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Genes
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Genetics and Epigenetics in Cancers
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Genetics and Epigenetics in Cancers

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 (20 July 2024) | Viewed by 5339

Special Issue Editor

Prof. Dr. Vilma Yuzbasiyan-Gurkan

E-Mail Website
Guest Editor
Department of Microbiology, Genetics and Immunology, Michigan State University, East Lansing, MI, USA
Interests: genetic diseases; cancer; genomic instability; epigenomics

Special Issue Information

Dear Colleagues,

Our understanding of cancer biology continues to grow with insights from studies of cancer genetics. Growing appreciation of epigenetic changes along with somatic mutations continues to contribute to our understanding of the mutational landscape in cancer. With this Special Issue of Genes, I invite you to submit your manuscripts on the genetic and epigenetic changes in any type of cancer, as well as approaches to manipulating and affecting these changes. In this Special Issue, we welcome review articles, original articles, and short reports on genetics and epigenetics of any cancer. We look forward to receiving contributions that provide insights on DNA methylation, histone modification, nucleosome remodeling, and RNA-mediated regulation of gene expression in cancers and how these changes may be exploited for novel therapeutic approaches as well as for prognostication.

Prof. Dr. Vilma Yuzbasiyan-Gurkan
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

  • cancer epigenetics and epigenomics
  • cancer genetics and genomics
  • DNA methylation in cancer
  • histone modification in cancer
  • nucleosome remodeling in cancer
  • RNA-mediated regulation of gene expression in cancer
  • drugs targeting epigenetic changes in cancer

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Published Papers (2 papers)

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Review

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13 pages, 899 KiB  
Review
Transient Myeloproliferative Disorder (TMD), Acute Lymphoblastic Leukemia (ALL), and Juvenile Myelomonocytic Leukemia (JMML) in a Child with Noonan Syndrome: Sequential Occurrence, Single Center Experience, and Review of the Literature
by Marta Arrabito, Nicolò Li Volsi, Manuela La Rosa, Piera Samperi, Giulio Pulvirenti, Emanuela Cannata, Giovanna Russo, Andrea Di Cataldo and Luca Lo Nigro
Genes 2024, 15(9), 1191; https://doi.org/10.3390/genes15091191 - 10 Sep 2024
Cited by 1 | Viewed by 2789
Abstract
Noonan syndrome (NS) is an autosomal dominant disorder that varies in severity and can involve multiple organ systems. In approximately 50% of cases, it is caused by missense mutations in the PTPN11 gene (12q24.13). NS is associated with a higher risk of cancer [...] Read more.
Noonan syndrome (NS) is an autosomal dominant disorder that varies in severity and can involve multiple organ systems. In approximately 50% of cases, it is caused by missense mutations in the PTPN11 gene (12q24.13). NS is associated with a higher risk of cancer occurrence, specifically hematological disorders. Here, we report a case of a child who was diagnosed at birth with a transient myeloproliferative disorder (TMD). After two years, the child developed hyperdiploid B-cell precursor acute lymphoblastic leukemia (BCP-ALL), receiving a two-year course of treatment. During her continuous complete remission (CCR), a heterozygous germline mutation in the PTPN11 gene [c.218 C>T (p.Thr73lle)] was identified. At the age of ten, the child presented with massive splenomegaly, hyperleukocytosis, and thrombocytopenia, resulting in the diagnosis of juvenile myelomonocytic leukemia (JMML). After an initial response to antimetabolite therapy (6-mercaptopurine), she underwent haploidentical hematopoietic stem cell transplantation (HSCT) and is currently in complete remission. The goal of this review is to gain insight into the various hematological diseases associated with NS, starting from our unique case. Full article
(This article belongs to the Special Issue Genetics and Epigenetics in Cancers)
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10 pages, 249 KiB  
Brief Report
SP1 Gene Methylation in Head and Neck Squamous Cell Cancer in HPV-Negative Patients
by Enar Jumaniyazova, Anna Aghajanyan, Sergey Kurevlev, Leyla Tskhovrebova, Andrey Makarov, Konstantin Gordon, Anastasiya Lokhonina and Timur Fatkhudinov
Genes 2024, 15(3), 281; https://doi.org/10.3390/genes15030281 - 23 Feb 2024
Cited by 3 | Viewed by 1868
Abstract
There is still much to learn about the epigenetic mechanisms controlling gene expression during carcinogenesis. When researching aberrant DNA methylation, active proliferative tumor cells from head and neck squamous cell cancer (HNSCC) can be used as a model. The aim of the study [...] Read more.
There is still much to learn about the epigenetic mechanisms controlling gene expression during carcinogenesis. When researching aberrant DNA methylation, active proliferative tumor cells from head and neck squamous cell cancer (HNSCC) can be used as a model. The aim of the study was to investigate the methylation status of CDKN1, CDKN2A, MYC, Smad3, SP1, and UBC genes in tumor tissue (control-normal tissue) in 50 patients (37 men and 13 women) with HPV-negative HNSCC. Methods: Bisulfite conversion methods and methyl-sensitive analysis of high-resolution melting curves were used to quantify the methylation of genes. In all patients and across various subgroups (tongue carcinoma, laryngeal and other types of carcinomas T2, T3, T4 status; age before and after 50 years; smoking and non-smoking), there are consistent differences in the methylation levels in the SP1 gene in tumor DNA compared to normal. Results: The methylation of the SP1 gene in tumor DNA suppresses its expression, hinders HNSCC cell proliferation regulation, and could be a molecular indicator of malignant cell growth. The study of DNA methylation of various genes involved in carcinogenesis is promising because hypermethylated promoters can serve as potential biomarkers of disease. Full article
(This article belongs to the Special Issue Genetics and Epigenetics in Cancers)
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