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Esophageal Cancer Research and Treatment / Gastric Cancer Management and Outcomes · Journal article
The Korean Journal of Helicobacter and Upper Gastrointestinal Research · September 9, 2026
A consensus or society position rather than new primary data.
This guidance synthesizes evidence that OLGA histological staging reliably stratifies gastric cancer risk in endoscopic populations and proposes a framework integrating serological monitoring (pepsinogens, gastrin) with endoscopy-based surveillance. The text acknowledges that serology's clinical utility at the individual patient level remains unresolved outside large epidemiological studies, and calls for a patient-specific serology approach within a structured follow-up protocol.
Journal article. Patients undergoing endoscopy for gastric cancer risk assessment, particularly those at risk from Helicobacter pylori infection..
OLGA staging classifies mucosal atrophy severity into five stages (0 to IV) with stepwise increasing cancer risk validated in international trials OLGA stages are reclassified as low-risk (0–I) and high-risk (III–IV), with stage II clinically controversial Helicobacter pylori prevalence is identified as the most significant population-specific risk factor affecting high-risk stage prevalence
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Clinicians should use OLGA histological staging from antral and corpus biopsies to stratify individual cancer risk and determine surveillance intervals. Serological markers may supplement but should not replace tissue-based staging; serology is proposed as a non-invasive interval monitoring tool, though its individual-level reliability requires further validation.
A narrative review synthesizing evidence on gastric atrophy staging and risk stratification to inform clinical surveillance strategy and serological monitoring in individual patients.
Clinicians should use OLGA histological staging from antral and corpus biopsies to stratify individual cancer risk and determine surveillance intervals. Serological markers may supplement but should not replace tissue-based staging; serology is proposed as a non-invasive interval monitoring tool, though its individual-level reliability requires further validation.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
What is missing. This record has no reported figures. That is a gap in the analysis, not a judgement about the study.
Gastric mucosa atrophy is the cancerization field for gastric cancer development. Atrophic changes in the gastric mucosa can be assessed endoscopically and histologically. Gastric serology (e.g., pepsinogens and their ratio, and gastrin) may provide information on the functional status of the mucosa. However, outside large-scale epidemiological studies, the clinical reliability of serology at the individual patient level remains controversial. Histology-based estimates of atrophy-associated neoplastic risk require mucosal specimens from both the antral/mucus-secreting and corpus/fundus oxyntic compartments. Inspired by the clinical–biological framework of cancer staging, the Operative Link on Gastritis Assessment (OLGA) staging system classifies the severity and topography of mucosal atrophy into five stages, ranging from 0 to IV. International trials have validated the stepwise increasing risk of cancer with disease progression. Based on this evidence, OLGA stages are classified into low-risk (0–I) and high-risk (III–IV), with stage II remaining clinically controversial. The prevalence of high-risk stages varies according to patient- and population-specific risk factors. Among these, the most significant is the prevalence of Helicobacter pylori, a recognized oncogenic agent. Bacterial infection at the time of the initial endoscopy requires eradication therapy regardless of the stage of gastritis. Histological stage reliably identifies the endoscopic population at a high risk of cancer progression and shapes the schedule of endoscopy/histology-based surveillance. Serology at the index endoscopy may circumvent the inherent inconsistencies of population-based studies. This patient-specific serology could serve as an interval for non-invasive monitoring within the endoscopy/histology follow-up framework.
Taken from the source record, never inferred. Follow any of these and new work involving them reaches your briefing.