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幽门螺杆菌会严重降低胃炎和胃癌中DNA修复蛋白PMS2和ERCC1的表达。

胃癌是世界上第三大导致癌症死亡的主要原因。幽门螺杆菌引起所有胃癌的60％以上。幽门螺杆菌在胃粘膜上定植会导致DNA损伤增加。幽门螺杆菌感染也可能减少DNA损伤的修复。减少的DNA修复与增加的DNA损伤相结合会导致致癌突变。在进展为胃癌的过程中，胃上皮经历病理增加的阶段。确定进展为胃癌的过程中DNA修复酶的水平可以阐明治疗方法。我们的目的是确定在H存在下DNA修复蛋白ERCC1（一种核苷酸切除修复酶）和PMS2（一种错配修复酶）在胃中的表达水平。在胃病理学的连续阶段和胃癌中感染幽门螺杆菌。我们分析了300人的胃组织，包括30例无消化不良，200例消化不良和70例胃癌。评估幽门螺杆菌的存在，胃病理学以及DNA修复蛋白ERCC1和PMS2的表达。在癌症之前的所有病理学阶段，携带共同的cagA基因的幽门螺杆菌感染将ERCC1和PMS2的中位核表达分别降低至正常水平的20％和15％以下。胃癌中ERCC1和PMS2的核表达为正常的0-5％。幽门螺杆菌可引起ERCC1和PMS2蛋白表达不足。这些缺陷与胃病理和癌症有关。DNA修复的减少可能导致致癌突变。