Autoimmune gastritis (AIG) has been traditionally recognised as a precursor to type I gastric neuroendocrine tumours and non-cardia gastric adenocarcinoma. However, emerging but scattered evidence suggests that its oncogenic footprint may extend beyond the gastric body to the cardia, gastro-oesophageal junction (GOJ) and oesophagus. In this review, we synthesise the available epidemiological and clinical studies linking AIG and its late manifestation, pernicious anaemia, to cardia/GOJ adenocarcinoma and oesophageal cancers. We discuss putative histopathological, immunological and other mechanisms, including corpus-predominant atrophy, intestinal metaplasia and vitamin B12 deficiency that may create a carcinogenic microenvironment not only in the distal stomach but also at the GOJ and beyond. We highlight diagnostic and epidemiologic challenges that have obscured these associations, including the difficulties in defining the gastric cardia, disentangling autoimmune versus other potential pathways and the under-recognition of AIG in routine practice. Finally, we outline a research agenda aimed at clarifying the malignancy risk across the stomach-cardia-oesophagus continuum, emphasising the need for well-phenotyped cohorts, biomarker-driven risk stratification and refined surveillance strategies. By reframing AIG as a potential hidden gateway to junctional and oesophageal malignancies, we argue that its true oncological significance may be broader than previously appreciated.
Lenti et al. (Wed,) studied this question.