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Cancers
Special Issues
Exploring the Genetic and Epigenetic Factors in Leukemia and Lymphoma
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Exploring the Genetic and Epigenetic Factors in Leukemia and Lymphoma

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: 31 July 2025 | Viewed by 1445

Special Issue Editor

Dr. Francesco E. Boccalatte

E-Mail Website
Guest Editor
NYU Grossman School of Medicine, New York, NY, YSA
Interests: hematopoiesis; leukemia; stem cells; epigenetics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Recent technological advances in the field of next-generation sequencing and chromatin conformation, together with refined computational tools, have greatly advanced our understanding of genetic and epigenetic alterations, leading to the establishment of new treatments to treat cancer. In the field of hematology in particular, many pioneering studies have shown that alterations of the DNA sequence and the elements that drive its transcription and translation are at the origin of cell identity, differentiation, and transformation. A better understanding of the genetic and epigenetic mechanisms that govern hematological malignancies is key to the field since it will provide new and improved strategies for prevention and personalized treatment. We are therefore pleased to invite you to contribute your original work to shed light on the molecular drivers of genetic and epigenetic aberrations and the strategies for their reversibility.

This Special Issue aims to offer an overview of the latest discoveries in the field, with particular attention to mechanistic approaches, discovery platforms, and diagnostic and therapeutic opportunities.

For this Special Issue, original research articles and reviews are welcome. Research areas may include (but are not limited to) the following:

  • Genetic and epigenetic alterations in hematological disease;
  • Novel mechanisms of gene regulation via DNA and RNA modifications (including DNA/RNA methylation, histone modifications, RNA alternative splicing, and noncoding RNAs);
  • Molecular mechanisms governing gene expression at the genetic and epigenetic levels and strategies for their reversibility;
  • Computational approaches for the analysis of genetic and epigenetic mechanisms in cancer;
  • Genetic and epigenetic alterations in response to environmental factors and drugs;
  • Molecular profiling of genetic and epigenetic markers for the discovery of biomarkers and therapeutic targets.

Should you have any questions, require further information, or need any assistance, please do not hesitate to reach out to us. We are here to support and facilitate your participation in this Special Issue.

Thank you for your attention to this matter, and we look forward to receiving your valuable submissions. 

Dr. Francesco E. Boccalatte
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 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. Cancers is an international peer-reviewed open access semimonthly 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 2900 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

  • hematology
  • leukemia
  • lymphoma
  • epigenetics
  • bioinformatics
  • gene expression
  • chromatin conformation

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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Research

