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Cancer Related Gene Regulation · Journal article
Genes · August 12, 2026
Encouraging direction, but not yet definitive.
This retrospective cohort study of 226 gastric cancer patients post-gastrectomy reports that high-risk m6A pathway genetic variants independently associate with poorer overall and disease-free survival over 38 months median follow-up. The effect sizes are substantial (HR 1.87 for OS, HR 1.94 for DFS) and survive multivariable adjustment, but the study is not yet validated externally and lacks mechanistic evidence of causality.
Retrospective cohort study with genotyping and multivariable Cox regression. 226 patients with gastric adenocarcinoma who underwent curative gastrectomy; setting and inclusion/exclusion criteria not specified in source.. Intervention: High-risk m6A pathway genotype (composite of SNPs in METTL3, METTL14, FTO, ALKBH5, YTHDF1). Compared with: Low-risk m6A pathway genotype. n = 226.
5-year overall survival was 68.2% in low-risk group versus 41.5% in high-risk group (p < 0.001) 5-year disease-free survival was 61.4% in low-risk group versus 36.8% in high-risk group (p < 0.001) High-risk m6A genotypes independently predicted worse overall survival (HR 1.87, 95% CI 1.28–2.74; p = 0.001)
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If validated externally, m6A genetic variants could serve as independent prognostic biomarkers to identify high-risk gastric cancer patients after surgery who might benefit from intensified adjuvant therapy or closer surveillance. Clinical adoption should await independent replication and prospective validation in external cohorts.
Retrospective cohort study with appropriate statistical methods and hard clinical endpoints (overall and disease-free survival) showing independent associations between m6A genetic variants and poor prognosis after gastrectomy, but limited by single-centre design, retrospective conduct, and lack of external validation.
As stated by the source record.
Quoted from the source exactly as published.
If validated externally, m6A genetic variants could serve as independent prognostic biomarkers to identify high-risk gastric cancer patients after surgery who might benefit from intensified adjuvant therapy or closer surveillance. Clinical adoption should await independent replication and prospective validation in external cohorts.
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.
Background/Objectives: N6-methyladenosine (m6A) RNA modification is a major epitranscriptomic regulator of mRNA stability and translation. Genetic variants in the m6A pathway may influence gastric cancer progression, but their prognostic significance after curative gastrectomy remains uncertain. Methods: This retrospective study included 226 patients with gastric adenocarcinoma who underwent curative gastrectomy. Single nucleotide polymorphisms in five m6A-related genes (METTL3, METTL14, FTO, ALKBH5, and YTHDF1) were genotyped. Overall survival (OS) and disease-free survival (DFS) were analyzed using Kaplan–Meier and log-rank tests. Multivariable Cox regression was performed after adjustment for age, sex, tumor stage, lymph node status, and adjuvant therapy. Results: During a median follow-up of 38 months, 78 patients (34.5%) died and 92 (40.7%) experienced recurrence. High-risk m6A genotypes were associated with significantly poorer survival. The 5-year OS was 68.2% in the low-risk group versus 41.5% in the high-risk group (p < 0.001), while 5-year DFS was 61.4% versus 36.8% (p < 0.001). High-risk genotypes independently predicted worse OS (HR 1.87, 95% CI 1.28–2.74; p = 0.001) and DFS (HR 1.94, 95% CI 1.36–2.78; p < 0.001). Patients with the highest genetic risk scores had the poorest outcomes, particularly those with stage III–IV disease. Conclusion: Genetic variants in the m6A RNA modification pathway are independently associated with poorer survival after curative gastrectomy and may serve as prognostic biomarkers for risk stratification and personalized management in gastric cancer.
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