No abstract available.
Methylation*

No abstract available.
Chromatin* ; DNA* ; Epigenomics* ; Histones* ; Methylation*

OBJECTIVE: Endometrial cancer (EC) is a common gynecologic cancer worldwide. However, the pathogenesis of EC has not been epigenetically elucidated. Here, this study aims to describe the DNA methylation profile and identify favorable gene signatures highly associated with aberrant DNA methylation changes in EC. METHODS: The data regarding DNA methylation and gene expression were downloaded from The Cancer Genome Atlas (TCGA) database. Differentially methylated CpG sites (DMCs), differentially methylated regions (DMRs), and differentially expressed genes (DEGs) were identified, and the relationship between the 2 omics was further analyzed. In addition, weighted CpG site co-methylation network (WCCN) was constructed followed by an integrated analysis of DNA methylation and gene expression data. RESULTS: Four hundred thirty-one tumor tissues and 46 tissues adjacent tumor of EC patients were analyzed. One thousand one hundred thirty-five DMCs (merging to 10 DMRs), and 1,488 DEGs were obtained between tumor and normal groups, respectively. One hundred forty-eight DMCs-DEGs correlated pairs and 13 regional DMCs-DEGs pairs were obtained. Interestingly, we found that some hub genes in 2 modules among 8 modules of WCCN analysis were down-regulated in tumor samples. Furthermore, protocadherins (PCDHs) clusters, DDP6, TNXB, and ZNF154 were identified as novel deregulated genes with altered methylation in EC. CONCLUSION: Based on the analysis of DNA methylation in a systematic view, the potential long-range epigenetic silencing (LRES) composed of PCDHs was reported in ECs for the first time. PCDHs clusters, DDP6, and TNXB were firstly found to be associated with tumorigenesis, and may be novel candidate biomarkers for EC.
Biomarkers ; Carcinogenesis ; DNA Methylation* ; DNA* ; Endometrial Neoplasms* ; Epigenomics ; Female ; Gene Expression* ; Genome ; Humans ; Methylation

Methylation of cytosine is a post-synthesis modification that does not affect the primary DNA sequence but greatly influences gene expression level and phenotypes of an organism. As high-throughput sequencing of bisulfite-treated DNA is the most efficient method to identify methylated sites, several tools to map sequencing reads on a reference are available. But tools to visualize and to interpret the methylation level of methylation sites are currently insufficient. Herein, we present a novel tool to visualize the methylation level of CpG sites.
Base Sequence ; Cytosine ; DNA ; DNA Methylation ; Epigenomics ; Gene Expression ; Methylation ; Phenotype ; Sulfites

Diverse somatic mutations have been reported to serve as cancer drivers. Recently, it has also been reported that epigenetic regulation is closely related to cancer development. However, the effect of epigenetic changes on cancer is still elusive. In this study, we analyzed DNA methylation data on colon cancer taken from The Caner Genome Atlas. We found that several promoters were significantly hypermethylated in colon cancer patients. Through clustering analysis of differentially methylated DNA regions, we were able to define subgroups of patients and observed clinical features associated with each subgroup. In addition, we analyzed the functional ontology of aberrantly methylated genes and identified the G-protein-coupled receptor signaling pathway as one of the major pathways affected epigenetically. In conclusion, our analysis shows the possibility of characterizing the clinical features of colon cancer subgroups based on DNA methylation patterns and provides lists of important genes and pathways possibly involved in colon cancer development.
Classification* ; Colon* ; Colonic Neoplasms* ; CpG Islands ; DNA ; DNA Methylation ; Epigenomics ; Genome ; Humans ; Methylation*

OBJECTIVE: Promoter methylation of Bcl-2 family genes in cancer cells were studied to verify possible correlation between DNA methylation pattern of Bcl-2 family members and cancer. METHODS: The genomic DNAs were extracted from different cancer cell lines, HeLa, CaSki and K562, and ovarian cancer tissue from patients. The cytosine residues were converted to uracil by sodium bisulfite treatment. MSP (methylation specific PCR) was performed to determine the methylation status of Bcl-2, Mcl-1, Noxa, and Harakiri promoters. Using primers that distinguish methylated DNA from unmethylated DNA after bisulfite modification of DNA, MSP was conducted to observe the methylation pattern of Bcl-2 family genes in different cancer cells. RESULTS: The promoter regions of Bcl-2 family genes including Mcl-1, Bcl-2, and Noxa were not methylated in cancer cells, whereas the proapoptotic Bcl-2 family gene Harakiri was detected as methylated in the cancer cell lines and hypomethylated in the ovarian cancer tissue. CONCLUSION: The present study demonstrated the differential methylation profiles of Bcl-2 family genes in cancerous cells, which suggests a possible connection between the methylation pattern of some of Bcl-2 family genes and ovarian cancer.
Cell Line ; Cytosine ; DNA Methylation* ; DNA* ; Humans ; Methylation ; Ovarian Neoplasms ; Promoter Regions, Genetic ; Sodium ; Uracil

