幽门螺杆菌介导炎症微环境调控胃癌发生机制：基于临床试验和类器官模型揭示机制及临床转化

Helicobacter pylori-Driven Inflammation in Gastric Tumorigenesis: Mechanisms and Clinical Translation Based on Clinical Trials and Organoid Models

摘要: 胃癌是一个严重的全球性健康问题，幽门螺杆菌(Helicobacter pylori, H. pylori)被认为是导致胃癌的最主要可控危险因素。据估计，全球有接近半数的人口受到H. pylori的影响，其产生和导致的慢性炎症在胃癌病变的过程中产生重要作用。近年来，关于H. pylori致炎机制、毒力因子CagA及相关信号通路的解析不断深入，根除治疗H. pylori在阻断Correa癌前病变级联反应中的证据亦日益充分。本文旨在讨论H. pylori感染相关胃癌发生的主要机制，结合临床试验和类器官模型总结根除治疗在胃癌预防中的证据，并在此基础上探讨未来精准防治策略的发展方向，以期为降低全球胃癌负担提供理论依据。

Abstract: Gastric cancer is a serious global health problem, and Helicobacter pylori (H. pylori) is considered the primary modifiable risk factor for gastric cancer. It is estimated that nearly half of the global population is affected by H. pylori, and the chronic inflammation induced plays a significant role in the development of gastric cancer. In recent years, the research on the inflammatory mechanisms of H. pylori, the virulence factor CagA, and related signaling pathways has been continuously deepening, and evidence supporting the role of H. pylori eradication therapy in interrupting the Correa cascade has become increasingly robust. In this review, we elaborate on the pivotal mechanisms driving H. pylori -related gastric tumorigenesis, consolidate preclinical and clinical evidence for gastric cancer prevention via H. pylori eradication with the application of gastric organoid systems, and highlight future advances in precision prevention and therapeutic modulation. This work intends to offer solid theoretical support for alleviating the worldwide burden of gastric cancer.