Ontology highlight
ABSTRACT:
PROVIDER: PRJNA148709 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:DNA hypermethylation in breast cancer: breast cancer tissues vs. normal breast tissues
| PRJNA154299 | ENA
Project description:This SuperSeries is composed of the following subset Series: GSE33445: DNA hypermethylation in breast cancer: breast cancer tissues vs. normal breast tissues GSE33447: Gene expression profiles in breast cancer: breast cancer tissues vs. normal breast tissues Refer to individual Series
2011-11-11 | E-GEOD-33450 | biostudies-arrayexpress
Project description:Gene expression profiles in breast cancer: breast cancer tissues vs. normal breast tissues
| PRJNA154301 | ENA
Project description:DNA hypermethylation in colorectal cancer: Colorectal cancer tissues vs. Adjacent non-tumor tissues
| PRJNA148895 | ENA
Project description:Microarray is widely used to monitor gene expression changes in breast cancer. The transcriptomic changes in breast cancer is commonly occured during the transition of normal cells to cancerous cells. This is the first study on gene expression profiling of multi ethnic of Malaysian breast cancer patients (Malays, Chinese and Indian). We aim to identify differentially expressed genes between tumors and normal tissues. We have identified a set of 33 significant differentially expressed genes in the tumor vs. normal group at p<0.001. We study the gene expression patterns of 43 breast tumors and their paired normal control by using Affymetrix genechip U133A. We have identified a set of 33 significant differentially expressed genes in the tumor vs. normal group at p<0.001.
2009-04-28 | GSE15852 | GEO
Project description:Breast cancer remains a leading cause of cancer-related death, for which the majority of deaths result from metastases. Von Willebrand factor C and EGF domain (VWCE) is a member of the Von Willebrand factor (VWF) gene family; however, its function, regulatory mechanism, and clinical value in breast cancer remain unclear. In the present study, we sought to elucidate the role of VWCE in breast cancer metastasis. We examined the expression of VWCE in breast cancer tissues and normal control tissues of 50 breast cancer patients. We found that VWCE expression was downregulated in breast cancer cells and tissues compared to normal breast epithelial cells or the adjacent normal tissues. To explore the role of VWCE in human breast cancer development, we introduced a VWCE-overexpressing or control lentiviral vector into the breast cancer MDA-MB-453 and MDA-MB-231 lines in vitro. The overexpression of VWCE inhibited the proliferation, migration, invasion, and chemoresistance of the breast cancer cell lines. More import
2020-09-29 | PXD021733 |
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:Aberrant DNA methylation is frequently observed in breast cancer. However, the relationship between methylation patterns and the heterogeneity of breast cancer has not been comprehensively characterized. Whole-genome DNA methylation analysis using 450K Illumina BeadArrays was performed on 188 human breast tumors. Unsupervised bootstrap consensus clustering was performed to identify DNA methylation epigenetic subgroups (epitypes). The Cancer Genome Atlas data, incluing methylation profiles of 669 human breast tumors, was utilized for validation. The identified epitypes were characterized by integration with publicly available genome-wide data, including gene expression levels, DNA copy numbers, whole-exome sequencing data, and chromatin states. We identified seven breast cancer epitypes. One epitype was distinctly associated with basal-like tumors and with BRCA1 mutations, one epitype contained a subset of ERBB2-amplified tumors characterized by multiple additional amplifications and the most complex genomes, and one epitype displayed a methylation profile similar to normal epithelial cells. Luminal tumors were stratified into the remaining four epitypes, with differences in promoter hypermethylation, global hypomethylation, proliferative rates and genomic instability. We observed two dominant patterns of aberrant methylation in breast cancer. One pattern, constitutively methylated in both basal-like and luminal breast cancer, was linked to genes with promoters in a Polycomb-repressed state in normal epithelial cells and displayed no correlation to gene expression levels. The second pattern correlated with gene expression levels and was associated with methylation in luminal tumors and genes with active promoters in normal epithelial cells. Our results suggest that hypermethylation patterns in basal-like breast cancer may have limited influence on tumor progression and instead reflects the repressed chromatin state of the tissue of origin. On the contrary, hypermethylation patterns specific to luminal breast cancer influence gene expression, may contribute to tumor progression, and may present an actionable epigenetic alteration in some luminal breast cancers.
2016-02-29 | GSE75067 | GEO
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
Project description:Aberrant DNA methylation is frequently observed in breast cancer. However, the relationship between methylation patterns and the heterogeneity of breast cancer has not been comprehensively characterized. Whole-genome DNA methylation analysis using 450K Illumina BeadArrays was performed on 188 human breast tumors. Unsupervised bootstrap consensus clustering was performed to identify DNA methylation epigenetic subgroups (epitypes). The Cancer Genome Atlas data, incluing methylation profiles of 669 human breast tumors, was utilized for validation. The identified epitypes were characterized by integration with publicly available genome-wide data, including gene expression levels, DNA copy numbers, whole-exome sequencing data, and chromatin states. We identified seven breast cancer epitypes. One epitype was distinctly associated with basal-like tumors and with BRCA1 mutations, one epitype contained a subset of ERBB2-amplified tumors characterized by multiple additional amplifications and the most complex genomes, and one epitype displayed a methylation profile similar to normal epithelial cells. Luminal tumors were stratified into the remaining four epitypes, with differences in promoter hypermethylation, global hypomethylation, proliferative rates and genomic instability. We observed two dominant patterns of aberrant methylation in breast cancer. One pattern, constitutively methylated in both basal-like and luminal breast cancer, was linked to genes with promoters in a Polycomb-repressed state in normal epithelial cells and displayed no correlation to gene expression levels. The second pattern correlated with gene expression levels and was associated with methylation in luminal tumors and genes with active promoters in normal epithelial cells. Our results suggest that hypermethylation patterns in basal-like breast cancer may have limited influence on tumor progression and instead reflects the repressed chromatin state of the tissue of origin. On the contrary, hypermethylation patterns specific to luminal breast cancer influence gene expression, may contribute to tumor progression, and may present an actionable epigenetic alteration in some luminal breast cancers. Genome-wide DNA methylation analysis of 188 breast cancers using Illumina Human Methylation 450K Beadchips.
2016-02-29 | E-GEOD-75067 | biostudies-arrayexpress