ReviewBiomarker research2025
Insights into KMT2A rearrangements in acute myeloid leukemia: from molecular characteristics to targeted therapies.
Review in Biomarker research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed.
- Wired to Survive: How AML Cytogenetics Shape Apoptotic Dependence and Venetoclax Resistance.Genes · 2026Review
- Plasticity under pressure: biology and detection of lineage switch in acute leukemia.Leukemia · 2026Review
- Review
- Characteristics and Prognostic Implications in Newly Diagnosed KMT2Ar AML: A Multicenter Study of the ECLA Group.American journal of hematology · 2026Article
- Wiedemann-Steiner Syndrome (WSS): A Neonatal Case Report Expanding the Phenotypic Spectrum of a Previously Reported Missense Variant.International journal of molecular sciences · 2026Review
- A Perturb-seq map of a differentiation hub reveals synergistic vulnerabilities in KMT2A-rearranged acute myeloid leukemia.Leukemia · 2026Article
- Acute Myeloid Leukemias with Alterations of Lysine Methyltransferase 2A (KMT2A): Recent Therapeutic Developments.Cancers · 2026Review
- Review
- Current perspectives on KMT2A fusion proteins and menin inhibition in paediatric acute myeloid leukaemia.The FEBS journal · 2026Review
- A Rare Case of De Novo Acute Myeloid Leukemia, Featuring aDiagnostics (Basel, Switzerland) · 2026Article
- Biomarkers and advances in AML-MRC: from bench to bedside.Annals of hematology · 2026Review
- Regulatory Potential of piRNAs TargetingGenes · 2026Article
- Menin Inhibition in Acute Myeloid MLL Rearranged Leukemias: A New Target for Precision Care.Cancers · 2026Review
- Review
- HS6ST1 regulates acute myeloid leukemia chemotherapy resistance via TGF-β1 signaling.Research square · 2026Article
- Review
- CharacterizingCancers · 2026Article
- Epigenetic alterations in Myeloid Malignancies.Advances in experimental medicine and biology · 2026Review
- The role of epigenetic modifications in hematological cancers.Frontiers in oncology · 2026Review
- KMT2A-Mediated transcriptional regulation in stemness and cancer: molecular mechanisms and therapeutic opportunities.Medical oncology (Northwood, London, England) · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myeloid leukemia (AML) with KMT2A rearrangements (KMT2A-r) represents a highly aggressive and prognostically unfavorable subtype of leukemia, often resistant to standard treatments and associated with high relapse rates. KMT2A-r, found in 3-10% of adult AML cases, disrupt epigenetic regulation by forming chimeric proteins that activate oncogenic pathways like HOXA and MEIS1. These fusion proteins recruit cofactors such as Menin and DOT1L, driving leukemogenesis through abnormal histone methylation. Diagnosing KMT2A-r AML requires precision, with traditional methods like FISH and RT-PCR being complemented by advanced technologies such as next-generation sequencing (NGS) and machine learning (ML). ML models, leveraging transcriptomic data, can predict KMT2A-r and identify biomarkers like LAMP5 and SKIDA1, improving risk stratification. Therapeutically, there is a shift from chemotherapy to targeted therapies. Menin inhibitors (e.g., Revumenib, Ziftomenib) disrupt the Menin-KMT2A interaction, suppressing HOXA/MEIS1 and promoting differentiation. DOT1L inhibitors (e.g., Pinometostat) show promise in combination therapies, while novel approaches like WDR5 inhibitors and PROTAC-mediated degradation are expanding treatment options. Despite progress, challenges remain, including optimizing minimal residual disease monitoring, overcoming resistance, and validating biomarkers. This review emphasizes the imperative to translate molecular insights into personalized therapeutic regimens, offering renewed hope for patients afflicted by this historically refractory malignancy.
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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.