Genome-wide profiling of DNA methylation and expression identifies CIMP in myelodysplastic syndrome [Illumina]
ABSTRACT: To identify genes hypermethylated and transcriptionally downregulated, we have employed the Illumina Infinium HumanMethylation450 BeadChip and Agilent SurePrint G3 Human Gene Expression 8x60K. And we validated selected genes in cases and controls. eventually we estalished CIMP of MDS. Bisulphite converted DNA from the 4 patients and 4 controls were hybridised to the Illumina Infinium 450k Human Methylation Beadchip
Project description:To identify genes hypermethylated and transcriptionally downregulated, we have employed the Illumina Infinium HumanMethylation450 BeadChip and Agilent SurePrint G3 Human Gene Expression 8x60K.And we validated selected genes in cases and controls. eventually we estalished CIMP of MDS. The gene expressions of four cases and four controls were measured.
Project description:Microarray methylation (Infinium®HumanMethylation 450 BeadChip from Illumina) was performed on 11 normal and 9 chronic periodontitis (CP) patients Bisulphite converted DNA from the 20 samples were hybridised to the Illumina Infinium 450k Human Methylation Beadchip
Project description:Microarray methylation (Infinium¨HumanMethylation 450 BeadChip from Illumina) was performed on 12 normal and 10 chronic periodontitis (CP) patients Bisulphite converted DNA from the 22 samples were hybridised to the Illumina Infinium 450k Human Methylation Beadchip
Project description:Genome wide DNA methylation profiling of 3 patient-derived colorectal cancer samples with different CIMP profiles. The Illumina Infinium 450k Human DNA methylation Beadchip was used to obtain DNA methylation profiles across approximately 450,000 CpGs Bisulphite converted DNA from the 3 samples were hybridised to the Illumina HumanMethylation450 BeadChip
Project description:Genome wide DNA methylation profiling of muscle cells extracted from healthy donors at different ages. The Illumina Infinium Human Methylation 450 BeadChip was used to obtain DNA methylation profiles across > 485,000 methylation sites. The muscle cells were extracted from young adults (18-40 years old) and elderly (>70 years old)(n=3 per group, 2 groups : Young and aged adult). Bisulphite converted DNA from the 6 samples were hybridized to the Illumina Infinium Human Methylation 450 BeadChip
Project description:With the whole genome SNP array information obtained from tumor and matched normal control, we could evaluate the acquired copy number variations (CNVs) and uniparental disomies (UPDs) . Seven MDS patients in a whole genome sequencing project were included in this experiment. To detect acquired CNVs and UPDs in MDS patients, we genotyped both CD34+ cell from bone marrow and matched skin tissue.
Project description:In short: Genome wide promoter DNA methylation profiling of 43 T-ALL samples and 5 T-cell controls (normal bone marrow and stimulated T-cells) . The Illumina Infinium 27k Human DNA methylation Beadchip v1.2 was used to obtain DNA methylation profiles across approximately 27,000 CpGs. Manuscript abstract: Background: Treatment of pediatric T-cell acute lymphoblastic leukemia (T-ALL) has improved, but there is a considerable fraction of patients experiencing a poor outcome. There is a need for better prognostic markers and aberrant DNA methylation is a candidate in other malignancies, but its potential prognostic significance in T-ALL is hitherto undecided. Design and Methods: Genome wide promoter DNA methylation analysis was performed in pediatric T-ALL samples (n=43) using arrays covering >27000 CpG sites. Clinical outcome was evaluated in relation to methylation status and compared with a contemporary T-ALL group not tested for methylation (n= 32). Results: Based on CpG island methylator phenotype (CIMP), T-ALL samples were subgrouped as CIMP+ (high methylation) and CIMP- (low methylation). CIMP- T-ALL patients had significantly worse overall and event free survival (p=0.02 and p=0.001, respectively) compared to CIMP+ cases. CIMP status was an independent factor for survival in multivariate analysis including age, gender and white blood cell count. Analysis of differently methylated genes in the CIMP subgroups showed an overrepresentation of transcription factors, ligands and polycomb target genes. Conclusions: We identified global promoter methylation profiling as being of relevance for subgrouping and prognostication of pediatric T-ALL. Bisulphite converted DNA from the 48 samples were hybridised to the Illumina Infinium 27k Human Methylation Beadchip v1.2
Project description:Both genetic and epigenetic aberrations are linked by intricate crosstalk, and can either individually or in synergy lead to the development of cancer. Accumulating evidence suggests that epigenetic changes such as alterations in DNA methylation play a crucial role in ESCC. We performed a Illumina Infinium HumanMethylation450 BeadChip to examine the global methylation signature of esophageal squamous cell carcinoma of Chinese patients. DNA methylation profiles of esophageal squamous cell carcinoma (4 samples), paired adjacent normal surrounding tissues (4 samples) and normal esophagus mucosa from healthy individuals (4 samples) were generated using Infinium methylation 450K BeadChips from Illumina (Illumina, San Diego, USA).
Project description:To address the global impact of PARP-1 on DNA methylation, we treated cells with PJ34 (PARylation inhibitor) and isolated genomic DNA from vehicle and PJ34 treated cells. This DNA was bisulfite treated and hybridized to the Illumina infinium Methylation 450 Beadchip. We next used these RNA-seq data sets (control, PARP-1 KD and PARylation inhibited) to assess whether PARP plays a role in DNA methylation by assessing differential methylation patterns. PARP1 mediates methylation patterns. DNA from vehicle and PJ34 (PARylation inhibited) cells. 750ng of geneomic DNA was bisulfite converted and used for the Illumia infinium HD methylation assay.
Project description:Glioma CIMP (G-CIMP) is a powerful determinant of tumor pathogenicity but the molecular cause of G-CIMP is a fundamental question that is unresolved. Here, we show that mutation of a single gene, isocitrate dehydrogenase 1 (IDH1), directly causes the G-CIMP in gliomas by remodeling the methylome. In this study 81 glioma clinic samples (49 CIMP+ and 32 CIMP-) were analyzed. Parental IDH1 wild-type and IDH1 mutant cells were passaged until passage 50.