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Targeting Epigenetics in Human Health and Diseases: From Mechanisms to...
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Targeting Epigenetics in Human Health and Diseases: From Mechanisms to Therapeutics and Beyond

A special issue of Diseases (ISSN 2079-9721).

Deadline for manuscript submissions: closed (30 December 2016) | Viewed by 39902

Special Issue Editor

Dr. Takeo Kubota

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Guest Editor
1. Past Professor, Department of Epigenetic Medicine, University of Yamanashi, Yamanashi 409-3898, Japan
2. Present Affiliation, Supervising Doctor, Kofu Office, Yamanashi Prefecture Red Cross Blood Center, Japanese Red Cross Society, 1-6-1 Ikeda, Kofu-city, Yamanashi 400-0062, Japan
Interests: neurodevelopmental disorder; epigenome; environmental stress; epigenetic reversibility; preemptive medicine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Epigenetics is a gene regulation mechanism that does not depend on genome (genomic DNA sequences) but depends on the epigenome (chemical modification of genomic DNA and histone proteins).

Recent studies indicate that epigenomic abnormalities, not only cause congenital diseases, but also cause acquired diseases, such as psychiatric diseases and type 2 diabetes, since the epigenome is more vulnerable to environmental stress than the genome.

Therefore, understanding of how the epigenome reacts to environmental stress and how we maintain the normal epigenome has become an important medical issue.

Since the epigenome has a reversible property, which is based on removable residues on genomic DNA, environmentally induced epigenomic alterations can be restored. In fact, some drugs, especially those for psychiatric diseases, are known to restore an altered epigenome, resulting in correction of gene expression.

In this Special Issue, I would like to focus on basic or clinical studies that contribute to human health and preemptive medicine through identification of the epigenomic markers or development of the epigenetic therapy.

Dr. Takeo Kubota
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. Diseases 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

  • epigenetics
  • epigenome
  • health
  • disease
  • mechanism
  • therapy
  • preemptive medicine

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Published Papers (3 papers)

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Review

549 KiB  
Review
Epigenetic Mechanisms of Tamoxifen Resistance in Luminal Breast Cancer
by Hany A. Abdel-Hafiz
Diseases 2017, 5(3), 16; https://doi.org/10.3390/diseases5030016 - 6 Jul 2017
Cited by 50 | Viewed by 10591
Abstract
Breast cancer is one of the most common cancers and the second leading cause of cancer death in the United States. Estrogen receptor (ER)-positive cancer is the most frequent subtype representing more than 70% of breast cancers. These tumors respond to endocrine therapy [...] Read more.
Breast cancer is one of the most common cancers and the second leading cause of cancer death in the United States. Estrogen receptor (ER)-positive cancer is the most frequent subtype representing more than 70% of breast cancers. These tumors respond to endocrine therapy targeting the ER pathway including selective ER modulators (SERMs), selective ER downregulators (SERDs) and aromatase inhibitors (AIs). However, resistance to endocrine therapy associated with disease progression remains a significant therapeutic challenge. The precise mechanisms of endocrine resistance remain unclear. This is partly due to the complexity of the signaling pathways that influence the estrogen-mediated regulation in breast cancer. Mechanisms include ER modifications, alteration of coregulatory function and modification of growth factor signaling pathways. In this review, we provide an overview of epigenetic mechanisms of tamoxifen resistance in ER-positive luminal breast cancer. We highlight the effect of epigenetic changes on some of the key mechanisms involved in tamoxifen resistance, such as tumor-cell heterogeneity, ER signaling pathway and cancer stem cells (CSCs). It became increasingly recognized that CSCs are playing an important role in driving metastasis and tamoxifen resistance. Understanding the mechanism of tamoxifen resistance will provide insight into the design of novel strategies to overcome the resistance and make further improvements in breast cancer therapeutics. Full article
(This article belongs to the Special Issue Targeting Epigenetics in Human Health and Diseases: From Mechanisms to Therapeutics and Beyond)
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2264 KiB  
Review
Milk’s Role as an Epigenetic Regulator in Health and Disease
by Bodo C. Melnik and Gerd Schmitz
Diseases 2017, 5(1), 12; https://doi.org/10.3390/diseases5010012 - 15 Mar 2017
Cited by 79 | Viewed by 20630
Abstract
It is the intention of this review to characterize milk’s role as an epigenetic regulator in health and disease. Based on translational research, we identify milk as a major epigenetic modulator of gene expression of the milk recipient. Milk is presented as an [...] Read more.
It is the intention of this review to characterize milk’s role as an epigenetic regulator in health and disease. Based on translational research, we identify milk as a major epigenetic modulator of gene expression of the milk recipient. Milk is presented as an epigenetic “doping system” of mammalian development. Milk exosome-derived micro-ribonucleic acids (miRNAs) that target DNA methyltransferases are implicated to play the key role in the upregulation of developmental genes such as FTO, INS, and IGF1. In contrast to miRNA-deficient infant formula, breastfeeding via physiological miRNA transfer provides the appropriate signals for adequate epigenetic programming of the newborn infant. Whereas breastfeeding is restricted to the lactation period, continued consumption of cow’s milk results in persistent epigenetic upregulation of genes critically involved in the development of diseases of civilization such as diabesity, neurodegeneration, and cancer. We hypothesize that the same miRNAs that epigenetically increase lactation, upregulate gene expression of the milk recipient via milk-derived miRNAs. It is of critical concern that persistent consumption of pasteurized cow’s milk contaminates the human food chain with bovine miRNAs, that are identical to their human analogs. Commercial interest to enhance dairy lactation performance may further increase the epigenetic miRNA burden for the milk consumer. Full article
(This article belongs to the Special Issue Targeting Epigenetics in Human Health and Diseases: From Mechanisms to Therapeutics and Beyond)
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1107 KiB  
Review
Targeting H19, an Imprinted Long Non-Coding RNA, in Hepatic Functions and Liver Diseases
by Chad Pope, Shashank Mishra, Joshua Russell, Qingqing Zhou and Xiao-Bo Zhong
Diseases 2017, 5(1), 11; https://doi.org/10.3390/diseases5010011 - 8 Mar 2017
Cited by 41 | Viewed by 7953
Abstract
H19 is a long non-coding RNA regulated by genomic imprinting through methylation at the locus between H19 and IGF2. H19 is important in normal liver development, controlling proliferation and impacting genes involved in an important network controlling fetal development. H19 also plays a [...] Read more.
H19 is a long non-coding RNA regulated by genomic imprinting through methylation at the locus between H19 and IGF2. H19 is important in normal liver development, controlling proliferation and impacting genes involved in an important network controlling fetal development. H19 also plays a major role in disease progression, particularly in hepatocellular carcinoma. H19 participates in the epigenetic regulation of many processes impacting diseases, such as activating the miR-200 pathway by histone acetylation to inhibit the epithelial-mesenchymal transition to suppress tumor metastasis. Furthermore, H19’s normal regulation is disturbed in diseases, such as hepatocellular carcinoma. In this disease, aberrant epigenetic maintenance results in biallelic expression of IGF2, leading to uncontrolled cellular proliferation. This review aims to further research utilizing H19 for drug discovery and the treatment of liver diseases by focusing on both the epigenetic regulation of H19 and how H19 regulates normal liver functions and diseases, particularly by epigenetic mechanisms. Full article
(This article belongs to the Special Issue Targeting Epigenetics in Human Health and Diseases: From Mechanisms to Therapeutics and Beyond)
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