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14 pages, 1144 KiB  
Article
Bone Marrow CD34+/lin− Cells of Patients with Chronic-Phase Chronic Myeloid Leukemia (CP-CML) After 12 Months of Nilotinib Treatment Exhibit a Different Gene Expression Signature Compared to the Diagnosis and the Corresponding Cells from Healthy Subjects
by Alessandra Trojani, Ester Pungolino, Barbara Di Camillo, Luca Emanuele Bossi, Cassandra Palumbo, Mariella D’adda, Alessandra Perego, Mauro Turrini, Chiara Elena, Lorenza Maria Borin, Alessandra Iurlo, Simona Malato, Francesco Spina, Maria Luisa Latargia, Pierangelo Spedini, Salvatore Artale, Michela Anghilieri, Maria Cristina Carraro, Cristina Bucelli, Alessandro Beghini and Roberto Cairoliadd Show full author list remove Hide full author list
Cancers 2025, 17(6), 1022; https://doi.org/10.3390/cancers17061022 - 18 Mar 2025
Viewed by 424
Abstract
Background: Chronic-Phase Chronic Myeloid Leukemia (C-PCML) is defined by the presence of the BCR-ABL1 fusion gene, which encodes a tyrosine kinase protein that drives the uncontrolled proliferation and survival of leukemic stem cells (LSCs). Nilotinib, a tyrosine kinase inhibitor, targets the activity of [...] Read more.
Background: Chronic-Phase Chronic Myeloid Leukemia (C-PCML) is defined by the presence of the BCR-ABL1 fusion gene, which encodes a tyrosine kinase protein that drives the uncontrolled proliferation and survival of leukemic stem cells (LSCs). Nilotinib, a tyrosine kinase inhibitor, targets the activity of BCR-ABL1 by reducing aberrant signaling pathways, which drive the regeneration of LSCs. Despite nilotinib’s action, a population of resilient LSCs persist in the bone marrow (BM) and can indeed drive relapse and progression in CML patients. Methods: Our study investigated the gene expression profiling (GEP) of BM CD34+/lin− cells from 79 CP-CML patients at diagnosis, compared to the BM CD34+/lin− cells from the same patients after 12 months of nilotinib treatment and to the normal counterpart cells from 10 donors (CTRLs). Results: GEP analyses identified 3012 significantly differentially expressed genes across these comparisons. Among these, we focused on certain key genes associated with eight crucial KEGG pathways: CML, cell cycle, JAK-STAT, PI3K-Akt, MAPK, Ras, NF-kB, and ABC transporters. Within these pathways, we observed the up-regulation of several genes at diagnosis compared to both 12 months of nilotinib treatment and the CTRLs. Conclusions: We observed that certain transcriptome features present at diagnosis persisted after 12 months of nilotinib treatment, compared to CTRLs. This suggests that nilotinib may exert selective pressure, potentially supporting the survival and self-renewal of LSCs. Future insights into these pathways could help identify therapeutic targets to improve outcomes in CML. Full article
(This article belongs to the Special Issue Exploring the Genetic and Epigenetic Factors in Leukemia and Lymphoma)
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Review

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27 pages, 1035 KiB  
Review
The Role of the Sirtuin Family Histone Deacetylases in Acute Myeloid Leukemia—A Promising Road Ahead
by Piotr Strzałka, Kinga Krawiec, Aneta Wiśnik, Dariusz Jarych, Magdalena Czemerska, Izabela Zawlik, Agnieszka Pluta and Agnieszka Wierzbowska
Cancers 2025, 17(6), 1009; https://doi.org/10.3390/cancers17061009 - 17 Mar 2025
Viewed by 609
Abstract
Acute myeloid leukemia (AML) corresponds to a heterogeneous group of clonal hematopoietic diseases, which are characterized by uncontrolled proliferation of malignant transformed myeloid precursors and their inability to differentiate into mature blood cells. The prognosis of AML depends on many variables, including the [...] Read more.
Acute myeloid leukemia (AML) corresponds to a heterogeneous group of clonal hematopoietic diseases, which are characterized by uncontrolled proliferation of malignant transformed myeloid precursors and their inability to differentiate into mature blood cells. The prognosis of AML depends on many variables, including the genetic features of the disease. Treatment outcomes, despite the introduction of new targeted therapies, are still unsatisfactory. Recently, there have been an increasing number of reports on enzymatic proteins of the sirtuin family and their potential importance in cancer in general. Sirtuins are a group of 7 (SIRT1-7) NAD+-dependent histone deacetylases with pleiotropic effects on metabolism, aging processes, and cell survival. They are not only responsible for post-translational modification of histones but also play various biochemical functions and interact with other proteins regulating cell survival, such as p53. Thus, their role in key mechanisms of tumorigenesis makes them a worthwhile topic in AML. Different sirtuins have been shown to act oppositely depending on the biological context, the mechanism of which requires further exploration. This review provides a comprehensive description of the significance and role of sirtuins in AML in light of the current state of knowledge. It focuses in particular on molecular mechanisms regulated by sirtuins and signaling pathways involved in leukemogenesis, as well as clinical aspects and potential therapeutic targets in AML. Full article
(This article belongs to the Special Issue Exploring the Genetic and Epigenetic Factors in Leukemia and Lymphoma)
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