Methylation profile in breast cancer
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE27374 | GEO | 2011/02/23
SECONDARY ACCESSION(S): PRJNA137279
REPOSITORIES: GEO
Similar Datasets
Project description:Agilent CpG microarray in combination with enriched methylated DNA by a MBD protein were carried out in each pool of genomic DNA from primary breast tumor and matched adjacent normal tissues. 1.Common reference vs enriched methylated DNA in tumor 2. Common reference vs enriched methylated DNA in adjacent normal 3. Then compare two data indirectly
2011-02-23 | E-GEOD-27374 | biostudies-arrayexpress
Project description:<p>Schizophrenia (SCZ) is a devastating psychiatric disorder. The aim of this study was to detect DNA methylation (5meC) profiles in whole blood associated with SCZ. The sample consisted of schizophrenia cases and controls selected from national population registers in Sweden. We employed MBD protein-based enrichment of the methylated DNA fraction, followed by single end sequencing (50 bp reads) on the SOLiD platform. To improve methylome-wide coverage we used an existing protocol variant, which increases the relative number of fragments from CpG poor regions. To analyze the data, we used an analysis pipeline described elsewhere7, that was designed specifically for MBD-seq and included alignment, quality control (QC) of reads and samples, coverage calculations for the 26,752,702 autosomal CpGs in the reference genome using a non-parametric estimate of the fragment size distribution, an in silico experiment to identify CpGs in loci with alignment problems, a 2-stage adaptive algorithm to combine data from correlated adjacent CpG sites in "blocks", principal component analysis (PCA), association testing, bioinformatics annotation and network analysis. After QC, 1459 subjects with on average 32.4 million high quality reads remained. Association testing was performed on 4.3 million high quality blocks after regressing out possible assay related technical artifacts, sex/age, and unmeasured confounders through the PCA components.</p>
| phs000608 | dbGaP
Project description:DNA methylation was assessed in genomic DNA obtained from the arcuate nucleus of heifers fed to gain body weight at high (HG, n = 4) and low (LG, n = 4) rates from 4.5 to 8.5 mo of age. A methyl-CpG binding domain-based (MBD) protein assay was performed to capture fragments of methylated DNA (methylated-enriched DNA). Input (total) and methylated-enriched DNA were labeled with two different dyes and co-hybridized to a custom-designed oligonucleotide array targeted to genes associated with nutritional inputs and the control of puberty. The ratio of the log2 (enriched/input) of the normalized intensities, were determined. Data was analyzed comparing values of HG versus LG heifers. Two nutritional schedules: HG (n=4 heifers) and LG (n=4 heifers); one array per heifer; methylated enriched DNA (enriched) and total DNA (input) co-hybridyzed into each array Methylated-enriched DNA obtained from a methyl-CpG binding domain-based (MBD) protein assay
2016-02-11 | E-GEOD-77782 | biostudies-arrayexpress
Project description:In order to gain insight into DNA methylation readout, we have established a controlled strategy for profiling genomic targeting of chromatin-interacting factors in vivo. With this approach we determined binding preferences for the methyl-CpG binding domain (MBD) family of proteins, including disease relevant mutants, deletions and isoforms. In vivo binding of MBD proteins occurs as a linear function of local methylation density, and is dependent on functional MBD domain – methyl-CpG interactions. This directs specificity of MBD proteins to methylated, CpG dense and inactive regulatory regions. In contrast, binding to unmethylated sites is MBD protein specific and mediated via alternative domains or protein-protein interactions. The latter is observed for NuRD complex-mediated MBD2 tethering to a subset of unmethylated, tissue-specific regulatory regions, similar to MBD3. These functional binding maps reveal methylation-dependent and -independent binding modes determined by distinct protein domains and revise current models of DNA methylation readout through MBD proteins.
2013-04-01 | GSE39610 | GEO
Project description:High-throughput analyses of concordant gene methylation and expression events were carried out for 91 human prostate specimens, including prostate cancer (T), matched normal adjacent to tumor (AT), and organ donor (OD). Methylated DNA in genomic DNA was immunoprecipitated with anti-methylcytidine antibodies and detected by Affymetrix human whole genome SNP 6.0 chips. Methylated genomic DNA was purified by 5-hmc antibodies and Affymetrix SNP arrays were performed according to the manufacturer's manual.
2013-08-01 | GSE45000 | GEO
Project description:DNA demethylating agents are epigenetic drugs for the therapy of myeloid leukemias. They not only induce DNA demethylation but also have significant cytostatic and cytotoxic effects, however, the relationships between these characteristics have not been established yet due to the lack of method to induce only DNA demethylation. Here we show that a fusion protein comprising the methyl-CpG binding domain (MBD) and the catalytic domain of Ten-eleven translocation protein 1 (TET1-CD) globally demethylates and upregulates a number of methylated genes. Gene expression microarray analyses using human embryonic kidney cell line 293T indicate that cells expressing wild-type (wt) TET1 catalytic domain with MBD (MBD-TET1-CDwt) upregulated more genes than ones expressing TET1-CDwt without MBD or catalytically inactive TET1-CD mutant (mut) with MBD (MBD-TET1-CDmut) and their upregulated genes frequently contained CpG islands (CGIs) within ± 1,000 bp of the transcription start site (TSS). Interestingly, 88% of genes upregulated 5-fold or more by MBD-TET1-CDwt were also reactivated after treatment with DNA demethylating agent, 5-azacytidine, suggesting that gene reactivation by both methods is primarily based on DNA demethylation.
