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Epigenomics, Epitranscriptomics and Novel Therapy Approaches in Hematology
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Epigenomics, Epitranscriptomics and Novel Therapy Approaches in Hematology

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Human Genomics and Genetic Diseases".

Deadline for manuscript submissions: closed (15 March 2023) | Viewed by 6758

Special Issue Editor

Dr. Haiyang Yun

E-Mail Website
Guest Editor
Department of Hematology, Oncology and Rheumatology, University Hospital Heidelberg, Heidelberg, Germany
Interests: epigenetics; chromatin biology; DNA topology; leukemia; hematopoiesis

Special Issue Information

Dear Colleagues,

The mammalian blood homeostasis is sustained by the constant and dynamic production of normal hematopoietic cells of all lineages. No cellular system is better characterized as a developmental hierarchy than the hematopoiesis, a process originating from a single precursor cell, termed the hematopoietic stem cell (HSC). Besides the ability to replenish its own pool, HSC can also differentiate into multi- and unipotent progenitors. Numerous reports have extensively documented the genetic and epigenetic factors regulating normal hematopoiesis. Technology advances enable the genome-wide scanning of hematopoietic cell genomes at an unprecedented resolution, allowing the identification of re-occurred genetic variations or inadequate gene expression in various hematological diseases. Many of these alterations could not only influence the cell genome and transcriptome, but also the epigenome and epitranscriptome, contributing to the disease initiation or progression. Though our treatment of hematological malignancies has been modestly improved, the development of more specific and potent therapeutic measures is still in high demand.

We launch this Special Issue with the aim to gain new insights into the epigenomics and epitranscriptomics in normal and malignant hematopoiesis, and to explore novel therapeutic approaches to treat hematological diseases. In this regard, we encourage the submission of research articles or reviews in the field of clinical or experimental hematology on the following topics: 1) gene mutations or polymorphisms impacting on epigenome or epitranscriptome; 2) functional characterization of regulators of epigenome or epitranscriptome; 3) clinical evaluation of epigenome or epitranscriptome in patients; 4) animal models to study altered epigenome or epitranscriptome; 5) novel or improved methodological development to quantify the epigenome or epitranscriptome; 6) novel gene therapies, gene manipulation, small molecules, or drug synergy with potency to tackle hematological disorders; and 7) clinical trials of novel targeted therapy drugs in hematology.

Dr. Haiyang Yun
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. Genes is an international peer-reviewed open access monthly 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 2600 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
  • epigenome
  • epitranscriptome
  • hematopoiesis
  • hematological diseases
  • target therapy
  • chromatin

Published Papers (3 papers)

