Role of Epigenetic Modifications in Cancers

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 4959

Special Issue Editors


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Guest Editor
Institut d'Investigació Germans Trias i Pujol, Badalona, Spain
Interests: precision oncology; translational oncology; cancer biomarkers; epigenomics; transcriptomics; pharmacoepigenetics.

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Guest Editor
Institut d'Investigació Josep Carreras, Badalona, Spain
Interests: epigenomics; molecular oncology; translational oncology; cancer biomarkers; pharmacoepigenetics

Special Issue Information

Dear Colleagues,

Cancer cells are simultaneously characterized by a massive overall loss of methylation in DNA and the acquisition of specific patterns of hypermethylation at CpG islands of certain gene promoters. Clearly established epigenetic mechanisms in human cancer, such as DNA methylation and histones methylation and acetylation, can reversibly or irreversibly alter gene function. Epigenetic abnormalities are set and maintained by multiple protein complexes and the interplay between their individual components, including DNA methylation machinery, histone modifiers, polycomb proteins and chromatin remodellers. Hence, DNA methylation mapping has revealed cancer-specific profiles of hypermethylated CpG islands (hypermethylomes) able to distinguish between different tumor types and to predict antineoplasic treatment responsiveness and patients’ outcome. It has been made achievable, by the introduction of next-generation technologies that have led to the generation of a large amount of information, to better appreciate the role of the epigenomics of cancer in the clinical scenario.

Given the importance of the epigenetics in neoplasia development, it is worth highlighting its attractive quality as a field of interest in personalized oncology. Pharmacoepigenetics, or the use of epigenetic biomarkers for the prediction of resistance to antineoplasic agents, is a potentially useful tool to be applied in the selection of cancer treatment in the clinical practice, allowing for the use of strategies that are suitable to be efficiently analysed in easy-getting samples in a non-invasive manner in order to make possible the use of biomarkers for the selection of the best treatment choice.

Taking into account the recent advances in this field, not only in a biological sense but also in technical terms, the purpose of this Special Issue is to put in context the role of epigenetic alterations in cancer, in both a translational and clinical setting, and emphasize the situation of pharmacoepigenomics in oncology, to generate interest in the health community for this discipline.

Dr. Anna Martínez-Cardús
Dr. Verónica Dávalos
Guest Editors

Manuscript Submission Information

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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

  • epigenomics
  • translational oncology
  • tailored therapy
  • epigenetic modifications
  • next generation techniques
  • pharmacoepigenomics
  • molecular oncology

Published Papers (2 papers)

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21 pages, 2483 KiB  
Article
Meta-Analysis of RNA-Seq Datasets Identifies Novel Players in Glioblastoma
by Magy Sallam, Mohamed Mysara, Sarah Baatout, Pieter-Jan Guns, Raghda Ramadan and Mohammed Abderrafi Benotmane
Cancers 2022, 14(23), 5788; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers14235788 - 24 Nov 2022
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Abstract
Glioblastoma is a devastating grade IV glioma with poor prognosis. Identification of predictive molecular biomarkers of disease progression would substantially contribute to better disease management. In the current study, we performed a meta-analysis of different RNA-seq datasets to identify differentially expressed protein-coding genes [...] Read more.
Glioblastoma is a devastating grade IV glioma with poor prognosis. Identification of predictive molecular biomarkers of disease progression would substantially contribute to better disease management. In the current study, we performed a meta-analysis of different RNA-seq datasets to identify differentially expressed protein-coding genes (PCGs) and long non-coding RNAs (lncRNAs). This meta-analysis aimed to improve power and reproducibility of the individual studies while identifying overlapping disease-relevant pathways. We supplemented the meta-analysis with small RNA-seq on glioblastoma tissue samples to provide an overall transcriptomic view of glioblastoma. Co-expression correlation of filtered differentially expressed PCGs and lncRNAs identified a functionally relevant sub-cluster containing DANCR and SNHG6, with two novel lncRNAs and two novel PCGs. Small RNA-seq of glioblastoma tissues identified five differentially expressed microRNAs of which three interacted with the functionally relevant sub-cluster. Pathway analysis of this sub-cluster identified several glioblastoma-linked pathways, which were also previously associated with the novel cell death pathway, ferroptosis. In conclusion, the current meta-analysis strengthens evidence of an overarching involvement of ferroptosis in glioblastoma pathogenesis and also suggests some candidates for further analyses. Full article
(This article belongs to the Special Issue Role of Epigenetic Modifications in Cancers)
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17 pages, 655 KiB  
Review
Histone Modifying Enzymes as Targets for Therapeutic Intervention in Oesophageal Adenocarcinoma
by Oliver J. Pickering, Stella P. Breininger, Timothy J. Underwood and Zoë S. Walters
Cancers 2021, 13(16), 4084; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers13164084 - 13 Aug 2021
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Abstract
Oesophageal adenocarcinoma (OAC) has a dismal prognosis, where curable disease occurs in less than 40% of patients, and many of those with incurable disease survive for less than a year from diagnosis. Despite the widespread use of systematic chemotherapy in OAC treatment, many [...] Read more.
Oesophageal adenocarcinoma (OAC) has a dismal prognosis, where curable disease occurs in less than 40% of patients, and many of those with incurable disease survive for less than a year from diagnosis. Despite the widespread use of systematic chemotherapy in OAC treatment, many patients receive no benefit. New treatments are urgently needed for OAC patients. There is an emerging interest in epigenetic regulators in cancer pathogenesis, which are now translating into novel cancer therapeutic strategies. Histone-modifying enzymes (HMEs) are key epigenetic regulators responsible for dynamic covalent histone modifications that play roles in both normal and dysregulated cellular processes including tumorigenesis. Several HME inhibitors are in clinical use for haematological malignancies and sarcomas, with numerous on-going clinical trials for their use in solid tumours. This review discusses the current literature surrounding HMEs in OAC pathogenesis and their potential use in targeted therapies for this disease. Full article
(This article belongs to the Special Issue Role of Epigenetic Modifications in Cancers)
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