Special Issue "Epigenetic Dysregulation in Cancer: From Mechanism to Therapy"

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

Deadline for manuscript submissions: 30 September 2019

Special Issue Editors

Guest Editor
Assist. Prof. Dr. Angeliki Magklara

Laboratory of Clinical Chemistry, Faculty of Medicine, School of Health Sciences, University of Ioannina and Institute of Molecular Biology and Biotechnology, Foundation of Research and Technology-Hellas, Ioannina 45110, Greece.
Website | E-Mail
Interests: cancer epigenetics, cancer stem cells, breast cancer, tumor heterogeneity, epigenetic therapies
Guest Editor
Assoc. Prof. Dr. Tugba Bagci-Onder

Koç University School of Medicine, Rumelifeneri Yolu, Sarıyer, Istanbul, 34450 TURKEY
Website | E-Mail
Interests: cancer drug resistance; epigenetics; brain cancer; glioblastoma; medulloblastoma; epigenetic therapies; drug delivery

Special Issue Information

Dear Colleagues,

The advent of new technologies has allowed for the genome-wide identification of a plethora of epigenetic alterations across many tumor types. Recurrent mutations and/or skewed expression patterns of chromatin regulators promote an aberrant epigenome that is now regarded as a major contributing factor in carcinogenesis and not as a mere by-product of genomic instability in cancer cells. Moving beyond the basic cataloguing of epigenetic defects in cancer, the research community is focusing its efforts on revealing the pathogenic mechanisms that link perturbations in the epigenome to the development of the cancer phenotype. The task at hand is of increasing significance, considering the reversible nature of DNA methylation and histone modifications and the prospects for "epigenetic therapies" that have the potential to restore the normal epigenetic and transcriptional landscape. Developing such epigenetic agents is bound to be a demanding project, as we are just at the beginning of appreciating the technical challenges and the biological and clinical implications of drugging the cancer epigenome.

In this Special Issue, we invite original research papers and reviews that advance our mechanistic understanding of epigenetic dysregulation in cancer and how it can be exploited for the development of novel, promising therapeutic modalities.

Assist. Prof. Dr. Angeliki Magklara
Assoc. Prof. Dr. Tugba Bagci-Onder
Guest Editors

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 papers will be 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. Cancers 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 1800 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 epigenome
  • DNA methylation
  • histone modifications
  • miRNAs
  • epigenetic regulators
  • epigenetic therapies

Published Papers (2 papers)

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Research

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Open AccessArticle Genes Located on 18q23 Are Epigenetic Markers and Have Prognostic Significance for Patients with Head and Neck Cancer
Cancers 2019, 11(3), 401; https://doi.org/10.3390/cancers11030401
Received: 10 February 2019 / Revised: 28 February 2019 / Accepted: 18 March 2019 / Published: 21 March 2019
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Abstract
Loss of heterozygosity (LOH) on chromosome 18q23 is associated with significantly decreased survival in head and neck cancer. In agreement with such tumor suppressive roles, the loss of function of genes located in this region can be achieved through LOH and promotor hypermethylation. [...] Read more.
Loss of heterozygosity (LOH) on chromosome 18q23 is associated with significantly decreased survival in head and neck cancer. In agreement with such tumor suppressive roles, the loss of function of genes located in this region can be achieved through LOH and promotor hypermethylation. In this study, the methylation status of promoters of 18q23 genes in 243 head and neck cancer patients was assessed by quantitative methylation-specific PCR. Promoter methylation was then compared to various clinical characteristics and patient survival. GALR1 and SALL3 promoter methylation correlated with reduced disease-free survival (log-rank test, p = 0.018 and p = 0.013, respectively). Furthermore, based on multivariate Cox proportional hazards analysis, these methylation events were associated with poor disease-free survival, with hazard ratios of 1.600 (95% confidence interval: CI, 1.027–2.493; p = 0.038) and 1.911 (95% CI, 1.155–3.162; p = 0.012), respectively. By comparison, GALR1 and SALL3 methylation were not prognostic for overall survival in The Cancer Genome Atlas (TCGA) cohort. Our findings suggest that the methylation status of 18q23 genes could serve as important biomarkers for the prediction of clinical outcomes in well-annotated head and neck squamous cell carcinoma cohorts. GALR1 and SALL3 methylation could thus help to facilitate risk stratification for individualized treatment. Full article
(This article belongs to the Special Issue Epigenetic Dysregulation in Cancer: From Mechanism to Therapy)
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Review

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Open AccessReview microRNA-23a in Human Cancer: Its Roles, Mechanisms and Therapeutic Relevance
Received: 26 November 2018 / Revised: 7 December 2018 / Accepted: 17 December 2018 / Published: 20 December 2018
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Abstract
microRNA-23a (miR-23a) is one of the most extensively studied miRNAs in different types of human cancer, and plays various roles in the initiation, progression, and treatment of tumors. Here, we comprehensively summarize and discuss the recent findings about the role of miR-23a in [...] Read more.
microRNA-23a (miR-23a) is one of the most extensively studied miRNAs in different types of human cancer, and plays various roles in the initiation, progression, and treatment of tumors. Here, we comprehensively summarize and discuss the recent findings about the role of miR-23a in cancer. The differential expression of tissue miR-23a was reported, potentially indicating cancer stages, angiogenesis, and metastasis. miR-23a in human biofluid, such as plasma and salivary fluid, may be a sensitive and specific marker for early diagnosis of cancer. Tissue and circulating miR-23a serves as a prognostic factor for cancer patient survival, as well as a predictive factor for response to anti-tumor treatment. The direct and indirect regulation of miR-23a on multiple gene expression and signaling transduction mediates carcinogenesis, tumor proliferation, survival, cell migration and invasion, as well as the response to anti-tumor treatment. Tumor cell-derived miR-23a regulates the microenvironment of human cancer through manipulating both immune function and tumor vascular development. Several transcriptional and epigenetic factors may contribute to the dysregulation of miR-23a in cancer. This evidence highlights the essential role of miR-23a in the application of cancer diagnosis, prognosis, and treatment. Full article
(This article belongs to the Special Issue Epigenetic Dysregulation in Cancer: From Mechanism to Therapy)
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