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Methylation detection Oligonucleotide Microarray Analysis: high resolution method for CpG island methylation detection

ABSTRACT: This SuperSeries is composed of the following subset Series: GSE15746: Methylation detection Oligonucleotide Microarray Analysis: high resolution method for CpG island methylation detection 1 GSE15747: Methylation detection Oligonucleotide Microarray Analysis: high resolution method for CpG island methylation detection 2 Refer to individual Series

ORGANISM(S): Homo sapiens

SUBMITTER: Chunlao Tang

PROVIDER: E-GEOD-15801 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Methylation detection oligonucleotide microarray analysis: a high-resolution method for detection of CpG island methylation.

Kamalakaran Sitharthan S Kendall Jude J Zhao Xiaoyue X Tang Chunlao C Khan Sohail S Ravi Kandasamy K Auletta Theresa T Riggs Michael M Wang Yun Y Helland Aslaug A Naume Bjørn B Dimitrova Nevenka N Børresen-Dale Anne-Lise AL Hicks Jim J Lucito Robert R

Nucleic acids research 20090527 12

Methylation of CpG islands associated with genes can affect the expression of the proximal gene, and methylation of non-associated CpG islands correlates to genomic instability. This epigenetic modification has been shown to be important in many pathologies, from development and disease to cancer. We report the development of a novel high-resolution microarray that detects the methylation status of over 25,000 CpG islands in the human genome. Experiments were performed to demonstrate low system ...[more]

PMID: 19474344

Similar Datasets

Methylation detection Oligonucleotide Microarray Analysis: high resolution method for CpG island methylation detection 2

Project description:Methylation of CpG islands associated with genes can affect the expression of the proximal gene, and methylation of non associated CpG islands correlates to genomic instability. This epigenetic modification has been shown to be important in many pathologies, from development and disease to cancer. We report the development of a novel high-resolution microarray that detects the methylation status of over 25,000 CpG islands in the human genome. Experiments were performed to demonstrate low system noise in the methodology and that the array probes have a high signal to noise ratio. Methylation measurements between different cell lines were validated demonstrating the accuracy of measurement. We then identified alterations in CpG islands, both those associated with gene promoters, as well as non-promoter associated islands in a set of breast and ovarian tumors. We demonstrate that this methodology accurately identifies methylation profiles in cancer and in principle it can differentiate any CpG methylation alterations and can be adapted to analyze other species. We have developed a method to profile genome wide methylation. 7 ovarian normal samples and 11 tumor samples from other individuals were analyzed for CpG methylation. After inter array normalization, the tumor samples were taken together and the methylation compared to that of the normal samples to identify regions of the CpG islands that are significantly altered between the two datasets. Some of these regions were validated for their methylation as a proof of principle for the method.

2010-05-19 | E-GEOD-15747 | biostudies-arrayexpress

Methylation detection Oligonucleotide Microarray Analysis: high resolution method for CpG island methylation detection 1

Project description:Methylation of CpG islands associated with genes can affect the expression of the proximal gene, and methylation of non associated CpG islands correlates to genomic instability. This epigenetic modification has been shown to be important in many pathologies, from development and disease to cancer. We report the development of a novel high-resolution microarray that detects the methylation status of over 25,000 CpG islands in the human genome. Experiments were performed to demonstrate low system noise in the methodology and that the array probes have a high signal to noise ratio. Methylation measurements between different cell lines were validated demonstrating the accuracy of measurement. We then identified alterations in CpG islands, both those associated with gene promoters, as well as non-promoter associated islands in a set of breast and ovarian tumors. We demonstrate that this methodology accurately identifies methylation profiles in cancer and in principle it can differentiate any CpG methylation alterations and can be adapted to analyze other species. We have developed a method to profile genome wide methylation. 12 breast normal samples and matching tumors from these individuals and an additional 28 tumor samples from other individuals were analyzed for CpG methylation. After inter array normalization, the tumor samples were taken together and the methylation compared to that of the normal samples to identify regions of the CpG islands that are significantly altered between the two datasets. Some of these regions were validated for their methylation as a proof of principle for the method.

