N6-methyladenosine (m6A) RNA methylation is the most prevalent internal modification of mammalian messenger RNA. The m6A modification affects multiple aspects of RNA metabolism, including processing, splicing, export, stability, and translation through the reversible regulation of methyltransferases (Writers), demethylases (Erasers), and recognition binding proteins (Readers). Accumulating evidence indicates that altered m6A levels are associated with a variety of human cancers. Recently, dysregulation of m6A methylation was shown to be involved in the occurrence and development of gastric cancer (GC) through various pathways. Thus, elucidating the relationship between m6A and the pathogenesis of GC has important clinical implications for the diagnosis, treatment, and prognosis of GC patients. In this review, we evaluate the potential role and clinical significance of m6A-related proteins which function in GC in an m6A-dependent manner. We discuss current issues regarding m6A-targeted inhibition of GC, explore new methods for GC diagnosis and prognosis, consider new targets for GC treatment, and provide a reasonable outlook for the future of GC research.

Background: To some extent, the robotic technique does offer certain benefits in rectal cancer surgery than laparoscopic one, while remains a topic of ongoing debate for rectal cancer patients who have undergone neoadjuvant chemoradiotherapy (NCRT). Methods: Potential studies published until January 2024 were obtained from Web of Science, Cochrane Library, Embase, and PubMed. Dichotomous and continuous variables were expressed as odds ratios (ORs) or weighted mean differences (WMDs) with 95% CIs, respectively. A random effects model was used if the I ² statistic >50%; otherwise, a fixed effects model was used. Results: Eleven studies involving 1079 patients were analysed. The robotic-assisted group had an 0.4 cm shorter distance from the anal verge (95% CI: −0.680 to −0.114, P =0.006) and 1.94 times higher complete total mesorectal excision (TME) rate (OR=1.936, 95% CI: 1.061–3.532, P =0.031). However, the operation time in the robotic-assisted group was 54 min longer (95% CI: 20.489–87.037, P =0.002) than the laparoscopic group. In addition, the robotic-assisted group had a lower open conversion rate (OR=0.324, 95% CI: 0.129–0.816, P =0.017) and a shorter length of hospital stay (WMD=−1.127, 95% CI: −2.071 to −0.184, P =0.019). Conclusion: Robot-assisted surgery offered several advantages over laparoscopic surgery for locally advanced mid-low rectal cancer following NCRT in terms of resection of lower tumours with improved TME completeness, lower open conversion rate, and shorter hospital stay, despite the longer operative time.

Available results on the association between the Mediterranean diet (MD) and gastric cancer (GC) incidence are controversial. The present study aimed to determine the correlation between different subtypes of GC and MD adherence. This meta-analysis was registered on PROSPERO (CRD42021284432). We searched Embase, PubMed, Cochrane Library, and Web of Science from inception through 22 April 2023 to retrieve relevant studies. A random-effects model was used to pool odds ratios (ORs) with 95% confidence intervals (CIs). Eleven studies were included in the meta-analysis. Pooled analyses revealed that adherence to the MD was inversely associated with GC risk (OR_cc, 0.43; 95% CI, 0.29 to 0.63; OR_coh, 0.84; 95% CI, 0.77 to 0.92). Higher MD adherence was significantly associated with a reduced GC risk in male (OR_cc, 0.78; 95% CI, 0.65 to 0.93; OR_coh, 0.81; 95% CI, 0.65 to 1.01), but not in female (OR_cc, 0.83; 95% CI, 0.68 to 1.01; OR_coh, 1.04; 95% CI, 0.82 to 1.31). Furthermore, adherence to the MD possibly decreased the risk of gastric cardia adenocarcinoma (GCA) (OR_cc, 0.64; 95% CI, 0.49 to 0.83; OR_coh, 0.88; 95% CI, 0.76 to 1.02) and gastric non-cardia adenocarcinoma (GNCA) (OR_cc, 0.68; 95% CI, 0.59 to 0.79; OR_coh, 0.85; 95% CI, 0.78 to 0.94). Our results indicate that adherence to the MD reduces the risk of GC and its subtypes.

