ArticleHaematologica2025
S-adenosylmethionine addiction confers sensitivity to methionine restriction in
Article in Haematologica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed.
- Traditional Chinese Medicine Intervention Based on Metabolic-Epigenetic Axis: Mechanism and Treatment Strategy of Chronic Heart Failure.Biomolecules · 2026Review
- Metabolic epigenome targeting hitsHaematologica · 2025Article
- The Phosphatidylinositol 3-Kinase (PI3K) Inhibitor Inavolisib Has Breast-cancer Synergy Combined With Recombinant Methioninase But Not on Normal Cells.In vivo (Athens, Greece)Article
- Ultra-low Concentrations of Cisplatinum Down to the ICIn vivo (Athens, Greece)Article
- Methionine Restriction Alone Induces T-cell-mediated Immunotherapy of Osteosarcoma in a Syngeneic Mouse Model.In vivo (Athens, Greece)Article
- The Combination of Methionine Adenosyltransferase 2A (MAT2A) Inhibitor AG-270 and Recombinant Methioninase Is Not Cancer-selective in a Co-culture Model of Colon Cancer Cells and Normal Fibroblasts.Cancer diagnosis & prognosisArticle
Corrections and comments
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Authors and funding
17 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Current intensive chemotherapy regimens have improved overall survival in pediatric acute lymphoblastic leukemia (ALL) but fail to cure some high-risk patient subgroups. We observed that lysine methyltransferase 2A-rearranged (KMT2A-r) leukemia, an aggressive subset with a dismal prognosis, is particularly vulnerable to perturbations of the methionine cycle. We demonstrate that this methionine dependency is driven by an increased need for S-adenosylmethionine (SAM) to maintain the hypermethylated state of KMT2A-r leukemias. Important pro-survival KMT2A-r target genes are repressed under methionine restriction, which, combined with other downstream metabolic changes, results in rapid cell death. FIDAS-5, an orally active methionine adenosyltransferase 2A (MAT2A) inhibitor that blocks SAM production, successfully impaired leukemia progression in patient-derived xenograft models, and a drug screen revealed strong synergy between MAT2A inhibition and histone deacetylase inhibitors. Our results identify the methionine cycle as a targetable vulnerability in KMT2A-r leukemia, which may increase the efficacy of epigenetic targeting agents.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.