ReviewSeminars in hematology2025
Epigenetic dysregulation in acute myeloid leukemia.
Review in Seminars in hematology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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.
Who cites it
11 citing papers in PubMed.
- Neem leaf glycoprotein mediated immunomodulation and epigenetic regulation in Acute Myeloid Leukemia.Molecular biology reports · 2026Article
- Epigenetic Regulation in Acute Myeloid Leukemia: Molecular Mechanisms and Clinical Implications.Cancers · 2026Review
- The nutrigenomic-epigenetic axis in cancer: from dietary bioactives to precision oncology.Nutrition & metabolism · 2026Review
- Lineage-specific CK2α deletion reshapes the transcriptome of hematopoietic stem cells toward an immune-primed state.bioRxiv : the preprint server for biology · 2026Article
- Harnessing genomics for early cancer detection, risk stratification and prevention.Nature genetics · 2026Review
- Measurable residual disease testing in acute myeloid leukemia: current state, foundational models, and tools for future development.Cancer metastasis reviews · 2026Review
- Gastrointestinal adverse reactions and metabolism-nutrition disorders associated with hypomethylating agents: a pharmacovigilance study with exploratory mechanistic analysis.Frontiers in nutrition · 2026Article
- Article
- Beyond the DNA sequence: mapping the dynamic epigenetic landscape for risk stratification and therapeutic intervention in acute myeloid leukemia.Clinical and experimental medicine · 2025Review
- Integrated Genomic and Transcriptomic Profiling of Isolated Trisomies in AML Reveals Cell Cycle Dysregulation and Therapeutic Vulnerabilities.Journal of cellular and molecular medicine · 2025Article
- Role and mechanism of the CBX4-HDAC5-CERS6 axis in disrupting sphingomyelin metabolism in acute myeloid leukemia.American journal of cancer research · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Acute myeloid leukemia (AML) is an aggressive hematologic malignancy defined by the clonal expansion of undifferentiated myeloid blasts with a block in differentiation and aberrant self-renewal. While recurrent genomic mutations are well-documented in AML, epigenetic dysregulation has emerged as an equally pivotal driver of leukemogenesis, a notion corroborated by the frequent recurrence of mutations in epigenetic regulators. Leukemic cells exhibit pervasive epigenetic alterations-including abnormal DNA methylation patterns, dysregulated histone modification, disrupted chromatin architecture and RNA-based regulatory mechanisms -which collectively rewire gene expression programs. These changes silence key differentiation genes and sustain self-renewal pathways, enforcing the developmental arrest and hyper-proliferation that are the hallmarks of AML. Importantly, epigenetic aberrations in AML are not merely downstream consequences of genetic lesions but actively contribute to the malignant phenotype. Somatic mutations frequently target epigenetic regulators (for example, DNA methyltransferases or histone modifiers), and these lesions cooperate with other genetic alterations to initiate and maintain the leukemic clone. Together, these insights highlight epigenetic dysregulation as a central mechanism in AML pathogenesis.
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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.