Gastric cancer (GC) ranks as the third most prevalent malignancy and a leading cause of cancer-related mortality worldwide. However, the majority of patients with GC are diagnosed at an advanced stage, highlighting the urgent need for effective perioperative and postoperative chemotherapy to prevent relapse and metastasis. The current treatment strategies have limited overall efficacy because of intrinsic or acquired drug resistance. Recent evidence suggests that dysregulated long non-coding RNAs (lncRNAs) play a significant role in mediating drug resistance in GC. Therefore, there is an imperative to explore novel molecular mechanisms underlying drug resistance in order to overcome this challenging issue. With advancements in deep transcriptome sequencing technology, lncRNAs—once considered transcriptional noise—have garnered widespread attention as potential regulators of carcinogenesis, including tumor cell proliferation, metastasis, and sensitivity to chemo- or radiotherapy through multiple regulatory mechanisms. In light of these findings, we aim to review the mechanisms by which lncRNAs contribute to drug therapy resistance in GC with the goal of providing new insights and breakthroughs toward overcoming this formidable obstacle.

Recently, attention has been paid to some medications and gastric cancer (GC) risk. This review aimed to evaluate associations between commonly used drugs and GC risk and to grade evidence from published systematic reviews and meta-analyses. This umbrella review was registered in PROSPERO (CRD42022320276). The systematic reviews and meta-analyses of observational studies were retrieved by searching Embase, PubMed, and Web of Science. The evidence strength of commonly used drugs and GC risk was categorized into four grades: weak, suggestive, highly suggestive, and strong. Of 19 associations between commonly used drugs and GC risk and its subtypes, none was supported by convincing or highly suggestive evidence. The risk of GC related to non-steroidal anti-inflammatory drugs (NSAIDs), non-aspirin NSAIDs, and acid-suppressive drugs, as well as the risk of non-cardia GC related to NSAIDs and aspirin, was supported by suggestive evidence. The results showed that a reduced GC risk was associated with two drug types (NSAIDs and non-aspirin NSAIDs), and an increased GC risk was associated with acid-suppressing drugs at the suggestive evidence level. Moreover, NSAIDs and aspirin reduced non-cardia GC risk as supported by suggestive evidence. However, the evidence supporting statins or metformin in reducing GC risk was weak, and thus future studies are required to clarify these associations.

Background: The albumin-to-alkaline phosphatase ratio (AAPR), a simple and cost-effective prognostic parameter, has not been thoroughly investigated in relation to gastrointestinal (GI) cancers. Methods: Relevant studies were retrieved from databases including Web of Science, Cochrane Library, Embase, and PubMed up to February 2025. Survival outcomes were presented as hazard ratios (HRs) with 95% confidence intervals (CIs). Heterogeneity was evaluated using the I ² statistic and Cochrane’s Q test. When significant heterogeneity was detected ( I ² ≥ 50% or P ≤ 0.05), a random-effects model was employed; otherwise, a fixed-effects model was utilized. Statistical analyses were conducted using STATA 18.0 software. Results: Eight studies involving 2267 patients with GI cancer were analysed. The pooled results of overall survival (OS) from both univariate and multivariate analyses indicated a significantly higher risk of death in the low-AAPR group than in the high-AAPR group (HR = 2.49, 95% CI: 1.67 to 3.71, P < 0.001, I ² = 84.3%; HR = 2.59, 95% CI: 1.55 to 4.35, P < 0.001, I ² = 80.3%). For recurrence-free survival (RFS), univariate analysis revealed worse outcomes in the low-AAPR group (HR = 1.58, 95% CI: 1.18 to 2.13, P = 0.002, I ² = 0.0%). However, multivariate analysis did not establish a significant correlation between the two groups (HR = 1.25, 95% CI: 0.33 to 4.77, P = 0.740, I ² = 51.5%). Subgroup analyses by country, tumor type, treatment method, and AAPR cut-off value consistently showed that low AAPR was significantly associated with poor OS. Although publication bias was detected in the OS meta-analysis, both the trim-and-fill method and sensitivity analysis confirmed a significant association between low AAPR and poor OS. Conclusion: A low AAPR is associated with poorer OS in GI cancer patients. Therefore, AAPR may serve as a promising serological parameter for prognostic assessment in GI cancer patients.