Buccal sample methylation from breast cancer cases
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ABSTRACT:
PROVIDER: EGAD00010002635 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:This study encompasses buccal sample DNA methylation (IlluminaMethylationEPIC array) from breast cancer cases and healthy age-matched controls.
| EGAS00001007658 | EGA
Project description:Raw methylation data from buccal samples.
| EGAD00010002231 | EGA
Project description:Buccal sample methylation data was generated from healthy controls
| EGAD00010002636 | EGA
Project description:Microarray data for inflammatory breast cancer cases
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Project description:Raw methylation data from blood samples in breast cancer cases.
| EGAD00010002470 | EGA
Project description:Prior candidate gene studies have shown tumor suppressor DNA methylation in breast milk related with history of breast biopsy, an established risk factor for breast cancer. To further establish the utility of breast milk as a tissue-specific biospecimen for investigations of breast carcinogenesis we measured genome-wide DNA methylation in breast milk from women with and without a diagnosis of breast cancer in two independent cohorts. In epigenome-wide analyses we identified 58 differentially methylated CpG sites associated with breast cancer diagnosis in the prospectively collected milk samples from the breast that would develop cancer compared with women without a diagnosis of breast cancer (q-value < 0.05), using linear mixed effects models adjusted for history of breast biopsy, age, age of the baby, cell type proportion estimates, array chip, and subject as random effect. Nearly all sites associated with breast cancer diagnosis were hypomethylated in cases compared with controls, and CpG sites were enriched for CpG islands. In addition, inferred repeat element methylation was lower in breast milk DNA from cases compared to controls, and cases exhibited increased estimated epigenetic mitotic tick rate as well as DNA methylation age compared with controls. Breast milk has promise as a biospecimen for prospective assessment of disease risk, and for understanding the underlying molecular basis of breast cancer risk factors and improving primary and secondary prevention of breast cancer.
2019-12-06 | GSE133918 | GEO
Project description:Genome-wide DNA Methylation analysis of 210 affected and unaffected individuals from 25 Australian families with multiple cases of breast cancer without carrying a mutation at breast cancer susceptibility genes. Genome-wide methylation was assessed using the Infinium HumanMethylation450K platform.
2017-10-14 | GSE104942 | GEO
Project description:The experiment was designed to discover deferentially methylated regions between DNA extracted from breast cancer tissues and DNA samples extracted from tissue obtained form breast reduction surgeries. The study involved 20 breast cancer samples and 5 tissue samples from breast reductions. Each of the samples was processed by the arrays and collected data were used to compare the genome wide methylation pattern cancer samples (cases) and breast reduction samples (controls). The methylation pattern of 5 DNA samples from breast reduction was compared with the methylation pattern of 20 DNA samples from breast cancer tumors
2012-12-22 | E-GEOD-43095 | biostudies-arrayexpress
Project description:Promoter methylation was assayed in a number of breast cancer and control normal samples along with the effects of 5'-aza-2'-deoxycytidine on breast cancer cell line transcriptomes. Aberrant promoter hypermethylation is frequently observed in cancer. The potential for this to contribute to tumour development depends on whether the genes affected are repressed because of their methylation. Many aberrantly methylated genes play important roles in development and are bivalently marked in ES cells suggesting that their aberrant methylation may reflect developmental processes. We investigated this possibility by analysing promoter methylation in 19 breast cancer cell lines, 10 normal tissues and 47 primary breast tumours. In order to determine the role of DNA methylation in silencing genes in breast cancer, we also examined the effects of the demethylating agent 5-aza-2?-deoxycytidine on gene expression in 3 breast cancer cell lines and HCT116 cells. Gene expression changes were also assayed in the DNA methyltransferase deficient HCT116 DKO cell line. Our findings implicate aberrant DNA methylation as a marker of cell lineage rather than tumour progression and suggest that, in most cases, it does not cause the repression with which it is associated. A number of human breast cancer cell lines, breast tumours and normal tissues were analysed on Illumina Infinium Methylation27 Beadchips to assay promoter methylation. Selected cell lines were analysed on expression arrays before and after treatment with 5-aza-2'-deoxycytidine.
2011-03-07 | E-GEOD-26990 | biostudies-arrayexpress
Project description:Promoter methylation was assayed in a number of breast cancer and control normal samples along with the effects of 5'-aza-2'-deoxycytidine on breast cancer cell line transcriptomes. Aberrant promoter hypermethylation is frequently observed in cancer. The potential for this to contribute to tumour development depends on whether the genes affected are repressed because of their methylation. Many aberrantly methylated genes play important roles in development and are bivalently marked in ES cells suggesting that their aberrant methylation may reflect developmental processes. We investigated this possibility by analysing promoter methylation in 19 breast cancer cell lines, 10 normal tissues and 47 primary breast tumours. In order to determine the role of DNA methylation in silencing genes in breast cancer, we also examined the effects of the demethylating agent 5-aza-2?-deoxycytidine on gene expression in 3 breast cancer cell lines and HCT116 cells. Gene expression changes were also assayed in the DNA methyltransferase deficient HCT116 DKO cell line. Our findings implicate aberrant DNA methylation as a marker of cell lineage rather than tumour progression and suggest that, in most cases, it does not cause the repression with which it is associated.
2011-03-07 | GSE26990 | GEO