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DNA methylation analysis of glioblastomas harboring FGFR3-TACC3 fusions identifies a methylation subclass with better patient survival.

ABSTRACT: DNA methylation analysis of glioblastomas harboring FGFR3-TACC3 fusions identifies a methylation subclass with better patient survival.

PROVIDER: PRJNA825641 | ENA |

REPOSITORIES: ENA

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DNA methylation analysis of glioblastomas harboring FGFR3-TACC3 fusions identifies a methylation subclass with better patient survival.

Project description:Genomewide DNA methylation array profiling of 244 gliobastoma and ganglioglioma samples to study FGFR3-TACC3 gene fusions and resolved into a new entity, glioblastoma IDH-wildtype, FGFR3-TACC3 fusion postive methylation outlier group (GBM-F3T3-O). GBM-F3T3-O showed a unique methylation profile and better survival than other glioblastoma patients. The methylation idat profiles were provided here.

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Microarray of Human astrocytes transduced with lentivirus expressing FGFR3-TACC3 treated with vehicle, FGFR3-TACC3 treated with the FGFR inhibitor PD173074 for 12h, FGFR3-TACC3-K508M treated with vehicle or empty vector treated with vehicle

Project description:In order to interrogate the transcriptional changes elicited by FGFR3-TACC3, we expressed the FGFR3-TACC3 fusion protein in human astrocytes and compared the global gene expression profiles of cells treated with a specific inhibitor of FGFR3-TK (PD173074) or vehicle. FGFR3-TACC3 expressing HA were also compared with HA that expressed the kinase-inactive FGFR3-TACC3 (FGFR3-TACC3-K508M) and HA transduced with the empty vector. Gene Ontology-guided enrichment map demonstrated that, besides the expected enrichment for mitotic activity, oxidative phosphorylation and mitochondrial biogenesis were the most significant biological functions enriched in HA expressing active FGFR3-TACC3.

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Project description:Gene expression profiling of SNB19 and U251 glioblastoma cell lines transfected with the FGFR3-TACC3 fusion, FGFR3 wildtype and TACC3 wildtype constructs.

2012-12-01 | GSE42401 | GEO

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Project description:To better understand the molecular mechanisms underlying altered-FGFR3 oncogenic activity in bladder carcinomas, we made use of RT112 cell lines, which were derived from a human bladder tumor and endogenously expressed the FGFR3-TACC3 fusion protein, the growth and transformation of these cell lines being dependent on activated-FGFR3 activity. We conducted a gene expression analysis using Affymetrix DNA arrays in this cell line treated or not with FGFR3 siRNAs.

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High resolution aCGH of the FGFR3-TACC3 locus in glioblastoma patients

Project description:Targeted high resolution array comparative genomic hybridization of the 4p16.3 locus in seven glioblastoma patients A custom Agilent CGH microarray based on the 105A backbone was designed with high probe coverage for 4p16.3. Tumor tissue from four FGFR3-TACC3 positive patients and three negative patients was hybridized onto the microarray for the purposes of identifying a tandem duplication causing the fusion gene.

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DNA Methylation subclass Receptor Tyrosine Kinase II (RTK II) is predictive for seizure development in glioblastoma patients

Project description:Background: Seizures can present at any time before or after the diagnosis of a glioma. Roughly, 25-30 % of glioblastoma (GBM) patients initially present with seizures, and an additional 30 % develop seizures during the course of the disease. Early studies failed to show an effect of general administration of anti-epileptic drugs for glioblastoma patients, since they were unable to stratify patients into high- or low- risk seizure groups. Methods: 112 patients, who underwent surgery for a GBM, were included. Genome- wide DNA methylation profiling was performed, before methylation subclasses and copy number changes inferred from methylation data were correlated with clinical characteristics. Independently, global gene expression was analyzed in GBM methylation subclasses from TCGA datasets (n=68). Results: Receptor tyrosine Kinase (RTK) II GBM showed a significantly higher incidence of seizures than RTK I and mesenchymal (MES) GBM (p<0.01). Accordingly, RNA expression datasets revealed an upregulation of genes involved in neurotransmitter synapses and vesicle transport in RTK II glioblastomas. In a multivariate analysis, temporal location (p=0.01, OR 6.35) and RTK II (p=0.03, OR 5.56) were most predictive for preoperative seizures. During postoperative follow-up, only RTK II remained significantly associated with the development of seizures (p<0.01, OR 8.23). Consequently, the need for antiepileptic medication and its increase due to treatment failure was highly associated with the RTK II methylation subclass (p<0.01). Conclusion: Our study shows a strong correlation of RTK II glioblastomas with preoperative and long-term seizures. These results underline the benefit of molecular glioblastoma profiling with important implications for postoperative seizure control.

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