DNA methylation is one of many epigenetic mechanisms that regulate gene expression in the human body. From the view of epigenetics, there are two phases of development, one for germ cell development and another for embryo development. This review will discuss the basic mechanism of methylation, its role in gene expression, and the role of methylation in embryonic reprogramming. Methylation of genes is very critical to embryo development and should be explored further in order to increase our understanding of development.
DNA ; DNA Methylation ; Embryonic Development ; Epigenomics ; Female ; Gene Expression ; Germ Cells ; Human Body ; Methylation ; Pregnancy

Aberrant DNA methylation, as an epigenetic marker of cancer, influences tumor development and progression. We downloaded publicly available DNA methylation and gene expression datasets of matched cancer and normal pairs from the Cancer Genome Atlas Data Portal and performed a systematic computational analysis. This study has three aims to screen genes that show hypermethylation and downregulated patterns in colorectal cancers, to identify differentially methylated regions in one of these genes, SFRP1, and to test whether the SFRP genes affect survival or not. Our results show that 31 hypermethylated genes had a negative correlation with gene expression. Among them, SFRP1 had a differentially methylated pattern at each methylation site. We also show that SFRP1 may be a potential biomarker for colorectal cancer survival.
Colorectal Neoplasms* ; Computer Simulation* ; Dataset ; DNA Methylation ; Epigenomics ; Gene Expression ; Genome ; Methylation ; Survival Analysis

BACKGROUND/AIMS: Methylation status plays a causal role in carcinogenesis in targeted tissues. However, the relationship between the DNA methylation status of multiple genes in blood leukocytes and colorectal cancer (CRC) susceptibility as well as interactions between dietary factors and CRC risks are unclear. METHODS: We performed a case-control study with 466 CRC patients and 507 cancer-free controls to investigate the association among the methylation status of individual genes, multiple CpG site methylation (MCSM), multiple CpG site heterogeneous methylation and CRC susceptibility. Peripheral blood DNA methylation levels were detected by performing methylation-sensitive high-resolution melting. RESULTS: Total heterogeneous methylation of CA10 and WT1 conferred a significantly higher risk of CRC (adjusted odds ratio [OR(adjusted)], 5.445; 95% confidence interval [CI], 3.075 to 9.643; OR(adjusted), 1.831; 95% CI, 1.100 to 3.047; respectively). Subjects with high-level MCSM (MCSM-H) status demonstrated a higher risk of CRC (OR(adjusted), 4.318; 95% CI, 1.529 to 12.197). Additionally, interactions between the high-level intake of fruit and CRH, WT1, and MCSM on CRC were statistically significant. CONCLUSIONS: The gene methylation status of blood leukocytes may be associated with CRC risk. MCSM-H of blood leukocytes was associated with CRC, especially in younger people. Some dietary factors may affect hypermethylation status and influence susceptibility to CRC.
Carcinogenesis ; Case-Control Studies ; China* ; Colorectal Neoplasms* ; DNA Methylation ; Freezing ; Fruit ; Humans ; Leukocytes ; Methylation* ; Odds Ratio

BACKGROUND/AIMS: Helicobacter pylori infection induces aberrant DNA methylation in gastric mucosa. We evaluated the long-term effect of H. pylori eradication on promotor CpG island hypermethylation in gastric carcinogenesis. METHODS: H. pylori-positive patients with gastric adenoma or early gastric cancer who underwent endoscopic resection were enrolled. According to H. pylori eradication after endoscopic resection, the participants were randomly assigned to H. pylori eradication or non-eradication group. H. pylori-negative gastric mucosa from normal participants provided the normal control. CpG island hypermethylation of tumor-related genes (p16, CDH1, and RUNX-3) was evaluated by quantitative MethyLight assay in non-tumorous gastric mucosa. The gene methylation rate and median values of hypermethylation were compared after one year by H. pylori status. RESULTS: In H. pylori-positive patients, hypermethylation of p16 was found in 80.6%, of CDH1 in 80.6%, and of RUNX-3 in 48.4%. This is significantly higher than normal control (p16, 10%; CDH1, 44%; RUNX-3, 16%) (p<0.05). In the H. pylori eradication group, methylation rates of p16 and CDH1 decreased in 58.1% and 61.3% of the patients, and the median values of hypermethylation were significantly lower at one year compared with the non-eradication group. However, RUNX-3 hypermethylation did not differ significantly at one year after H. pylori eradication. The non-eradication group hypermethylation did not change after one year. CONCLUSIONS: H. pylori infection was associated with promotor hypermethylation of genes in gastric carcinogenesis, and H. pylori eradication might reverse p16 and CDH1 hypermethylation.
Adenoma ; Carcinogenesis* ; CpG Islands* ; DNA Methylation ; Gastric Mucosa ; Helicobacter pylori* ; Helicobacter* ; Humans ; Methylation ; Stomach Neoplasms