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.
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.
Project description:Gene expression profiling of SNB19 and U251 glioblastoma cell lines transfected with the FGFR3-TACC3 fusion, FGFR3 wildtype and TACC3 wildtype constructs.
Project description:Gene expression profiling of SNB19 and U251 glioblastoma cell lines transfected with the FGFR3-TACC3 fusion, FGFR3 wildtype and TACC3 wildtype constructs. SNB19 and U251 cells were transfected with different clones of the FGFR3-TACC3 fusion and with wildtype FGFR3 and TACC3 constructs. Total RNA was extracted and hybridized onto Agilent dual channel gene expression microarrays. In each hybridization, empty vector transfected SNB19 or U251 cells were hybridized into the reference channel.
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.
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.
