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Cancers
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Epigenomic Studies of Gynecological Cancer
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Epigenomic Studies of Gynecological Cancer

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Informatics and Big Data".

Deadline for manuscript submissions: closed (31 October 2021) | Viewed by 19477

Special Issue Editors

Assoc. Prof. Dylan Glubb

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Guest Editor
1. Department of Genetics and Computational, Biology, QIMR Berghofer Medical Research Institute, Brisbane, Australia
2. Honorary Associate Professor, School of Biomedical Sciences, University of Queensland, Brisbane, Australia
3. Adjunct Associate Professor, School of Biomedical Sciences, Queensland University of Technology, Brisbane, Australia
Interests: endometrial cancer; hormone-related cancers; post-GWAS functional analysis; epigenomics; chromatin looping; transcriptional regulation
Assoc. Prof. Tracy O’Mara

E-Mail Website
Guest Editor
1. Department of Genetics and Computational, Biology, QIMR Berghofer Medical Research Institute, Brisbane, Australia
2. Honorary Associate Professor, School of Biomedical Sciences, University of Queensland, Brisbane, Australia
3. Adjunct Associate Professor, School of Biomedical Sciences, Queensland University of Technology, Brisbane, Australia
Interests: endometrial cancer; hormone-related cancers; genome-wide association studies; integrative molecular genomics; cross-cancer genetic analysis; epigenomics; chromatin looping

Special Issue Information

Dear Colleagues,

The last decade has seen major developments in high-throughput sequencing, spurring many new applications. In particular, the development of new epigenomic analyses (e.g., bisulfite sequencing, chromosome conformation capture sequencing, and ChIP-seq) has led to a remarkable growth in whole genome studies of methylation, chromatin looping, transcription factor binding, and histone modifications. Through epigenomic studies, it has become apparent that epigenetic features play important roles in cancer etiology, development, and progression. Recently, epigenomics has also helped to provide insights into findings from genome-wide association studies of cancer risk and whole genome sequencing of tumors.

Compared with the epigenomics of some other common cancer types, gynecological cancer has been much less well studied. Therefore, we welcome articles that generate novel epigenomic datasets using gynecological cancer cell lines, organoids or tissue, in particular those that integrate these data with large-scale genetic or “omic” datasets to further our understanding of gynecological cancer.

Assoc. Prof. Dylan Glubb
Assoc. Prof. Tracy O’Mara
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 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

  • epigenomics
  • gynecological cancer
  • endometrial cancer
  • ovarian cancer
  • chromatin looping
  • histone modifications
  • transcription factor binding
  • genome-wide association studies
  • whole genome sequencing

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Published Papers (4 papers)

