Mbulaiteye Sam M, Hisada Michie, El-Omar Emad M
Infections and Immunoepidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland, USA.
Front Biosci (Landmark Ed). 2009 Jan 1;14(4):1490-504. doi: 10.2741/3320.
Helicobacter pylori infection is ubiquitous, infecting close to one-half of the world's population, but its prevalence is declining in developed countries. Chronic H. pylori infection is etiologically linked to gastric adenocarcinoma, especially non-cardia type (63% of all stomach cancer or ~5.5% of the global cancer burden: ~25% of cancers associated with infectious etiology), and to gastric mucosal associated lymphoid tissue (MALT) lymphoma, which accounts for up to 8% of all non-Hodgkin lymphoma. Epidemiological, clinical, and animal studies have established a central role for H. pylori in gastric carcinogenesis and provided insights into the mechanisms and biologic relationships between bacterial infection, host genetics, nutrition, and environmental factors. These discoveries invite strategies to prevent infection to be the logical primary goals in a multi-pronged effort to curtail suffering and death from H. pylori infection-associated cancers.
幽门螺杆菌感染十分普遍，全球近一半人口受其感染，但在发达国家其感染率正在下降。幽门螺杆菌慢性感染在病因上与胃腺癌相关，尤其是非贲门型（占所有胃癌的63%或全球癌症负担的约5.5%：约25%的癌症与感染病因相关），还与胃黏膜相关淋巴组织（MALT）淋巴瘤相关，后者占所有非霍奇金淋巴瘤的比例高达8%。流行病学、临床和动物研究已证实幽门螺杆菌在胃癌发生过程中起核心作用，并为细菌感染、宿主遗传学、营养和环境因素之间的机制及生物学关系提供了深入见解。这些发现促使预防感染的策略成为多项举措中旨在减少幽门螺杆菌感染相关癌症所致痛苦和死亡的合理首要目标。
