{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T04:20:36Z","timestamp":1787026836747,"version":"build-2736575974"},"reference-count":61,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2025,10,21]],"date-time":"2025-10-21T00:00:00Z","timestamp":1761004800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Microbiol."],"abstract":"<jats:p>\n                    <jats:italic>Fusobacterium nucleatum<\/jats:italic>\n                    and\n                    <jats:italic>Helicobacter pylori<\/jats:italic>\n                    are two microbial species increasingly recognized for their roles in gastrointestinal (GI) carcinogenesis, particularly in colorectal cancer (CRC) and gastric cancer (GC), respectively. While\n                    <jats:italic>H. pylori<\/jats:italic>\n                    has been long classified as a Group 1 carcinogen due to its well-characterized pathogenic mechanisms,\n                    <jats:italic>F. nucleatum<\/jats:italic>\n                    has more recently emerged as a key microbial contributor to CRC, with growing evidence linking it to tumor progression, immune evasion, and poor clinical outcomes. Despite occupying anatomically distinct niches within the GI tract, both bacteria converge on similar oncogenic pathways, including the activation of NF-\u03baB signaling, \u03b2-catenin pathway dysregulation, and epithelial barrier disruption. In parallel, dietary factors \u2013 particularly the consumption of red and processed meats \u2013 contribute additional oncogenic pressure via carcinogenic compounds such as heme iron, N-nitroso compounds, and polycyclic aromatic hydrocarbons. These dietary components not only damage host tissue but may also potentiate bacterial virulence and promote microbial persistence. This review provides a comparative analysis of the oncogenic strategies employed by\n                    <jats:italic>F. nucleatum<\/jats:italic>\n                    and\n                    <jats:italic>H. pylori<\/jats:italic>\n                    , with an emphasis on their interactions with diet-derived carcinogens and implications for therapeutic interventions targeting the microbiota\u2013diet\u2013host axis in GI cancers.\n                  <\/jats:p>","DOI":"10.3389\/fmicb.2025.1677795","type":"journal-article","created":{"date-parts":[[2025,10,21]],"date-time":"2025-10-21T05:36:38Z","timestamp":1761024998000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":8,"title":["Comparative insights into Fusobacterium nucleatum and Helicobacter pylori in human cancers"],"prefix":"10.3389","volume":"16","author":[{"given":"Alua","family":"Gusmaulemova","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Botakoz","family":"Kurentay","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dina","family":"Bayanbek","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gulmira","family":"Kulmambetova","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2025,10,21]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"23","DOI":"10.1007\/s12029-020-00518-5","article-title":"Molecular mechanism of Helicobacter pylori-induced gastric cancer.","volume":"52","author":"Alipour","year":"2021","journal-title":"J. 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