2009-04-28 | E-GEOD-15746 | biostudies-arrayexpress

Identification of Tumor Suppressors and Oncogenes from Genomic and Epigenetic Features in Ovarian Cancer

Project description:This SuperSeries is composed of the following subset Series: GSE27940: Methylation detection Oligonucleotide Microarray Analysis: high resolution method for CpG island methylation detection 3. GSE27943: Gene Expression Array of Human Ovarian Cancer. GSE28013: Representational Oligonucleotide Microarray Analysis (ROMA) array for Copy Number Variation Detection. Refer to individual Series

2011-10-16 | E-GEOD-28015 | biostudies-arrayexpress

Methylation detection Oligonucleotide Microarray Analysis: high resolution method for CpG island methylation detection 3.

Project description:The identification of genetic and epigenetic alterations from primary tumor cells has become a common method to identify genes critical to the development and progression of cancer. We provide a bioinformatic analysis of copy number variation and DNA methylation covering the genetic landscape of ovarian cancer tumor cells. We individually examined the copy number variation and DNA methylation for 44 primary ovarian cancer samples and 7 ovarian normal samples using our MOMA-ROMA technology and Affymetrix expression data as well as 379 tumor samples analyzed by The Cancer Genome Atlas. We have identified 346 genes with significant deletions or amplifications among the tumor samples. Utilizing associated gene expression data we predict 156 genes with significantly altered copy number and correlated changes in expression. We identify changes in DNA methylation and expression for all amplified and deleted genes. We predicted 615 potential oncogenes and tumor suppressors candidates by integrating these multiple genomic and epigenetic data types. We have developed a method to profile genome wide methylation. 7 ovarian normal samples and 44 tumor samples from other individuals were analyzed for CpG methylation. After inter array normalization, the tumor samples were taken together and the methylation compared to that of the normal samples to identify regions of the CpG islands that are significantly altered between the two datasets. Some of these regions were validated for their methylation as a proof of principle for the method. Kamalakaran S., et. al. Mol Oncol. 2011;5:77-92 (PMID: 21169070).

2011-10-16 | E-GEOD-27940 | biostudies-arrayexpress

Suppression of the chromatin remodeling protein CHD3 and platinum resistance in ovarian cancer

Project description:Epithelial ovarian cancer is the leading cause of death from gynecological malignancies. Currently platinum-based chemotherapy, coupled with a taxane based drug is the primary treatment for ovarian cancer. Approximately 25% of patients either present with or rapidly develop resistance to platinum based chemotherapy and all recurrent tumors ultimately become resistant. Epigenetic modifications have been associated with tumor formation and progression and may contribute to therapy response. We performed a methylation screen on a set of tumors and have found a number of genes and family members differentially methylated between resistant patients and sensitive patients. Here we show that loss of expression of CHD3, a member of the Mi-2/NuRD complex, causes increased resistance to platinum chemotherapy drugs. Additionally, ovarian cell lines transcriptionally silenced for CHD3 are more invasive, have migratory ability, and display a transformed epithelial to mesenchymal (EMT) phenotype. Taken together, we provide the first evidence of a role for CHD3 as an important epigenetic regulator of chemoresistance in ovarian cancer and hypothesize EMT as one of the underlying mechanisms. Furthermore, CHD3 expression might represent a therapy response predictor and could be a future therapeutic target for ovarian cancer. We have developed a method to profile genome wide methylation. 71 ovarian tumor samples and 9 normal tissue samples from individuals were analyzed for CpG methylation. Some of these regions were validated for their methylation as a proof of principle for the method. Kamalakaran S., et. al. Mol Oncol. 2011;5:77-92 (PMID: 21169070).

2012-05-14 | E-GEOD-33011 | biostudies-arrayexpress

Transcription profiling of wild type and ZakA and GskA knock-out Dictyostelium discoideum to investigate the Zak1-GSK-3 signalling pathway

Project description:GskA, the Dictyostelium GSK-3 orthologue, is modified and activated by the dual-specificity tyrosine kinase Zak1 and the two kinases form part of a signalling pathway that responds to extracellular cAMP. We identify potential cellular effectors for the two kinases by analysing their null mutants. There are proteins and mRNAs that are altered in abundance in only one or other of the two mutants, indicating that each kinase has some unique functions. However, proteomic and micro-array analysis respectively identified 3 proteins and 37 genes that are similarly mis-regulated in both mutant strains. The positive correlation between the array data and the proteomics data is consistent with the Zak1-GskA signalling pathway functioning by directly or indirectly regulating gene expression. The discoidin 1 genes are positively regulated by the pathway while the abundance of the H5 protein is negatively regulated. Two of the targets, H5 and discoidin 1, are well-characterised markers for early development, indicating that the Zak1-GskA pathway plays a role in development earlier than previously observed.

