ReviewCurrent oncology reports2026
Targeting the Epigenetic-Immune Axis in Acute Myeloid Leukemia: Current Advances and Future Directions.
Review in Current oncology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
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0 citing papers in PubMed.
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purpose of reviewAcute myeloid leukemia (AML) exemplifies how malignant transformation can be driven by both epigenetic deregulation and genetic mutation. Aberrant DNA methylation, histone modifications, and chromatin remodelling cooperate to block myeloid differentiation, sustain leukemic self-renewal, and promote immune evasion. This review examines the molecular mechanisms underlying epigenetic dysregulation in AML and highlights recent advances in epigenetic and immune-based therapeutic strategies. RECENT
findingsRecent studies have identified multiple druggable epigenetic regulators, including DNA methyltransferases, TET dioxygenases, histone methyltransferases and demethylases, and histone acetyltransferases and deacetylases. These discoveries have led to the development of hypomethylating agents, mutant IDH1/2 inhibitors, menin-MLL and DOT1L antagonists, EZH2 and LSD1 inhibitors, and class-specific HDAC inhibitors, several of which are approved or undergoing advanced clinical evaluation. Beyond reprogramming leukemic transcriptional networks, epigenetic therapies also remodel the immune microenvironment by influencing antigen presentation and immune checkpoint pathways, providing a rationale for combination approaches with antibody-drug conjugates, bispecific T-cell or NK-cell engagers, aptamer-directed therapeutics, vaccines, and CAR-T/NK cell therapies targeting CD33, CD123, FLT3, CLL-1, and other AML-associated antigens. The integration of epigenetic modulation with immunotherapeutic and precision medicine approaches represents a promising strategy to overcome disease heterogeneity and therapeutic resistance in AML. By bridging mechanistic insights with translational advances, clinical trial evidence, and emerging patent landscapes, this review highlights epigenetic dysregulation as both a fundamental driver of leukemogenesis and a clinically actionable therapeutic interface that may enable more rational treatment sequencing and personalized AML management.
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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.