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High-resolution Nanopore methylome-maps reveal random hyper-methylation at CpG-poor regions as driver of chemoresistance in leukemias.[RNA-Seq]

ABSTRACT: Aberrant DNA-methylation at CpG dinucleotides is a hallmark of cancer and is associated with the emergence of resistance to anti-cancer treatment, though molecular mechanisms and biological signifi- cance remain elusive. Genome-scale methylation maps by currently used methods are based on chemical modification of DNA and are best suited for analyses of methylation at CpG-rich regions (CpG islands). We report the first high-coverage whole-genome map in cancer using the long-read nanopore technol- ogy, which allows simultaneous DNA-sequence and -methylation analyses on native DNA. We analyzed clonal epigenomic/genomic evolution in Acute Myeloid Leukemias (AMLs) at diagnosis and relapse, af- ter chemotherapy. Long-read sequencing coupled to a novel computational method allowed definition of differential methylation at unprecedented resolution (> 99% CpGs), extending analyses of CpG is- lands to sparse CpGs, which represent half of all differentially-methylated regions. We showed that the

ORGANISM(S): Homo sapiens

PROVIDER: GSE213684 | GEO | 2023/04/12

REPOSITORIES: GEO

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High-resolution Nanopore methylome-maps reveal random hyper-methylation at CpG-poor regions as driver of chemoresistance in leukemias. [methylation]

Project description:Aberrant DNA-methylation at CpG dinucleotides is a hallmark of cancer and is associated with the emergence of resistance to anti-cancer treatment, though molecular mechanisms and biological signifi- cance remain elusive. Genome-scale methylation maps by currently used methods are based on chemical modification of DNA and are best suited for analyses of methylation at CpG-rich regions (CpG islands). We report the first high-coverage whole-genome map in cancer using the long-read nanopore technol- ogy, which allows simultaneous DNA-sequence and -methylation analyses on native DNA. We analyzed clonal epigenomic/genomic evolution in Acute Myeloid Leukemias (AMLs) at diagnosis and relapse, af- ter chemotherapy. Long-read sequencing coupled to a novel computational method allowed definition of differential methylation at unprecedented resolution (> 99% CpGs), extending analyses of CpG is- lands to sparse CpGs, which represent half of all differentially-methylated regions. We showed that the

2023-04-12 | GSE213685 | GEO

Epigenetic analysis of gastric cancer cell lines

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Methylation analysis of cancer and control samples.

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Project description:Genome wide DNA methylation profiling of gastric cancer cell lines. The Illumina Goldengate DNA methylation Beadchip was used to obtain DNA methylation profiles across 1,505 CpG CpGs in 20 gastric cancer cell lines. Bisulphite converted DNA from the 20 gastric cancer cell lines were hybridised to the Illumina Goldengate Methylation Beadchip

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Non-CpG island promoter hypomethylation and miR-149 regulate the expression of SRPX2 in colorectal cancer

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Methylation analysis of cancer and control samples.

Project description:DNA methylation profiling of cancer and control samples. The Illumina GoldenGate Methylation Cancer Panel I was used to obtain DNA methylation profiles across 1,505 CpG sites CpGs distributed across 807 genes in blood DNA specimens. DNA samples were extracted from blood specimens, bisulfite treated and subsequently used for GoldenGate Methylation Cancer Panel I Array (Illumina) according to manufacturer’s protocol together with normalization methylated, hemimethylated and unmethylated DNA controls (Qiagen).

2012-11-01 | E-GEOD-33614 | biostudies-arrayexpress

Non-CpG island promoter hypomethylation and miR-149 regulate the expression of SRPX2 in colorectal cancer

Project description:We used Illumina Infinium 27k Human DNA Methylation BeadChip v1.2 to assess genome-wide DNA methylation profiling of normal colon epithelial, adenomas and colorectal adenocarcinomas across approximately 27,000 CpGs in fresh frozen colorectal tissue samples. We found that cancer-associated methylation changes with impact on transcription occur nearly as frequent at non-CpG island as CpG island promoters in colorectal cancer (CRC). Samples included 6 normal colon epithelial tissue samples, 6 adenomas, and 30 colorectal adenocarcinomas. Bisulfite-converted DNA from the 42 samples were hybridised to the Illumina Infinium 27k Human Methylation Beadchip v1.2.

