Gastric cancer (GC) is a major public health problem worldwide, with high mortality rates due to late diagnosis and limited treatment options. Biomarker research is essential to improve the early detection of GC. Technological advances and research methodologies have improved diagnostic tools, identifying several potential biomarkers for GC, including microRNA, DNA methylation markers, and protein-based biomarkers. Although most studies have focused on identifying biomarkers in biofluids, the low specificity of these markers has limited their use in clinical practice. This is because many cancers share similar alterations and biomarkers, so obtaining them from the site of disease origin could yield more specific results. As a result, recent research efforts have shifted towards exploring gastric juice (GJ) as an alternative source for biomarker identification. Since GJ is a waste product during a gastroscopic examination, it could provide a “liquid biopsy” enriched with disease-specific biomarkers generated directly at the damaged site. Furthermore, as it contains secretions from the stomach lining, it could reflect changes associated with the developmental stage of GC. This narrative review describes some potential biomarkers for gastric cancer screening identified in gastric juice.

Introduction: The risk stratification of gastric cancer (GC) is graded by assessing well‐established precursor lesions, glandular atrophy (GA), and intestinal metaplasia (IM), resulting in both the operative link on gastritis assessment (OLGA), and intestinal metaplasia (OLGIM) systems. Although the OLGIM stage is reproducible among pathologists, the OLGA system is laborious to calculate and has poor reproducibility. In addition, it does not comprehensively address the severity of both GA and IM as recommended by the Sydney consensus. We aimed to propose the Operative Link on Gastric Intestinal Metaplasia and Glandular Atrophy Assessment (OLGIMA) system, which identifies OLGIM III–IV and upstages 0–II with advanced GA. Methods: A cross‐sectional study of consecutive diagnostic gastroscopies in adults was designed. Systematic gastric biopsies were taken. The updated Sydney guidelines were used for histological grading of GA and IM. Higher GC risk was defined as OLGIM III–IV and advanced GA. Results: The OLGIMA stage was assessed based on the most severe GA and/or IM findings in both antrum and corpus. We included 998 patients (median age 57; 64% women; 35% Helicobacter pylori infection). Thirty‐nine (3.9%) patients had higher GC risk: 17 (1.7%) with OLGIM III–IV; 12 (1.2%) with advanced GA, and 10 (1%) meeting both criteria. Among OLGIM 0‐II, 12 (1.2%) patients had advanced GA. The OLGIMA system upstaged 39 (3.9%) patients to III–IV, being more sensitive than OLGIM. Conclusions: The new OLGIMA system identifies patients at higher GC risk (OLGIMA III–IV), encompassing all OLGIM III–IV patients, and upstaging those OLGIM 0–II with advanced GA. This approach addresses the OLGA and OLGIM limitations by integrating GA and IM severity as recommended by the Updated Sydney consensus.

Background: Post‐endoscopy gastric cancer (PEGC) is a gastric cancer (GC) diagnosed within 3 years after an esophago‐gastro‐duodenoscopy (EGD) negative for cancer. Post‐endoscopy gastric cancer has a prevalence of 9%–11% in the western population and is potentially reducible through adequate surveillance and high‐quality endoscopy. However, Post‐Endoscopy Gastric Cancer features are not well defined. Objectives: Define Post‐Endoscopy Gastric Cancer prevalence in a gastric cancer low‐risk area as Spain, describe its characteristics and associated factors. Evaluate adherence to current recommendations for surveillance of preneoplastic gastric lesions and endoscopic quality indicators. Methods: A descriptive and analytical study included patients who met PEGC criteria and enrolled in the EpiGASTRIC registry—a national multicentric GC cohort—between April 2021 and May 2024. Results: Of 289 gastric cancer patients analyzed, 21 (7.3%) presented with PEGC. No differences were found between PEGCs and new‐onset gastric cancers (NOGC) regarding clinical‐demographic characteristics (males 52.4%, 65 years, caucasians 78.9%, previous Helicobacter pylori infection 56.3%) except for use of proton pump inhibitors (PPI) (81.0% vs. 44.9%, p ‐value = 0.002). Distal stomach (antrum and/or incisure) was more frequently affected in PEGC compared with NOGC (71.4% vs. 46.2%; p ‐value = 0.022), without differences in tumoral staging (I–II 52.4%) or histology (intestinal type 47.6%). Median time from last negative‐for‐cancer EGD to diagnosis was 13.6 months (interquartile range 4.1–26.8), with 38.1% of precursor lesions in previous endoscopy (19% chronic atrophic gastritis with metaplasia, 19% dysplasia). Considering last negative‐for‐cancer EGD, adherence to current recommendations was 66.6% for the surveillance of gastric lesions, and 14.3% for quality indicators (complete procedure 100%, high‐definition 38.1%, chromoendoscopy 10.0%). Conclusions: PEGC patients present a higher rate of distal stomach involvement and use of PPIs. Although precursor gastric lesions are commonly identified, adherence to current recommendations for their surveillance and to established quality indicators in EGDs is scarce. Despite its low prevalence, there is room for improvement to enhance the early detection and prevention strategies for PEGC.