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Epigenomes, Volume 1, Issue 1 (March 2017)

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Editorial

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Open AccessEditorial Welcome to the New Journal Epigenomes
Epigenomes 2017, 1(1), 1; doi:10.3390/epigenomes1010001
Received: 16 February 2016 / Accepted: 16 February 2016 / Published: 7 April 2016
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Abstract We are excited to introduce Epigenomes, a new journal that will serve the growing community of researchers who use omic approaches to dissect the epigenetic mechanisms underlying developmental and pathological processes.[...] Full article

Research

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Open AccessArticle Helicase Lymphoid-Specific Enzyme Contributes to the Maintenance of Methylation of SST1 Pericentromeric Repeats That Are Frequently Demethylated in Colon Cancer and Associate with Genomic Damage
Epigenomes 2017, 1(1), 2; doi:10.3390/epigenomes1010002
Received: 27 July 2016 / Revised: 8 September 2016 / Accepted: 14 September 2016 / Published: 22 September 2016
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Abstract
DNA hypomethylation at repetitive elements accounts for the genome-wide DNA hypomethylation common in cancer, including colorectal cancer (CRC). We identified a pericentromeric repeat element called SST1 frequently hypomethylated (>5% demethylation compared with matched normal tissue) in several cancers, including 28 of 128 (22%)
[...] Read more.
DNA hypomethylation at repetitive elements accounts for the genome-wide DNA hypomethylation common in cancer, including colorectal cancer (CRC). We identified a pericentromeric repeat element called SST1 frequently hypomethylated (>5% demethylation compared with matched normal tissue) in several cancers, including 28 of 128 (22%) CRCs. SST1 somatic demethylation associated with genome damage, especially in tumors with wild-type TP53. Seven percent of the 128 CRCs exhibited a higher (“severe”) level of demethylation (≥10%) that co-occurred with TP53 mutations. SST1 demethylation correlated with distinct histone marks in CRC cell lines and primary tumors: demethylated SST1 associated with high levels of the repressive histone 3 lysine 27 trimethylation (H3K27me3) mark and lower levels of histone 3 lysine 9 trimethylation (H3K9me3). Furthermore, induced demethylation of SST1 by 5-aza-dC led to increased H3K27me3 and reduced H3K9me3. Thus, in some CRCs, SST1 demethylation reflects an epigenetic reprogramming associated with changes in chromatin structure that may affect chromosomal integrity. The chromatin remodeler factor, the helicase lymphoid-specific (HELLS) enzyme, called the “epigenetic guardian of repetitive elements”, interacted with SST1 as shown by chromatin immunoprecipitation, and down-regulation of HELLS by shRNA resulted in demethylation of SST1 in vitro. Altogether these results suggest that HELLS contributes to SST1 methylation maintenance. Alterations in HELLS recruitment and function could contribute to the somatic demethylation of SST1 repeat elements undergone before and/or during CRC pathogenesis. Full article
(This article belongs to the Special Issue Biological Methylation in Development and Cancer)
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Review

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Open AccessReview New Frontiers in Melanoma Epigenetics—The More We Know, the More We Don’t Know
Epigenomes 2017, 1(1), 3; doi:10.3390/epigenomes1010003
Received: 31 December 2016 / Accepted: 25 January 2017 / Published: 30 January 2017
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Abstract
Skin cancer is one of the most common neoplasms worldwide, with a surprising tendency to increase its incidence. As with many cancer types nowadays, early diagnosis and proper management carries an excellent prognosis, up to 5-year survival rate of above 95% for most
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Skin cancer is one of the most common neoplasms worldwide, with a surprising tendency to increase its incidence. As with many cancer types nowadays, early diagnosis and proper management carries an excellent prognosis, up to 5-year survival rate of above 95% for most skin cancers, even though the long-term survival rate among metastatic melanoma patients remains only 5%. This review aims to summarize recent discoveries in epigenetic changes connected with cutaneous malignant melanoma (CMM), comprising of DNA methylation, histone modifications, miRNA regulation, nucleosome positioning and chromatin remodelling. Undoubtedly, personalised medicine based on both genetic and epigenetic changes of cancer is the future, the question remains: how long will it take to transport this treatment from the bench to the bedside? Full article
(This article belongs to the Special Issue Biological Methylation in Development and Cancer)

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