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7.4
5.2
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Cancers
Special Issues
Cancer Epigenetics
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Cancer Epigenetics

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

Deadline for manuscript submissions: closed (28 February 2013) | Viewed by 77483

Special Issue Editor

Prof. Dr. Taiping Chen

E-Mail Website
Guest Editor
Department of Epigenetics and Molecular Carcinogenesis, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX 77030, USA
Interests: DNA methylation; histone modifications; genomic imprinting; mammalian development; cancer epigenetics

Special Issue Information

Dear Colleagues,

The role of genetic alterations in cancer is well established. It is generally accepted, however, that genetic changes alone do not fully account for malignancy. Growing evidence has indeed implicated the involvement of epigenetic alterations in cancer. Unlike irreversible genetic mutations, epigenetic alterations are potentially reversible, which makes epigenetic therapy (modulation of epigenetic states) an appealing strategy for cancer treatment. Alterations of epigenetic marks could also serve as biomarkers for diagnosis, prognosis, and responses to therapies. To realize the potential of epigenetics in clinical applications, it is essential to understand the fundamental aspects of cancer epigenetics. For this special issue of Cancers dedicated to cancer epigenetics, we invite manuscripts that address various epigenetic mechanisms, such as DNA methylation, histone modifications, chromatin remodeling, and non-coding RNAs, in cancer. We are particularly interested in manuscripts that aim to document epigenetic alterations in cancer, elucidate the mechanisms underlying such alterations, and understand the roles of such alterations in the initiation and progression of cancer.

Prof. Dr. Taiping Chen
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. 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

  • DNA methylation
  • histone modifications
  • genomic imprinting
  • mammalian development
  • cancer epigenetics

Published Papers (6 papers)

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Research

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603 KiB  
Article
Epigenetics and Colorectal Cancer Pathogenesis
by Kankana Bardhan and Kebin Liu
Cancers 2013, 5(2), 676-713; https://doi.org/10.3390/cancers5020676 - 05 Jun 2013
Cited by 191 | Viewed by 18529
Abstract
Colorectal cancer (CRC) develops through a multistage process that results from the progressive accumulation of genetic mutations, and frequently as a result of mutations in the Wnt signaling pathway. However, it has become evident over the past two decades that epigenetic alterations of [...] Read more.
Colorectal cancer (CRC) develops through a multistage process that results from the progressive accumulation of genetic mutations, and frequently as a result of mutations in the Wnt signaling pathway. However, it has become evident over the past two decades that epigenetic alterations of the chromatin, particularly the chromatin components in the promoter regions of tumor suppressors and oncogenes, play key roles in CRC pathogenesis. Epigenetic regulation is organized at multiple levels, involving primarily DNA methylation and selective histone modifications in cancer cells. Assessment of the CRC epigenome has revealed that virtually all CRCs have aberrantly methylated genes and that the average CRC methylome has thousands of abnormally methylated genes. Although relatively less is known about the patterns of specific histone modifications in CRC, selective histone modifications and resultant chromatin conformation have been shown to act, in concert with DNA methylation, to regulate gene expression to mediate CRC pathogenesis. Moreover, it is now clear that not only DNA methylation but also histone modifications are reversible processes. The increased understanding of epigenetic regulation of gene expression in the context of CRC pathogenesis has led to development of epigenetic biomarkers for CRC diagnosis and epigenetic drugs for CRC therapy. Full article
(This article belongs to the Special Issue Cancer Epigenetics)
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1160 KiB  
Article
Global Decrease of Histone H3K27 Acetylation in ZEB1-Induced Epithelial to Mesenchymal Transition in Lung Cancer Cells
by Joëlle Roche, Patrick Nasarre, Robert Gemmill, Aleksander Baldys, Julien Pontis, Christopher Korch, Joëlle Guilhot, Slimane Ait-Si-Ali and Harry Drabkin
Cancers 2013, 5(2), 334-356; https://doi.org/10.3390/cancers5020334 - 03 Apr 2013
Cited by 55 | Viewed by 15766
Abstract
The epithelial to mesenchymal transition (EMT) enables epithelial cells with a migratory mesenchymal phenotype. It is activated in cancer cells and is involved in invasion, metastasis and stem-like properties. ZEB1, an E-box binding transcription factor, is a major suppressor of epithelial genes in [...] Read more.
The epithelial to mesenchymal transition (EMT) enables epithelial cells with a migratory mesenchymal phenotype. It is activated in cancer cells and is involved in invasion, metastasis and stem-like properties. ZEB1, an E-box binding transcription factor, is a major suppressor of epithelial genes in lung cancer. In the present study, we show that in H358 non-small cell lung cancer cells, ZEB1 downregulates EpCAM (coding for an epithelial cell adhesion molecule), ESRP1 (epithelial splicing regulatory protein), ST14 (a membrane associated serine protease involved in HGF processing) and RAB25 (a small G-protein) by direct binding to these genes. Following ZEB1 induction, acetylation of histone H4 and histone H3 on lysine 9 (H3K9) and 27 (H3K27) was decreased on ZEB1 binding sites on these genes as demonstrated by chromatin immunoprecipitation. Of note, decreased H3K27 acetylation could be also detected by western blot and immunocytochemistry in ZEB1 induced cells. In lung cancers, H3K27 acetylation level was higher in the tumor compartment than in the corresponding stroma where ZEB1 was more often expressed. Since HDAC and DNA methylation inhibitors increased expression of ZEB1 target genes, targeting these epigenetic modifications would be expected to reduce metastasis. Full article
(This article belongs to the Special Issue Cancer Epigenetics)
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Review

