I thoroughly reviewed the paper by Zhang et al published in the recent issue of World Journal of Gastrointestinal Oncology , and commend the authors for their in-depth analysis of the oncogenic functions of GEN1 in gastric cancer (GC). The recent work by Zhang et al sheds light on the oncogenic role of GEN1 in GC, which is involved in cell cycle progression, mitochondrial function, ferroptosis, and chemotherapeutic sensitivity. The findings of this study are of scientific interest and future studies to increase the translational relevance of the work are proposed.
BACKGROUND Human epidermal growth factor receptor 2 (HER2)-negative advanced gastric cancer lacks convenient prognostic biomarkers. Peripheral blood neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), lymphocyte-to-monocyte ratio (LMR) and systemic immune-inflammation index (SII) reflect tumour inflammatory status. This study hypothesizes the four indicators independently predict overall survival (OS) of such patients. AIM To determine the predictive value of NLR, PLR, LMR, and SII for survival in HER2-negative advanced gastric cancer. METHODS We retrospectively enrolled 262 HER2-negative advanced gastric cancer patients (2021-2024) split into disease control (n = 203) and progression (n = 59) groups. Baseline and inflammatory markers were collected. Kaplan-Meier, Cox regressions, nomogram and receiver operating characteristic curve analyses were performed to assess survival predictors. RESULTS In the disease progress group, the NLR, PLR and SII were significantly higher than in the disease control group, whilst the LMR was significantly lower; the median OS in the disease control group (19.1 months) was significantly longer than in the disease progress group (9.2 months). Multivariate Cox regression analysis revealed that elevated NLR, elevated PLR and elevated SII were independent risk factors for OS, whilst a reduced LMR was an independent protective factor. The nomogram constructed using these four indicators demonstrated good predictive performance, with a combined area under the curve of 0.764 (95% confidence interval: 0.676-0.853). CONCLUSION Pretreatment NLR, PLR, LMR, and SII predict survival in HER2-negative advanced gastric cancer; combined use with a nomogram aids prognosis, screening, and treatment.
A recent study identified taurine as a potential drug for suppressing gastric intestinal metaplasia (GIM) in patient-derived organoids and Atp4a-/- mice. Gastric cancer is one of the leading causes of cancer-related deaths worldwide. GIM is a reversible stage in the Correa cascade of gastric carcinogenesis, which is a research hotspot. Previous research models, which included animals and cells, to some extent limited the progress of GIM. Currently, the rapid development of organoid technology has significantly overcome the limitations of the research models in GIM. Organoid technology provides a novel research model for GIM studies that can preserve molecular characteristics of GIM patients with high similarity, thereby offering experimental evidence to support individualized diagnosis and treatment in the clinic. Here, we discuss research models, current therapeutic drugs, and treatment prospects for GIM. Our view is that future research should focus on patient-derived organoids to conduct more accurate studies of GIM pathogenesis and to advance drug development.
BACKGROUND Gastric adenocarcinoma with enteroblastic differentiation (GAED) is a rare histological subtype of gastric cancer with unique embryonic characteristics, and its clinicopathological features and prognostic significance remain unclear to date. AIM To compare the clinicopathological features and survival outcomes between GAED and conventional gastric adenocarcinoma. METHODS A retrospective analysis was conducted on 330 patients who underwent radical gastrectomy at a single center from 2015 to 2024, including 81 GAED patients and 249 patients with conventional gastric adenocarcinoma. The clinicopathological features of the two groups were compared, and Kaplan-Meier analysis and Cox proportional hazards model were used to evaluate overall survival and progression-free survival. RESULTS Compared with the conventional gastric adenocarcinoma group, GAED patients had higher proportions of smoking history (25.9% vs 12.9%, P = 0.008) and drinking history (18.5% vs 8.8%, P = 0.024); lesions were mostly located in the distal stomach (51.9% vs 26.5%), and the proportion of cross-site lesions was lower (19.7% vs 39.0%; P < 0.001 for inter-group difference in tumor location); the proportion of intestinal type in Lauren classification was higher (60.0% vs 37.1%, P = 0.001), the proportion of signet ring cell features was lower (9.9% vs 28.5%, P = 0.001), and there was a difference in the distribution of HER2 scores (P = 0.012); the operation time was shorter (median 190 minutes vs 215 minutes, P = 0.002), the rates of perineural invasion (17.3% vs 36.5%, P < 0.001) and vascular tumor thrombus (11.1% vs 53.4%, P < 0.001) were lower, but the metastasis or recurrence rate was higher (45.7% vs 30.9%, P = 0.022). Kaplan-Meier analysis showed that overall survival and progression-free survival of GAED patients were significantly worse than those of patients with conventional gastric adenocarcinoma; multivariate analysis confirmed that GAED was an independent prognostic factor for both survival outcomes. CONCLUSION Compared with conventional gastric adenocarcinoma, GAED has unique clinicopathological features and worse survival outcomes. As an independent adverse prognostic factor, GAED patients require closer monitoring and more individualized management.
Upper gastrointestinal (UGI) cancers remain a major global health burden, particularly in high-incidence regions. Traditionally, endoscopic screening has been positioned as a secondary prevention strategy aimed at detecting premalignant lesions and early-stage cancers. However, emerging evidence suggests that the role of endoscopic screening may extend beyond early diagnosis and into the realm of primary cancer prevention. Recent prospective data suggest that participation in UGI endoscopic screening programs may be associated with reductions in modifiable behavioral risk factors, including cigarette smoking, alcohol consumption, and unhealthy dietary habits. These findings challenge the conventional paradigm that screening solely identifies disease and instead support the concept that screening encounters may serve as critical behavioral intervention windows (i.e. , brief, clinician-delivered risk communication and counseling opportunities during and after screening). From an oncologic perspective, this raises important questions regarding how screening programs can be optimized to function as structured risk-modification platforms. This review examines the evolving concept of endoscopy as a catalyst for primary prevention, integrating behavioral science, risk stratification models, and population-based cancer control strategies. We discuss how screening-triggered health education, individualized risk communication, and integration with molecular and epidemiologic risk profiling could transform UGI cancer prevention frameworks. Furthermore, we explore the implications of redefining screening programs as multidimensional interventions rather than purely diagnostic tools. As precision oncology advances, cancer prevention must evolve accordingly. Reframing UGI endoscopic screening from a detection-centered approach to a precision prevention platform may conceptually enhance long-term cancer control, reduce population-level risk exposure, and improve cost-effectiveness in high-risk regions. Future implementation research is warranted to validate sustainable models that integrate behavioral modification into structured screening pathways.