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DNA methylation profiling reveals novel biomarkers and important roles for DNA methyltransferases in prostate cancer

Project description:Genome wide DNA methylation profiling of normal and tumor prostate samples, as well as cultured primary prostate cells overexpressing DNA Methyltransferases (DNMTs) and EZH2 Candidate gene based studies have identified a handful of aberrant CpG DNA methylation events in prostate cancer. However, DNA methylation profiles have not been compared on a large scale between prostate tumor and normal prostate, and the mechanisms behind these alterations are unknown. In this study, we quantitatively profiled 95 primary prostate tumors and 86 healthy prostate tissue samples for their DNA methylation levels at 26,333 CpGs representing 14,104 gene promoters by using the Illumina HumanMethylation27 platform. A 2-class Significance Analysis of this dataset revealed 5,912 CpG sites with increased DNA methylation and 2,151 CpG sites with decreased DNA methylation in tumors (FDR < 0.8%). Prediction Analysis of this dataset identified 87 CpGs that are the most predictive diagnostic methylation biomarkers of prostate cancer. By integrating available clinical follow-up data, we also identified 69 prognostic DNA methylation alterations that correlate with biochemical recurrence of the tumor. To identify the mechanisms responsible for these genome-wide DNA methylation alterations, we measured the gene expression levels of several DNA methyltransferases (DNMTs) and their interacting proteins by TaqMan qPCR and observed increased expression of DNMT3A2, DNMT3B, and EZH2 in tumors. Subsequent transient transfection assays in cultured primary prostate cells revealed that DNMT3B1 and DNMT3B2 overexpression resulted in increased methylation of a substantial subset of CpG sites that also showed tumor-specific increased methylation. Bisulfite converted DNA from 193 samples were hybridized to the Illumina Infinium 27k Human Methylation Beadchip v1.2. The tissue samples (first 181) and the cultured cell samples (last 12) were normalized independently.

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Mapping of variable DNA methylation across multiple cell types defines a dynamic regulatory landscape of the human genome

Project description:DNA methylation is an important epigenetic modification involved in many biological processes and diseases. Many studies have mapped DNA methylation changes associated with embryogenesis, cell differentiation and cancer at a genome-wide scale. Our understanding of genome-wide DNA methylation changes in a developmental or disease-related context has been steadily growing. However, the investigation of which CpGs are variably methylated in different normal cell or tissue types is still limited. Here we present an in-depth analysis of 54 single-CpG-resolution DNA methylomes of normal human cell types by integrating high-throughput sequencing-based methylation data. We find that the percentage of unmethylated CpGs is relatively fixed regardless of cell type. However, which CpGs are unmethylated is cell-type specific. We categorize the 26 million human autosomal CpGs based on their methylation levels across multiple cell types to identify variably methylated CpGs. Among all the autosomal CpGs, 22.6% exhibit variable DNA methylation across cell types included in our study. These variably methylated CpGs form 66 thousand variably methylated regions (VMRs), encompassing 11% of the genome. By integrating a multitude of genomic data, we found that VMRs enrich for histone modifications indicative of enhancers, suggesting their role as regulatory elements marking cell type specificity. VMRs enrich for transcription factor binding sites in a tissue-dependent manner. Importantly, they enrich for GWAS variants, suggesting VMRs could potentially be implicated in disease and complex traits. Taken together, our results highlight the link among CpG methylation variation, genetic variation and disease risk in a tissue-specific manner for many human cell types. Processed data includes new Samples and 75 Samples from GSE16368 and 2 Samples from GSE51565.

2016-04-06 | E-GEOD-69894 | biostudies-arrayexpress

DNA methylation profiling reveals novel biomarkers and important roles for DNA methyltransferases in prostate cancer

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