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783 KiB  
Review
The Interactions of microRNA and Epigenetic Modifications in Prostate Cancer
by Prashant Kumar Singh and Moray J. Campbell
Cancers 2013, 5(3), 998-1019; https://doi.org/10.3390/cancers5030998 - 09 Aug 2013
Cited by 32 | Viewed by 10559
Abstract
Epigenetic modifiers play important roles in fine-tuning the cellular transcriptome. Any imbalance in these processes may lead to abnormal transcriptional activity and thus result in disease state. Distortions of the epigenome have been reported in cancer initiation and progression. DNA methylation and histone [...] Read more.
Epigenetic modifiers play important roles in fine-tuning the cellular transcriptome. Any imbalance in these processes may lead to abnormal transcriptional activity and thus result in disease state. Distortions of the epigenome have been reported in cancer initiation and progression. DNA methylation and histone modifications are principle components of this epigenome, but more recently it has become clear that microRNAs (miRNAs) are another major component of the epigenome. Interactions of these components are apparent in prostate cancer (CaP), which is the most common non-cutaneous cancer and second leading cause of death from cancer in the USA. Changes in DNA methylation, altered histone modifications and miRNA expression are functionally associated with CaP initiation and progression. Various aspects of the epigenome have also been investigated as biomarkers for different stages of CaP detection, though with limited success. This review aims to summarize key aspects of these mechanistic interactions within the epigenome and to highlight their translational potential as functional biomarkers. To this end, exploration of TCGA prostate cancer data revealed that expression of key CaP miRNAs inversely associate with DNA methylation. Given the importance and prevalence of these epigenetic events in CaP biology it is timely to understand further how different epigenetic components interact and influence each other. Full article
(This article belongs to the Special Issue Cancer Epigenetics)
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371 KiB  
Review
Role of Hydroxamate-Based Histone Deacetylase Inhibitors (Hb-HDACIs) in the Treatment of Solid Malignancies
by Antonino Grassadonia, Pasquale Cioffi, Felice Simiele, Laura Iezzi, Marinella Zilli and Clara Natoli
Cancers 2013, 5(3), 919-942; https://doi.org/10.3390/cancers5030919 - 25 Jul 2013
Cited by 35 | Viewed by 9180
Abstract
Hydroxamate-based histone deacetylase inhibitors (Hb-HDACIs), such as vorinostat, belinostat and panobinostat, have been previously shown to have a wide range of activity in hematologic malignancies such as cutaneous T-cell lymphoma and multiple myeloma. Recent data show that they synergize with a variety of [...] Read more.
Hydroxamate-based histone deacetylase inhibitors (Hb-HDACIs), such as vorinostat, belinostat and panobinostat, have been previously shown to have a wide range of activity in hematologic malignancies such as cutaneous T-cell lymphoma and multiple myeloma. Recent data show that they synergize with a variety of cytotoxic and molecular targeted agents in many different solid tumors, including breast, prostate, pancreatic, lung and ovarian cancer. Hb-HDACIs have a quite good toxicity profile and are now being tested in phase I and II clinical trials in solid tumors with promising results in selected neoplasms, such as hepatocarcinoma. This review will focus on their clinical activity and safety in patients with advanced solid neoplasms. Full article
