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Most infections are asymptomatic, but in 1%\u20132% of infected individuals, inflammation can lead to a cascade of tissue changes that culminates in the development of metaplasia (pre-cancer) and finally gastric cancer, a highly fatal disease. It has been posited that\n                      <jats:italic toggle=\"yes\">Hp<\/jats:italic>\n                      \u2019s role in the process is merely to initiate inflammation, and once the later stages of disease develop,\n                      <jats:italic toggle=\"yes\">Hp<\/jats:italic>\n                      becomes dispensable. However, epidemiological and molecular studies support a different paradigm: that in at least some individuals,\n                      <jats:italic toggle=\"yes\">Hp<\/jats:italic>\n                      actively drives metaplasia and carcinogenesis. Molecular profiling shows that\n                      <jats:italic toggle=\"yes\">Hp<\/jats:italic>\n                      is prevalent during gastric cancer. In individuals with metaplasia, successful antibiotic eradication of\n                      <jats:italic toggle=\"yes\">Hp<\/jats:italic>\n                      prevents the development of gastric cancer; antibiotic eradication after cancer appears can even significantly reduce the likelihood of tumor recurrence. In rodent models of gastric cancer,\n                      <jats:italic toggle=\"yes\">Hp<\/jats:italic>\n                      infection accelerates carcinogenesis, and in a metaplasia model,\n                      <jats:italic toggle=\"yes\">Hp<\/jats:italic>\n                      infection alters the metaplastic lineages present and causes increased dysplasia (abnormal cells). Taken together, these data point to an active role for\n                      <jats:italic toggle=\"yes\">Hp<\/jats:italic>\n                      infection in driving gastric cancer development, at least in some individuals. Therefore, studies investigating host-pathogen interactions in the context of\n                      <jats:italic toggle=\"yes\">Hp<\/jats:italic>\n                      -driven carcinogenesis should encompass the entire spectrum of disease development, not just the establishment of gastric infection and initiation of inflammation. Understanding the complete picture of\n                      <jats:italic toggle=\"yes\">Hp<\/jats:italic>\n                      -driven disease will enable us to tackle this highly fatal cancer.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1128\/iai.00032-26","type":"journal-article","created":{"date-parts":[[2026,7,13]],"date-time":"2026-07-13T14:01:58Z","timestamp":1783951318000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["Bad bugs mean business: gastric cancer is an intended consequence of\n                    <i>Helicobacter pylori<\/i>\n                    infection"],"prefix":"10.1128","volume":"94","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0502-2690","authenticated-orcid":true,"given":"Valerie P.","family":"O'Brien","sequence":"first","affiliation":[{"name":"Borch Department of Medicinal Chemistry and Molecular Pharmacology, Purdue University College of Pharmacy","place":["West Lafayette, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.3322\/caac.21834"},{"key":"e_1_3_2_3_2","unstructured":"2023. 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