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目的：探讨幽门螺杆菌L型（Hp-L型）可能的致癌机理。方法：应用免疫组化S-P法对Hp-L型阳性和阴性胃病变组织的PCNA、P21、P53表达进行对比分析。结果：胃癌、癌前病变的PCNA、P21、P53表达显著高于慢性浅表性胃炎和正常粘膜；Hp-L型阳性组的PCNA、P21、P53表达也明显高于Hp-L型阴性组（P＜0．01，P＜0·05）。表明Hp-L型感染与胃病变组织的PCNA、P21、P53过度表达存在着相关性。提示，Hp-L型感染时胃粘膜处于高增殖状态。结论：Hp-L型参与了ras原癌基因激活和P53抑癌基因的失活，基因突变可能是Hp-L型致胃癌作用的机制之一。
Objective: To investigate the possible mechanism of H. pylori L-type (Hp-L) carcinogenesis. Methods: The expression of PCNA, P21 and P53 in Hp-L positive and negative gastric lesions was analyzed by immunohistochemical S-P method. Results: The expressions of PCNA, P21 and P53 in gastric cancer and precancerous lesions were significantly higher than those in chronic superficial gastritis and normal mucosa. The expressions of PCNA, P21 and P53 in Hp-L positive group were also significantly higher than those in Hp-L negative group P <0.01, P <0.05). The results showed that there was a correlation between Hp-L infection and PCNA, P21, P53 overexpression in gastric tissue. Tip, Hp-L infection in gastric mucosa in a high proliferative state. Conclusion: Hp-L is involved in the activation of oncogene ras and the inactivation of p53 suppressor oncogene. Mutation may be one of the mechanisms of Hp-L-induced gastric cancer.