Epigenetic Dysregulation in Hematological Malignancies: Mechanisms and Therapeutic Implications
A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Therapy".
Deadline for manuscript submissions: 30 April 2026 | Viewed by 31
Special Issue Editors
2. Department of Laboratory Hematology, University Health Network, Toronto, ON, Canada
Interests: myeloma; molecular cytogenetics; prognostic factors; small molecule inhibitors
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Epigenetic dysregulation is a hallmark of hematologic malignancies (HMs), driving their initiation, progression, and therapeutic resistance.
Epigenetic alterations—including DNA methylation, histone modification, and chromatin remodeling—play a fundamental role in the pathogenesis of hematological malignancies (HMs). Recurrent mutations in epigenetic regulators such as DNMT3A, TET2, EZH2, and ASXL1 have been identified in both myeloid and lymphoid neoplasms, leading to widespread transcriptional dysregulation. These mutations promote leukemogenesis by enhancing the self-renewal of leukemic stem cells (LSCs), impairing normal hematopoietic differentiation, and activating oncogenic pathways.
Environmental and systemic factors—such as chronic inflammation and metabolic syndrome—may further exacerbate malignant transformation by triggering epigenetic changes that favor oncogene activation and tumor suppressor silencing. Aberrant histone modifications and mutations in chromatin remodeling complexes (e.g., SWI/SNF components) further destabilize chromatin architecture and contribute to disease progression.
Exosomes, nano-sized extracellular vesicles, have emerged as key mediators of epigenetic communication within the tumor microenvironment. These vesicles transport various bioactive molecules, including non-coding RNAs, which can post-transcriptionally modulate gene expression in recipient cells. A subset of these, known as epimiRNAs, are selectively packaged and can induce pro-oncogenic epigenetic reprogramming, such as silencing tumor suppressor genes or promoting therapy resistance, thereby supporting clonal expansion and disease persistence.
The clinical importance of epigenetic dysregulation is underscored by the development of targeted epigenetic therapies, including hypomethylating agents (e.g., azacitidine, decitabine) and histone deacetylase inhibitors (e.g., vorinostat, romidepsin), which have shown efficacy in treating certain HMs. Additionally, exosomal miRNAs are being investigated as non-invasive biomarkers for diagnosis, prognosis, and monitoring treatment response.
Advancing our understanding of these mechanisms offers significant promises for improving outcomes through precision epigenetic therapies and biomarker discoveries. In this Special Issue, we invite original research and comprehensive reviews that explore the following:
- Novel insights into epigenetic drivers of hematologic malignancies;
- Mechanisms of therapy resistance mediated by epigenetic dysregulation;
- Clinical applications of epigenetic biomarkers and emerging therapies;
- Interplay between environmental factors, lifestyles, and epigenetic alterations in HMs.
We seek contributions that bridge basic science with translational advances, ultimately paving the way for personalized therapeutic approaches in hematologic oncology.
Dr. Hong Chang
Dr. Shamila D. Alipoor
Guest Editors
Manuscript Submission Information
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Keywords
- epigenetic dysregulation
- hematologic malignancies
- epigenetic therapy
- DNA methylation
- histone modification
- non-coding RNAs
- exosomes
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