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Research

12 pages, 2635 KiB  
Article
Preliminary Interpretations of Epigenetic Profiling of Cord Blood in Preeclampsia
by Junrui Ma, Zhongqun Zhan, Ning Li, Yanli Huang, Yan Li, Lu Liu, Qi Shen, Qiao Chu, Xiaonan Wang, Benqing Wu and Hui Zhang
Genes 2022, 13(5), 888; https://0-doi-org.brum.beds.ac.uk/10.3390/genes13050888 - 16 May 2022
Cited by 1 | Viewed by 2147
Abstract
Preeclampsia (PE) is characterized by new-onset hypertension after 20 weeks of pregnancy and results in high maternal and fetal mortality worldwide. It has been reported that PE is associated with abnormalities in the umbilical cord and cord blood. However, previous studies were focused [...] Read more.
Preeclampsia (PE) is characterized by new-onset hypertension after 20 weeks of pregnancy and results in high maternal and fetal mortality worldwide. It has been reported that PE is associated with abnormalities in the umbilical cord and cord blood. However, previous studies were focused primarily on the transcriptomics level, while the underlying gene regulatory landscapes are still unclear. Thus, we performed the Assay for Transposase-Accessible Chromatin with high-throughput sequencing (ATAC-seq) using the umbilical cord blood samples collected from a patient with superimposed PE and three healthy donors to uncover the chromatin accessibility changes attributed to PE. We have identified genes associated with immunomodulation and hypoxia response that have higher chromatin accessibility close to their transcription start sites. Motif analysis indicated that the GATA family transcription factor binding was enriched in PE and may play an essential regulatory role in the disease progression. Overall, our findings provide an overview of gene regulatory programs and the corresponding downstream pathways associated with PE that may influence the placenta function and fetal growth. Full article
(This article belongs to the Special Issue Epigenomics, Epitranscriptomics and Novel Therapy Approaches in Hematology)
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10 pages, 1304 KiB  
Article
Loss of Heterozygosity in the Tumor DNA of De Novo Diagnosed Patients Is Associated with Poor Outcome for B-ALL but Not for T-ALL
by Natalya Risinskaya, Yana Kozhevnikova, Olga Gavrilina, Julia Chabaeva, Ekaterina Kotova, Anna Yushkova, Galina Isinova, Ksenija Zarubina, Tatiana Obukhova, Sergey Kulikov, Hunan Julhakyan, Andrey Sudarikov and Elena Parovichnikova
Genes 2022, 13(3), 398; https://0-doi-org.brum.beds.ac.uk/10.3390/genes13030398 - 23 Feb 2022
Cited by 3 | Viewed by 1849
Abstract
Despite the introduction of new technologies in molecular diagnostics, one should not underestimate the traditional routine methods for studying tumor DNA. Here we present the evidence that short tandem repeat (STR) profiling of tumor DNA relative to DNA from healthy cells might identify [...] Read more.
Despite the introduction of new technologies in molecular diagnostics, one should not underestimate the traditional routine methods for studying tumor DNA. Here we present the evidence that short tandem repeat (STR) profiling of tumor DNA relative to DNA from healthy cells might identify chromosomal aberrations affecting therapy outcome. Tumor STR profiles of 87 adult patients with de novo Ph-negative ALL (40 B-ALL, 43 T-ALL, 4 mixed phenotype acute leukemia (MPAL)) treated according to the “RALL-2016” regimen were analyzed. DNA of tumor cells was isolated from patient bone marrow samples taken at diagnosis. Control DNA samples were taken from the buccal swab or the blood of patients in complete remission. Overall survival (OS) analysis was used to assess the independent impact of the LOH as a risk factor. Of the 87 patients, 21 were found with LOH in various STR loci (24%). For B-ALL patients, LOH (except 12p LOH) was an independent risk factor (OS hazard ratio 3.89, log-rank p-value 0.0395). In contrast, for T-ALL patients, the OS hazard ratio was 0.59 (log-rank p-value 0.62). LOH in particular STR loci measured at the onset of the disease could be used as a prognostic factor for poor outcome in B-ALL, but not in T-ALL. Full article
(This article belongs to the Special Issue Epigenomics, Epitranscriptomics and Novel Therapy Approaches in Hematology)
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12 pages, 22542 KiB  
Article
Epigenetic Silencing of Tumor Suppressor lncRNA NKILA: Implication on NF-κB Signaling in Non-Hodgkin’s Lymphoma
by Min-Yue Zhang, George Calin, Ming-Dan Deng, Rex K. H. Au-Yeung, Lu-Qian Wang and Chor-Sang Chim
Genes 2022, 13(1), 128; https://0-doi-org.brum.beds.ac.uk/10.3390/genes13010128 - 11 Jan 2022
Cited by 4 | Viewed by 1857
Abstract
The long non-coding RNA (lncRNA) NKILA, localized to 20q13.31, is a negative regulator of NF-κB signaling implicated in carcinogenesis. As a CpG island is embedded in the promoter region of NKILA, it is hypothesized as a tumor suppressor lncRNA silenced by promoter [...] Read more.
The long non-coding RNA (lncRNA) NKILA, localized to 20q13.31, is a negative regulator of NF-κB signaling implicated in carcinogenesis. As a CpG island is embedded in the promoter region of NKILA, it is hypothesized as a tumor suppressor lncRNA silenced by promoter DNA methylation in non-Hodgkin’s lymphoma (NHL). By pyrosequencing-verified methylation-specific PCR, NKILA methylation was detected in 1/10 (10%) NHL cell lines, but not in normal peripheral blood buffy coats or tonsils. NKILA methylation correlated with the repression of NKILA in cell lines. Hypomethylation treatment with 5-Aza-2′-deoxycytidine resulted in promoter demethylation and the re-expression of NKILA. In 102 NHL primary samples, NKILA was methylated in 29 (51.79%) diffuse large B-cell lymphoma (DLBCL) and 4 (20%) peripheral T-cell lymphoma cases, but unmethylated in all 26 mantle cell lymphoma cases. Mechanistically, the knockdown of NKILA resulted in promoting IkBα phosphorylation, associated with nucleus translocation of total p65 and phosphorylated p65 in SU-DHL-1 cells, hence constitutive NF-κB activation. Functionally, the knockdown of NKILA in SU-DHL-1 cells led to decreased cell death and increased cellular proliferation. Collectively, NKILA was a tumor suppressor lncRNA frequently hypermethylated in DLBCL. Promoter DNA methylation-mediated NKILA silencing resulted in increased cellular proliferation and decreased cell death via the repression of NF-κB signaling in NHL. Full article
(This article belongs to the Special Issue Epigenomics, Epitranscriptomics and Novel Therapy Approaches in Hematology)
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