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Abstract：
Helicobacter pylori has been classified as a class I carcinogen by WHO because of its primary involvement in the development of gastric cancer and mucosa-associated lymphoid tissue (MALT) lymphoma. This review focuses on understanding the molecular pathophysiological mechanisms that operate within intracellular transduction pathways and their relevance in the treatment strategies for the two main diseases caused by H. pylori. H. pylori virulence factors such as cytotoxin-associated gene A and vacuolating cytotoxin A genotypes, inflammatory mediators, H. pylori-induced microRNA deregulation, alterations in autophagy proteins and regulators, and changes in DNA methylation are some of the molecular mechanisms that play essential roles in H. pylori infection and gastric carcinogenesis. The discovery of novel treatment strategies that target the deregulated intracellular transduction pathways in gastric carcinogenesis and MALT lymphoma is critical. H. pylori eradication (HPE) is not limited to H. pylori-dependent low-grade MALT lymphoma and may be used in patients with high-grade diffuse large B-cell lymphoma (DLBCL) (de novo or DLBCL-MALT lymphoma). The loss of H. pylori dependency and high-grade transformation appear to be distinct events in the progression of gastric lymphoma. Interestingly, patients with H. pylori-positive gastric DLBCL without histological evidence of MALT lymphoma (pure gastric DLBCL) may respond to HPE therapy.
摘要：
幽门螺杆菌因其主要参与胃癌和粘膜相关淋巴组织（MALT）淋巴瘤的发展而被WHO归类为I类致癌物。这篇综述的重点是了解在细胞内转导途径中起作用的分子病理生理机制及其在幽门螺杆菌引起的两种主要疾病的治疗策略中的相关性。幽门螺杆菌毒力因子，如细胞毒素相关基因A和空泡细胞毒素A基因型，炎症介质，幽门螺杆菌诱导的microRNA失调，自噬蛋白和调节因子的改变，和DNA甲基化的变化是在幽门螺杆菌感染和胃癌发生中起重要作用的一些分子机制。发现针对胃癌发生和MALT淋巴瘤中失调的细胞内转导途径的新治疗策略至关重要。幽门螺杆菌根除(HPE)不限于幽门螺杆菌依赖性低度MALT淋巴瘤,并且可用于患有高度弥漫性大B细胞淋巴瘤(DLBCL)(从头或DLBCL-MALT淋巴瘤)的患者。幽门螺杆菌依赖性的丧失和高级转化似乎是胃淋巴瘤进展中的不同事件。有趣的是,没有组织学证据的幽门螺杆菌阳性胃DLBCL患者MALT淋巴瘤(纯胃DLBCL)可能对HPE治疗有反应.