(This article belongs to the Special Issue Cancer Epigenetics)
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1678 KiB  
Review
Alterations of 5-Hydroxymethylcytosine in Human Cancers
by Christopher J. Mariani, Jozef Madzo, Erika L. Moen, Ali Yesilkanal and Lucy A. Godley
Cancers 2013, 5(3), 786-814; https://doi.org/10.3390/cancers5030786 - 25 Jun 2013
Cited by 33 | Viewed by 10882
Abstract
Prior to 2009, 5-methylcytosine (5-mC) was thought to be the only biologically significant cytosine modification in mammalian DNA. With the discovery of the TET enzymes, which convert 5-methylcytosine (5-mC) to 5-hydroxymethylcytosine (5-hmC), however, intense interest has emerged in determining the biological function of [...] Read more.
Prior to 2009, 5-methylcytosine (5-mC) was thought to be the only biologically significant cytosine modification in mammalian DNA. With the discovery of the TET enzymes, which convert 5-methylcytosine (5-mC) to 5-hydroxymethylcytosine (5-hmC), however, intense interest has emerged in determining the biological function of 5-hmC. Here, we review the techniques used to study 5-hmC and evidence that alterations to 5-hmC physiology play a functional role in the molecular pathogenesis of human cancers. Full article
(This article belongs to the Special Issue Cancer Epigenetics)
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954 KiB  
Review
Epigenetic Modulating Agents as a New Therapeutic Approach in Multiple Myeloma
by Ken Maes, Eline Menu, Els Van Valckenborgh, Ivan Van Riet, Karin Vanderkerken and Elke De Bruyne
Cancers 2013, 5(2), 430-461; https://doi.org/10.3390/cancers5020430 - 15 Apr 2013
Cited by 47 | Viewed by 11657
Abstract
Multiple myeloma (MM) is an incurable B-cell malignancy. Therefore, new targets and drugs are urgently needed to improve patient outcome. Epigenetic aberrations play a crucial role in development and progression in cancer, including MM. To target these aberrations, epigenetic modulating agents, such as [...] Read more.
Multiple myeloma (MM) is an incurable B-cell malignancy. Therefore, new targets and drugs are urgently needed to improve patient outcome. Epigenetic aberrations play a crucial role in development and progression in cancer, including MM. To target these aberrations, epigenetic modulating agents, such as DNA methyltransferase inhibitors (DNMTi) and histone deacetylase inhibitors (HDACi), are under intense investigation in solid and hematological cancers. A clinical benefit of the use of these agents as single agents and in combination regimens has been suggested based on numerous studies in pre-clinical tumor models, including MM models. The mechanisms of action are not yet fully understood but appear to involve a combination of true epigenetic changes and cytotoxic actions. In addition, the interactions with the BM niche are also affected by epigenetic modulating agents that will further determine the in vivo efficacy and thus patient outcome. A better understanding of the molecular events underlying the anti-tumor activity of the epigenetic drugs will lead to more rational drug combinations. This review focuses on the involvement of epigenetic changes in MM pathogenesis and how the use of DNMTi and HDACi affect the myeloma tumor itself and its interactions with the microenvironment. Full article
(This article belongs to the Special Issue Cancer Epigenetics)
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