<i>Helicobacter pylori</i> in esophageal carcinogenesis: Potential culprit or forceful defender?

<i>Helicobacter pylori (H. pylori)</i>, a recognized gastric pathogen, has been extensively documented pertaining to its association with a spectrum of gastrointestinal disorders. Given its predominant dissemination via fecal-oral and oral-oral pathways, <i>H. pylori</i> colonization experiences transient esophageal transit prior to its gastric mucosal establishment, while reflux-mediated recrudescence may result in repetitive exposure. The interplay and causality between <i>H. pylori</i> infection and the onset and development of esophageal carcinoma (EC) has emerged as an area of intense scrutiny. Substantial evidence indicates subtype-dependent associations. <i>H. pylori</i> infection (particularly cytotoxin-associated gene A (<i>CagA</i>)-positive strains) reduces the risk of esophageal adenocarcinoma. However, its relationship with esophageal squamous cell carcinoma remains controversial, with studies reporting positive impact, irrelevance, or even an inverse correlation. This review elucidates <i>H. pylori</i> interactions with EC, summarizes protective and pathogenic mechanisms, discerns extant controversies and clinical implications, to inform novel therapeutic strategies for EC prevention and management.