ArticleThe Journal of clinical investigation2026
Histone lysine methyltransferases KMT2C and KMT2D join the all-star tumor suppressor team in gastrointestinal cancer.
Article in The Journal of clinical investigation, 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
Members of the type 2 histone lysine methyltransferase family (KMT2s) are key drivers of enhancer activation and are the most mutated group of epigenetic regulators in different cancer types. Within this family, KMT2C and KMT2D have the highest mutational incidence across various cancers. To evaluate their role in gastric cancer, Wang et al. developed a Pten deficiency-driven genetically engineered mouse model with inducible loss of Kmt2c and Kmt2d in gastric epithelial cells. Through extensive in vitro, in vivo, and in silico analyses, the authors revealed that the concomitant loss of Kmt2c and Kmt2d promotes gastric carcinogenesis while enhancing antigen presentation and sensitivity to immunotherapy and targeted approaches like mTOR inhibition, highlighting the tumor-suppressive roles of KMT2C/D in gastric cancer and uncovering a vulnerability for this dismal condition.
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