SynthesisFrontiers in pharmacology2026
Novel roles of SETD2 in tumor metabolism and immunotherapy: a systematic review and meta-analysis.
Synthesis in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: SET domain-containing 2 (SETD2), the sole histone H3 lysine 36 trimethyltransferase, has emerged as a critical tumor suppressor across multiple cancer types. Recent evidence suggests SETD2 orchestrates complex interactions between metabolic reprogramming and immune evasion in the tumor microenvironment. Methods: Following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA)2020 guidelines, we systematically searched PubMed, EMBASE, Web of Science, and Cochrane databases from inception through April 2024. We included studies investigating SETD2's role in tumor metabolism and immunotherapy response. Meta-analysis was performed using random-effects models to assess the association between SETD2 status and clinical outcomes. Protocol was developed Results: Of 2,847 initially identified records, 78 studies met inclusion criteria, encompassing approximately 12,400 patients across 12 cancer types. SETD2 loss was associated with metabolic reprogramming (pooled OR: 2.34, 95% confidence interval (CI): 1.89-2.89, p < 0.001) and decreased immunotherapy response (hazard ratio (HR): 1.56, 95% CI: 1.32-1.84, p < 0.001). Substantial heterogeneity was observed (I-squared heterogeneity statistic (I Conclusion: This meta-analysis identifies SETD2 as an epigenetic regulator linking tumor metabolic reprogramming to antitumor immunity. SETD2 loss was associated with altered metabolic states and reduced clinical benefit from immune checkpoint inhibitors, with the strongest translational relevance observed in ccRCC and substantial evidence in NSCLC and CRC. These findings support further prospective validation and standardized assessment of SETD2, as well as exploration of rational metabolic-immunotherapy combination strategies in SETD2-deficient tumors.
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