Epigenetics in Hematologic Malignancies

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

Deadline for manuscript submissions: closed (31 May 2023) | Viewed by 5314

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 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. Analysis of genomic data from these patients reveals that recurrent somatic mutations which affect 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

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Epigenomes is an international peer-reviewed open access quarterly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1500 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

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

Published Papers (2 papers)

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Research

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17 pages, 3533 KiB  
Article
Ikaros Regulates microRNA Networks in Acute Lymphoblastic Leukemia
by Sophie Kogut, Hana Paculova, Princess Rodriguez, Joseph Boyd, Alyssa Richman, Amrita Palaria, Hilde Schjerven and Seth Frietze
Epigenomes 2022, 6(4), 37; https://doi.org/10.3390/epigenomes6040037 - 19 Oct 2022
Cited by 2 | Viewed by 2488
Abstract
The hematopoietic transcription factor Ikaros (IKZF1) regulates normal B cell development and functions as a tumor suppressor in precursor B cell acute lymphoblastic leukemia (B-ALL). MicroRNAs (miRNAs) are small regulatory RNAs that through post-transcriptional gene regulation play critical roles in intracellular [...] Read more.
The hematopoietic transcription factor Ikaros (IKZF1) regulates normal B cell development and functions as a tumor suppressor in precursor B cell acute lymphoblastic leukemia (B-ALL). MicroRNAs (miRNAs) are small regulatory RNAs that through post-transcriptional gene regulation play critical roles in intracellular processes including cell growth in cancer. However, the role of Ikaros in the regulation of miRNA expression in developing B cells is unknown. In this study, we examined the Ikaros-regulated miRNA targets using human IKZF1-mutated Ph+ B-ALL cell lines. Inducible expression of wild-type Ikaros (the Ik1 isoform) caused B-ALL growth arrest and exit from the cell cycle. Global miRNA expression analysis revealed a total of 31 miRNAs regulated by IK1, and ChIP-seq analysis showed that Ikaros bound to several Ik1-responsive miRNA genes. Examination of the prognostic significance of miRNA expression in B-ALL indicate that the IK1-regulated miRNAs hsa-miR-26b, hsa-miR-130b and hsa-miR-4649 are significantly associated with outcome in B-ALL. Our findings establish a potential regulatory circuit between the tumor-suppressor Ikaros and the oncogenic miRNA networks in IKZF1-mutated B-ALL. These results indicate that Ikaros regulates the expression of a subset of miRNAs, of which several may contribute to B-ALL growth. Full article
(This article belongs to the Special Issue Epigenetics in Hematologic Malignancies)
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Review

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17 pages, 765 KiB  
Review
Epigenetic Mechanisms in Hematologic Aging and Premalignant Conditions
by Bowen Yan, Qingchen Yuan and Olga A. Guryanova
Epigenomes 2023, 7(4), 32; https://doi.org/10.3390/epigenomes7040032 - 12 Dec 2023
Cited by 1 | Viewed by 2264
Abstract
Hematopoietic stem cells (HSCs) are essential for maintaining overall health by continuously generating blood cells throughout an individual’s lifespan. However, as individuals age, the hematopoietic system undergoes significant functional decline, rendering them more susceptible to age-related diseases. Growing research evidence has highlighted the [...] Read more.
Hematopoietic stem cells (HSCs) are essential for maintaining overall health by continuously generating blood cells throughout an individual’s lifespan. However, as individuals age, the hematopoietic system undergoes significant functional decline, rendering them more susceptible to age-related diseases. Growing research evidence has highlighted the critical role of epigenetic regulation in this age-associated decline. This review aims to provide an overview of the diverse epigenetic mechanisms involved in the regulation of normal HSCs during the aging process and their implications in aging-related diseases. Understanding the intricate interplay of epigenetic mechanisms that contribute to aging-related changes in the hematopoietic system holds great potential for the development of innovative strategies to delay the aging process. In fact, interventions targeting epigenetic modifications have shown promising outcomes in alleviating aging-related phenotypes and extending lifespan in various animal models. Small molecule-based therapies and reprogramming strategies enabling epigenetic rejuvenation have emerged as effective approaches for ameliorating or even reversing aging-related conditions. By acquiring a deeper understanding of these epigenetic mechanisms, it is anticipated that interventions can be devised to prevent or mitigate the rates of hematologic aging and associated diseases later in life. Ultimately, these advancements have the potential to improve overall health and enhance the quality of life in aging individuals. Full article
(This article belongs to the Special Issue Epigenetics in Hematologic Malignancies)
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