Epigenetic Mechanisms of Hematologic Malignancies

A special issue of Epigenomes (ISSN 2075-4655).

Deadline for manuscript submissions: closed (31 March 2025) | Viewed by 815

Special Issue Editor


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Guest Editor
Division of Hematology and Oncology, Department of Medicine, University of Florida, Gainesville, FL, USA
Interests: cancer epigenetics; molecular cell biology; cancer cell signaling
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Hematologic malignancies that include leukemia, lymphoma, and multiple myeloma account for approximately 9% of cancers in the U.S. and Europe. The analysis of genomic data from these patients reveals that recurrent somatic mutations, which affect the epigenetic regulation of gene expression, play a central role in the pathogenesis of lymphoid and myeloid neoplasms. These mutations may affect key proteins involved in DNA methylation, chromatin architecture, histone post-translational modification, or chromatin remodeling to alter chromatin accessibility and gene expression. Importantly, emerging therapeutic strategies target aberrant epigenetic mechanisms found in hematological malignancies to restore a more normal epigenetic state and either inhibit malignant cell growth or render these malignancies more tractable to other anti-cancer therapies, such as chemotherapies or immunotherapies.

This Special Issue will focus on the role of epigenetic mechanisms in hematologic malignancies and anti-cancer therapeutics that target aberrant epigenetic mechanisms in these cancers. We welcome high-quality manuscripts (reviews, research, and technology tool articles) with a focus on the following areas:

  • Epigenetic mechanisms that drive or contribute to hematologic malignancies;
  • Novel epigenetic targets in hematological malignancies;
  • Development or use of targeted epigenetic therapies for hematologic malignancy;
  • Methods for identifying aberrant epigenetic mechanisms in hematological malignancies.

Dr. Richard L. Bennett
Guest Editor

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Keywords

  • epigenetics
  • myeloid neoplasms
  • lymphoid neoplasms
  • multiple myeloma
  • epigenetic therapies
  • DNA methylation
  • histone acetylation
  • histone methylation
  • chromatin remodeling

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Published Papers (1 paper)

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Review

19 pages, 476 KiB  
Review
Genetics and Epigenetics of Chemoinduced Oral Mucositis in Paediatric Patients with Haematological Malignancies—A Review
by Juliana Ramalho Guimarães, José Maria Chagas Viana Filho and Naila Francis Paulo de Oliveira
Epigenomes 2025, 9(2), 16; https://doi.org/10.3390/epigenomes9020016 - 30 May 2025
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Abstract
Background: Oral mucositis (OM) is a painful inflammation resulting from chemotherapy. It is dependent on factors such as age, gender, chemotherapy regimen, oral health, immunological and nutritional status, and genetics. Objectives: The aim of the study was to conduct a narrative review to [...] Read more.
Background: Oral mucositis (OM) is a painful inflammation resulting from chemotherapy. It is dependent on factors such as age, gender, chemotherapy regimen, oral health, immunological and nutritional status, and genetics. Objectives: The aim of the study was to conduct a narrative review to compile studies on the contribution of genetic and epigenetic aspects to the pathogenesis of OM in children with haematological malignancies undergoing chemotherapy treatment. Methods: The literature search was performed in Pubmed, Scopus, Web of Science, Cochrane, Lilacs, and grey literature databases covering articles published since 2010. Results: Twenty-two studies investigating polymorphisms and four studies investigating DNA methylation were included. Polymorphisms in the MTHFR, ABCB1, ABCC2, ABCG2, SLCO1B, miR-1206, miR-3683, CAT, and VDR genes were associated as risk factors for OM and polymorphisms in the TYMS and miR-4268 genes were associated as protective factors. With regard to DNA methylation, associations such as protection or susceptibility to OM have not yet been proven. However, studies have shown that DNMT1 methylation and hypomethylation in total DNA and in the TNF-α gene are associated with recovery of the oral mucosa. Conclusions: Genetic variants are associated with OM in various biological pathways, such as folate metabolism, transport proteins, epigenetic machinery, oxidative stress, and vitamin D metabolism. The DNA methylation profile, which is still poorly understood in the pathogenesis of OM, is associated with mucosal recovery (inflammation and epigenetic machinery). Genetic and epigenetic markers may be tools to indicate a patient’s susceptibility to developing OM, and epigenetic markers may be a target for therapies. Full article
(This article belongs to the Special Issue Epigenetic Mechanisms of Hematologic Malignancies)
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