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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Cytosine methylation data generated by HELP-tagging from human osteosarcoma biopsy samples

ABSTRACT: Osteosarcoma is the most common primary malignant bone tumor in children. Validated markers for disease prognosis available at diagnosis are lacking. No genome-wide DNA methylation studies linked to clinical outcomes have been reported in osteosarcoma. To address this, we tested the methylome at over 1.1 million loci in 15 osteosarcoma biopsy samples obtained prior to the initiation of therapy and correlated these molecular data with disease outcomes. At the tested loci, samples obtained from patients who experienced disease relapse were generally more methylated than those from patients who did not have recurrence. In samples from patients who went on to have recurrent disease, increased DNA methylation was found at gene bodies, intergenic regions and empirically-annotated candidate enhancers, whereas candidate gene promoters were unusual for a more balanced distribution of increased and decreased DNA methylation. A locus at the TLR4 gene demonstrates one of strongest associations between DNA methylation and five year event-free survival, with empirical annotation of this locus showing promoter characteristics. Our data indicate that DNA methylation information has potential to be predictive of outcome in pediatric osteosarcoma, and that both promoters and non-promoter loci are potentially informative in DNA methylation studies. 15 samples. HpaII libraries were compared to at least 3 MspI libraries from the same sample

ORGANISM(S): Homo sapiens

SUBMITTER: Jeremy Rosenblum

PROVIDER: E-GEOD-59200 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Human cervical cells HELP-tagging cytosine methylation data

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2016-08-22 | E-GEOD-76986 | biostudies-arrayexpress

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2015-09-20 | E-GEOD-67277 | biostudies-arrayexpress

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2015-12-22 | E-GEOD-64412 | biostudies-arrayexpress

Human embryonic stem cells HELP-tagging cytosine methylation data (Albert Einstein College of Medicine)

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2010-04-12 | E-GEOD-19937 | biostudies-arrayexpress

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2015-02-13 | E-GEOD-62592 | biostudies-arrayexpress

A restricted repertoire of cytosine methylation changes in neonates following intrauterine growth restriction

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2010-02-17 | E-GEOD-17727 | biostudies-arrayexpress

Tissue-specific dysregulation of DNA methylation in aging

Project description:The normal aging process is a complex phenomenon associated with physiological alterations in the function of cells and organs over time. Although an attractive candidate for mediating transcriptional dysregulation, the contribution of epigenetic dysregulation to these progressive changes in cellular function remains unclear. In this study, we employed the genome-wide HELP assay to define patterns of cytosine methylation throughout the rat genome, and the LUMA assay to measure global levels of DNA methylation in the same samples. We studied both liver and visceral adipose tissue, and demonstrated significant differences in DNA methylation with age at >5% of sites analyzed. Furthermore, we showed that epigenetic dysregulation with age is a highly tissue-dependent phenomenon. The most distinctive loci were located at intergenic sequences and conserved non-coding elements, and not at promoters nor at CG-dinucleotide dense loci. Finally, we demonstrated that changes in methylation occur consistently near genes that are involved in metabolism and metabolic regulation, implicating their potential role in the pathogenesis of age-related diseases. We conclude that different patterns of epigenetic dysregulation occur in each tissue over time and may cause some of the physiological changes associated with normal aging. Direct comparison of DNA methylation in 18 samples belonging to four groups: young liver (n=6), young adipose tissue (n=4), old liver (n=5), old adipose tissue (n=3), isolated from F344*BN rats (young at ~3 months, old at ~18 months). Each microarray consists of a two-color comparison of a methylation-sensitive representation of the genome (HpaII) with an internal methylation-insensitive control/reference (MspI).

2010-05-01 | E-GEOD-17332 | biostudies-arrayexpress

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