2017-02-09 | GSE74744 | GEO
Project description:Lung cancer occurs in never-smokers. Epigenetic changes in lung cancer potentially represent important diagnostic, prognostic, and therapeutic targets. We compared DNA methylation profiles of 28 adenocarcinomas of the lungs of never-smokers with paired adjacent nonmalignant lung tissue. We correlated differential methylation changes with gene expression changes from the same 28 samples. We observed a distinct separation in methylation profiles between tumor and adjacent nonmalignant lung tissue using principal component analysis. Tumors were generally hypomethylated compared with adjacent nonmalignant tissue. Of 1,906 differentially methylated CpG sites between tumor and nonmalignant tissue, 1,198 were within classically defined CpG islands where tumors were hypermethylated compared with nonmalignant tissue. A total of 708 sites were outside CpG islands where tumors were hypomethylated compared with nonmalignant tissue. There were significant differences in expression of 351 genes (23%) of the 1,522 genes matched to the differentially methylated CpG sites. Genes that were not significantly differentially expressed and were hypermethylated within CpG sites were enriched for homeobox genes. These results suggest that the methylation profiles of lung adenocarcinomas of never-smokers and adjacent nonmalignant lung tissue are significantly different. Despite the differential methylation of homeobox genes, no significant changes in expression of these genes were detected. Twenty eight pairs of tumor and adjacent normal lungs were profiled for lung adenocarcinoma patients by gene expression and DNA methylation microarray
2015-02-03 | E-GEOD-62948 | biostudies-arrayexpress
Project description:Lung cancer occurs in never-smokers. Epigenetic changes in lung cancer potentially represent important diagnostic, prognostic, and therapeutic targets. We compared DNA methylation profiles of 28 adenocarcinomas of the lungs of never-smokers with paired adjacent nonmalignant lung tissue. We correlated differential methylation changes with gene expression changes from the same 28 samples. We observed a distinct separation in methylation profiles between tumor and adjacent nonmalignant lung tissue using principal component analysis. Tumors were generally hypomethylated compared with adjacent nonmalignant tissue. Of 1,906 differentially methylated CpG sites between tumor and nonmalignant tissue, 1,198 were within classically defined CpG islands where tumors were hypermethylated compared with nonmalignant tissue. A total of 708 sites were outside CpG islands where tumors were hypomethylated compared with nonmalignant tissue. There were significant differences in expression of 351 genes (23%) of the 1,522 genes matched to the differentially methylated CpG sites. Genes that were not significantly differentially expressed and were hypermethylated within CpG sites were enriched for homeobox genes. These results suggest that the methylation profiles of lung adenocarcinomas of never-smokers and adjacent nonmalignant lung tissue are significantly different. Despite the differential methylation of homeobox genes, no significant changes in expression of these genes were detected. Twenty eight pairs of tumor and adjacent normal lungs were profiled for lung adenocarcinoma patients by gene expression and DNA methylation microarray
2015-02-03 | E-GEOD-62949 | biostudies-arrayexpress
Project description:Methyl CpG Binding (MBD) proteins are a class of protein that binds with methylated DNA. In the model plant Arabidopsis thaliana there are 13 MBD proteins are there. To understand the gene regulation we performed microarray analysis of mutants of three genes (atmbd4, atmbd6 and atmbd11). Ten day old seedlings of these three mutant were compared with the wild type plants grown in same condition.
2014-07-09 | GSE59133 | GEO
Project description:In order to gain insight into DNA methylation readout, we have established a controlled strategy for profiling genomic targeting of chromatin-interacting factors in vivo. With this approach we determined binding preferences for the methyl-CpG binding domain (MBD) family of proteins, including disease relevant mutants, deletions and isoforms. In vivo binding of MBD proteins occurs as a linear function of local methylation density, and is dependent on functional MBD domain M-bM-^@M-^S methyl-CpG interactions. This directs specificity of MBD proteins to methylated, CpG dense and inactive regulatory regions. In contrast, binding to unmethylated sites is MBD protein specific and mediated via alternative domains or protein-protein interactions. The latter is observed for NuRD complex-mediated MBD2 tethering to a subset of unmethylated, tissue-specific regulatory regions, similar to MBD3. These functional binding maps reveal methylation-dependent and -independent binding modes determined by distinct protein domains and revise current models of DNA methylation readout through MBD proteins. Comparative binding analysis for the MBD family of proteins utilizing recombinase-assisted mapping of biotin-tagged proteins (RAMBiO). This set contains maps for 29 samples including wild type MBD proteins, mutants and domain variants in mouse ES cells, derived neurons (NP and TN) and Dnmt1/3a/3b triple-KO ES cells (TKO).
2013-04-01 | E-GEOD-39610 | biostudies-arrayexpress