Differential gene methylation in paired glioblastomas suggests a role of microenvironment in tumor progression
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Agusti Alentorn
PROVIDER: E-MTAB-3476 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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2016-02-26 | E-MTAB-3274 | biostudies-arrayexpress
Project description:Systemic lupus erythematosus (SLE) is a chronic-relapsing autoimmune disease of incompletely understood etiology. Recent evidence strongly supports an epigenetic contribution to the pathogenesis of lupus. To understand the extent and nature of dysregulated DNA methylation in lupus T cells, we performed a genome-wide DNA methylation study in CD4+ T cells from 12 lupus patients and 12 normal healthy controls. Cytosine methylation was quantified in 27,578 CG pairs located within the promoter regions of 14,495 genes. We identified 236 hypomethylated and 105 hypermethylated CG sites in lupus CD4+ T cells compared to normal controls, consistent with a global hypomethylation in lupus T cells. Further analysis identified hypomethylation in genes involved in connective tissue development including CD9, MMP9, and PDGFRA. Hypermethylated genes highlight “response to nutrients” ontology such as folate biosynthesis, suggesting a link between environmental factor and lupus and emphasizing the role of folate in DNA methylation. In addition, the transcription factor RUNX3 was hypermethylated in lupus CD4+ T cells. Protein-protein interaction maps identified a transcription factor, HNF4a, as a regulatory hub affecting a number of differentially methylated genes. Functional annotations such as apoptosis is also overrepresented. Further, our data indicate that the methylation status of certain genes predicts disease activity in lupus patients. This work provides a foundation to begin identifying novel pathogenic pathways in lupus T cells and developing novel epigenetic biomarkers for disease activity in lupus. We employed microarray-based technologies to perform a genome-wide DNA methylation assay and quantify CD4+ T cell DNA methylation levels at 27,578 CG sites spanning 14,495 genes of 11 lupus patients and 12 healthy controls.
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Project description:A Cartes d'Identite des Tumeurs (CIT) project from the french Ligue Nationale Contre le Cancer (http://cit.ligue-cancer.net: Anaplastic oligodendrogliomas (AOs) are rare primary brain tumors which are generally incurable with few treatment targets identified. Most oligodendrogliomas have chromosome 1p/19q co-deletion and IDH mutation. We analyzed 51 AOs by whole-exome and/or transcriptome sequencing identifying previously reported frequent somatic mutations in CIC and FUBP1 genes. We also identified recurrent mutations in TCF12 (11% of IDHmut-codel) which encodes basic helix-loop-helix (bHLFH) transcription factor 12 which is an oligodendrocyte-related transcription factor in IDHmut-codel tumors. Strikingly, the somatic mutations (encoding E548R and R602M substitutions) have not been reported previously in cancer but are identical to germline mutations causing craniosynostosis. Incorporating TCGA data on 43 AO tumors also implicates functional mutation of SMARCA4, NOTCH1, NOTCH2, SETD2, RBPJ and ARID1A/1B. These data are compatible with the combined deregulation of metabolism, chromatin organization/remodeling and Notch-pathway genes in AO oncogenesis. Our analysis provides further insights into the unique and shared pathways driving AO and new targets for therapeutic intervention.
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