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Research

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14 pages, 1532 KiB  
Article
Exploring Differentially Methylated Genes in Vulvar Squamous Cell Carcinoma
by Shatavisha Dasgupta, Patricia C. Ewing-Graham, Sigrid M. A. Swagemakers, Thierry P. P. van den Bosch, Peggy N. Atmodimedjo, Michael M. P. J. Verbiest, Marit de Haan, Helena C. van Doorn, Peter J. van der Spek, Senada Koljenović and Folkert J. van Kemenade
Cancers 2021, 13(14), 3580; https://doi.org/10.3390/cancers13143580 - 16 Jul 2021
Cited by 5 | Viewed by 4188
Abstract
DNA methylation is the most widely studied mechanism of epigenetic modification, which can influence gene expression without alterations in DNA sequences. Aberrations in DNA methylation are known to play a role in carcinogenesis, and methylation profiling has enabled the identification of biomarkers of [...] Read more.
DNA methylation is the most widely studied mechanism of epigenetic modification, which can influence gene expression without alterations in DNA sequences. Aberrations in DNA methylation are known to play a role in carcinogenesis, and methylation profiling has enabled the identification of biomarkers of potential clinical interest for several cancers. For vulvar squamous cell carcinoma (VSCC), however, methylation profiling remains an under-studied area. We sought to identify differentially methylated genes (DMGs) in VSCC, by performing Infinium MethylationEPIC BeadChip (Illumina) array sequencing, on a set of primary VSCC (n = 18), and normal vulvar tissue from women with no history of vulvar (pre)malignancies (n = 6). Using a false-discovery rate of 0.05, beta-difference (Δβ) of ±0.5, and CpG-island probes as cut-offs, 199 DMGs (195 hyper-methylated, 4 hypo-methylated) were identified for VSCC. Most of the hyper-methylated genes were found to be involved in transcription regulator activity, indicating that disruption of this process plays a vital role in VSCC development. The majority of VSCCs harbored amplifications of chromosomes 3, 8, and 9. We identified a set of DMGs in this exploratory, hypothesis-generating study, which we hope will facilitate epigenetic profiling of VSCCs. Prognostic relevance of these DMGs deserves further exploration in larger cohorts of VSCC and its precursor lesions. Full article
(This article belongs to the Special Issue Epigenomic Studies of Gynecological Cancer)
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16 pages, 3239 KiB  
Article
ROR2 Is Epigenetically Regulated in Endometrial Cancer
by Dongli Liu, Luis Enriquez and Caroline E. Ford
Cancers 2021, 13(3), 383; https://doi.org/10.3390/cancers13030383 - 21 Jan 2021
Cited by 9 | Viewed by 3657
Abstract
The Wnt signalling receptor ROR2 has been identified as a possible therapeutic target in numerous cancers; however, its exact role remains unclear. The aim of this study was to investigate the role of ROR2 in endometrial cancer (EC) and the potential mechanism associated [...] Read more.
The Wnt signalling receptor ROR2 has been identified as a possible therapeutic target in numerous cancers; however, its exact role remains unclear. The aim of this study was to investigate the role of ROR2 in endometrial cancer (EC) and the potential mechanism associated with its altered expression. The association between ROR2 mRNA expression levels and clinicopathological parameters, including overall survival (OS), in EC was analysed in The Cancer Genome Atlas Uterine Corpus Endometrial Carcinoma (TCGA-UCEC) cohort and GEO dataset GSE17025. Four EC cell lines (KLE, MFE-296, Ishikawa and ARK-1) and eight clinical EC samples were analysed for ROR2 methylation via Combined Bisulphite Restriction Analysis (COBRA) and bisulphite genomic sequencing (BGS). In addition, the functional effects of ROR2 overexpression were investigated in Ishikawa and ARK-1 cells following ectopic ROR2 expression. ROR2 promoter methylation or reduced ROR2 expression were both found to correlate with shorter OS, high grade and serous subtype in the TCGA-UCEC and GEO datasets. ROR2 was epigenetically silenced by promoter methylation in both patient samples and cell lines. A significant correlation between ROR2 expression levels and promoter methylation was observed in patient samples (r = −0.797, p = 0.018). ROR2 restoration in ARK-1 significantly decreased invasion ability, with associated changes in epithelial-mesenchymal transition (EMT) markers. ROR2 plays a tumour-suppressor role in EC and is epigenetically suppressed with the development of disease. It may represent a diagnostic or therapeutic candidate for EC. Full article
(This article belongs to the Special Issue Epigenomic Studies of Gynecological Cancer)
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25 pages, 2612 KiB  
Article
Global DNA Hypomethylation in Epithelial Ovarian Cancer: Passive Demethylation and Association with Genomic Instability
by Wa Zhang, David Klinkebiel, Carter J. Barger, Sanjit Pandey, Chittibabu Guda, Austin Miller, Stacey N. Akers, Kunle Odunsi and Adam R. Karpf
Cancers 2020, 12(3), 764; https://doi.org/10.3390/cancers12030764 - 24 Mar 2020
Cited by 52 | Viewed by 6954
Abstract
A hallmark of human cancer is global DNA hypomethylation (GDHO), but the mechanisms accounting for this defect and its pathological consequences have not been investigated in human epithelial ovarian cancer (EOC). In EOC, GDHO was associated with advanced disease and reduced overall and [...] Read more.
A hallmark of human cancer is global DNA hypomethylation (GDHO), but the mechanisms accounting for this defect and its pathological consequences have not been investigated in human epithelial ovarian cancer (EOC). In EOC, GDHO was associated with advanced disease and reduced overall and disease-free survival. GDHO (+) EOC tumors displayed a proliferative gene expression signature, including FOXM1 and CCNE1 overexpression. Furthermore, DNA hypomethylation in these tumors was enriched within genomic blocks (hypomethylated blocks) that overlapped late-replicating regions, lamina-associated domains, PRC2 binding sites, and the H3K27me3 histone mark. Increased proliferation coupled with hypomethylated blocks at late-replicating regions suggests a passive hypomethylation mechanism. This hypothesis was further supported by our observation that cytosine DNA methyltransferases (DNMTs) and UHRF1 showed significantly reduced expression in GDHO (+) EOC after normalization to canonical proliferation markers, including MKI67. Finally, GDHO (+) EOC tumors had elevated chromosomal instability (CIN), and copy number alterations (CNA) were enriched at the DNA hypomethylated blocks. Together, these findings implicate a passive DNA demethylation mechanism in ovarian cancer that is associated with genomic instability and poor prognosis. Full article
(This article belongs to the Special Issue Epigenomic Studies of Gynecological Cancer)
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Review

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21 pages, 842 KiB  
Review
Histone Modifying Enzymes in Gynaecological Cancers
by Priya Ramarao-Milne, Olga Kondrashova, Sinead Barry, John D. Hooper, Jason S. Lee and Nicola Waddell
Cancers 2021, 13(4), 816; https://doi.org/10.3390/cancers13040816 - 16 Feb 2021
Cited by 10 | Viewed by 3777
Abstract
Genetic and epigenetic factors contribute to the development of cancer. Epigenetic dysregulation is common in gynaecological cancers and includes altered methylation at CpG islands in gene promoter regions, global demethylation that leads to genome instability and histone modifications. Histones are a major determinant [...] Read more.
Genetic and epigenetic factors contribute to the development of cancer. Epigenetic dysregulation is common in gynaecological cancers and includes altered methylation at CpG islands in gene promoter regions, global demethylation that leads to genome instability and histone modifications. Histones are a major determinant of chromosomal conformation and stability, and unlike DNA methylation, which is generally associated with gene silencing, are amenable to post-translational modifications that induce facultative chromatin regions, or condensed transcriptionally silent regions that decondense resulting in global alteration of gene expression. In comparison, other components, crucial to the manipulation of chromatin dynamics, such as histone modifying enzymes, are not as well-studied. Inhibitors targeting DNA modifying enzymes, particularly histone modifying enzymes represent a potential cancer treatment. Due to the ability of epigenetic therapies to target multiple pathways simultaneously, tumours with complex mutational landscapes affected by multiple driver mutations may be most amenable to this type of inhibitor. Interrogation of the actionable landscape of different gynaecological cancer types has revealed that some patients have biomarkers which indicate potential sensitivity to epigenetic inhibitors. In this review we describe the role of epigenetics in gynaecological cancers and highlight how it may exploited for treatment. Full article
(This article belongs to the Special Issue Epigenomic Studies of Gynecological Cancer)
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