2007-10-24 | E-SGRP-4 | biostudies-arrayexpress

Transcription profiling of Dictyostelium discoides mutant cell type aspidocyte induced by heavy meatals and antibiotics

Project description:We describe the serendipitous discovery and first characterization of a new resistant cell type from Dictyostelium, which we propose to call the aspidocyte (aspida: Greek for shield). These cells are induced from amoebae by a range of toxins including heavy metals and antibiotics, and were first detected by their striking resistance to detergent lysis. Aspidocytes are separate, rounded or irregular shaped cells that are immotile but remain fully viable; once the toxic stress is removed, they revert to amoeboid cells within an hour. Induction takes a few hours and is completely blocked by the protein synthesis inhibitor cycloheximide. Aspidocytes lack a cell wall and their resistance to detergent lysis is active, requiring continued energy metabolism, and may be assisted by a complete cessation of endocytosis, as measured by uptake of the dye FM1-43. Microarray analysis shows that aspidocytes have a distinct pattern of gene expression with a number of genes up-regulated that are predicted to be involved in lipid metabolism. Aspidocytes were initially detected in a hypersensitive mutant, in which the AMP deaminase gene is disrupted, suggesting that the inductive pathway involves AMP levels or metabolism. Since aspidocytes can also be induced from wild-type cells and are much more resistant than amoebae to a membrane disrupting antibiotic, it is possible that they are an adaptation allowing Dictyostelium cells to survive a sudden onslaught of toxins in the wild.

2007-02-06 | E-SGRP-5 | biostudies-arrayexpress

Identification of Myc-regulated microRNAs in human P493 cells

Project description:We previously described the use of a spotted oligonucleotide array to identify the mir-17 cluster as a direct transcriptional target of Myc. In order to determine whether Myc regulates additional miRNAs, we produced custom microarrays with an expanded set of probes capable of assaying the expression of 313 human miRNAs and 233 mouse miRNAs. P493-6 cells which are Epstein-Barr virus-immortalized human B cells that harbor a tetracycline (tet)-repressible allele of Myc were studied. These cells are tumorigenic in immunocompromised mice and represent a model of human B cell lymphoma. miRNA expression profiles were examined in the high Myc (-tet) and low Myc (+tet) state. Keywords: Dose response P493 cells with high Myc (-tet) and low Myc (+tet) were compared.

2007-12-05 | E-GEOD-9070 | biostudies-arrayexpress

Mesenchymal stem cell labelings with ferritin

Project description:Mesenchymal stem cells (MSC) omplexed to different transfection agents (R60, R200, DOSPER, jetPei, Pulsin). Two MSC populations (h21 and h24) and two passages (P2 and P4) were tested with different labelings. In a direct design experiment each sample was compared to its unlabeled control sample. Keywords: Human gene expression study Reference design with unlabeled cells in the Cy3 reference channel, and labeled cells in the Cy5 channel.

2010-05-16 | E-GEOD-11470 | biostudies-arrayexpress

Clock genes in human oral mucosa

Project description:Circadian rhythms are daily oscillations of multiple biological processes driven by endogenous clocks. Imbalance of these rhythms has been associated with cancerogenesis in humans. To further elucidate the role of the circadian clock in cellular growth control, tumor suppression and cancer treatment, a standard of circadian gene regulations in healthy men is essential. Comparative microarray analyses were conducted investigating the relative mRNA expression of clock genes throughout a 24-hour period in biopsies obtained from oral mucosa of eight healthy diurnally active male study participants. A custom-designed oligo-based microarray which in addition to oncogenes and inflammatory genes contains probes for 20 clock genes and 70 clock-associated genes in human was used. Keywords: Human gene expression study Reference design with Cy3 labeled uniRNA and Cy5 labeled sample RNA.

2010-05-16 | E-GEOD-11469 | biostudies-arrayexpress

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