Moss Steven F
Gastroenterology Division, Rhode Island Hospital, Brown University, Providence, Rhode Island.
Cell Mol Gastroenterol Hepatol. 2016 Dec 27;3(2):183-191. doi: 10.1016/j.jcmgh.2016.12.001. eCollection 2017 Mar.
Gastric cancer has long been recognized to be accompanied and preceded by chronic gastritis, lasting decades. Arguably, the most important development in our understanding of gastric cancer pathogenesis over the past 50 years has been the realization that, for most cases of gastric cancer, is the cause of the underlying gastritis. Gastritis can promote gastric carcinogenesis, typically via the Correa cascade of atrophic gastritis, intestinal metaplasia, and dysplasia. Nested case-control studies have shown that infection increases the risk of gastric cancer significantly, both of the intestinal and diffuse subtypes, and that is responsible for approximately 90% of the world's burden of noncardia gastric cancer. Based largely on randomized studies in high gastric cancer prevalence regions in East Asia, it appears that primary and tertiary intervention to eradicate can halve the risk of gastric cancer. Some public health authorities now are starting screening and treatment programs to reduce the burden of gastric cancer in these high-risk areas. However, there is currently much less enthusiasm for initiating similar attempts in the United States. This is partially because gastric cancer is a relatively less frequent cause of cancer in the United States, and in addition there are concerns about theoretical downsides of eradication, principally because of the consistent inverse relationship noted between and esophageal adenocarcinoma. Nevertheless, establishing a link between chronic infection and gastric cancer has led to novel insights into cancer biology, the gastrointestinal microbiome, and on individual and population-based gastric cancer prevention strategies.
长期以来，人们一直认识到胃癌常伴有慢性胃炎，且在其之前就已存在，这种情况可持续数十年。可以说，在过去50年里，我们对胃癌发病机制认识的最重要进展是意识到，对于大多数胃癌病例来说，[此处原文缺失关键信息]是潜在胃炎的病因。胃炎可促进胃癌发生，通常是通过萎缩性胃炎、肠化生和发育异常的科雷亚级联反应。巢式病例对照研究表明，[此处原文缺失关键信息]感染显著增加胃癌风险，包括肠型和弥漫型亚型，并且[此处原文缺失关键信息]导致了全球约90%的非贲门胃癌负担。主要基于东亚胃癌高发地区的随机研究，根除[此处原文缺失关键信息]的一级和三级干预似乎可使胃癌风险减半。一些公共卫生当局现在开始启动筛查和治疗项目，以减轻这些高危地区的胃癌负担。然而，目前在美国开展类似尝试的热情要低得多。部分原因是胃癌在美国是相对不常见的癌症病因，此外，人们担心根除[此处原文缺失关键信息]存在理论上的不利之处，主要是因为[此处原文缺失关键信息]与食管腺癌之间存在持续的负相关关系。尽管如此，建立慢性[此处原文缺失关键信息]感染与胃癌之间的联系，为癌症生物学、胃肠道微生物群以及基于个体和人群的胃癌预防策略带来了新的见解。
