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

ABSTRACT: Targeted high resolution array comparative genomic hybridization of the 4p16.3 locus in seven glioblastoma patients

ORGANISM(S): Homo sapiens

PROVIDER: GSE42400 | GEO | 2012/12/01

SECONDARY ACCESSION(S): PRJNA181294

REPOSITORIES: GEO

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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.

2012-12-01 | E-GEOD-42400 | biostudies-arrayexpress

Gene expression profiling of glioblastoma cell lines transfected with FGFR3-TACC3

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.

2012-12-01 | E-GEOD-42401 | biostudies-arrayexpress

Gene expression profiling of glioblastoma cell lines transfected with FGFR3-TACC3

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

Gene expression profiling of glioblastoma cell lines transfected with FGFR3-TACC3

| S-ECPF-GEOD-42401 | biostudies-other

The tumorigenic FGFR3-TACC3 gene fusion escapes miR-99a regulation in glioblastoma.

Project description:Fusion genes are chromosomal aberrations that are found in many cancers and can be used as prognostic markers and drug targets in clinical practice. Fusions can lead to production of oncogenic fusion proteins or to enhanced expression of oncogenes. Several recent studies have reported that some fusion genes can escape microRNA regulation via 3'-untranslated region (3'-UTR) deletion. We performed whole transcriptome sequencing to identify fusion genes in glioma and discovered FGFR3-TACC3 fusions in 4 of 48 glioblastoma samples from patients both of mixed European and of Asian descent, but not in any of 43 low-grade glioma samples tested. The fusion, caused by tandem duplication on 4p16.3, led to the loss of the 3'-UTR of FGFR3, blocking gene regulation of miR-99a and enhancing expression of the fusion gene. The fusion gene was mutually exclusive with EGFR, PDGFR, or MET amplification. Using cultured glioblastoma cells and a mouse xenograft model, we found that fusion protein expression promoted cell proliferation and tumor progression, while WT FGFR3 protein was not tumorigenic, even under forced overexpression. These results demonstrated that the FGFR3-TACC3 gene fusion is expressed in human cancer and generates an oncogenic protein that promotes tumorigenesis in glioblastoma.

| S-EPMC3561838 | biostudies-literature

The tumorigenic fusion FGFR3-TACC3 escapes miR-99a regulation in glioblastoma

Project description:This SuperSeries is composed of the SubSeries listed below.

2012-12-01 | GSE42402 | GEO

Extra-CNS and dural metastases in <i>FGFR3::TACC3</i> fusion+ adult glioblastoma, IDH-wildtype.

Project description:BackgroundAdult glioblastomas (GBMs), IDH-wildtype, WHO grade 4 with FGFR3::TACC3 fusion have a better prognosis than standard GBMs. Whether this extended survival leads to late biological consequences is unknown. Although constituting only 4% of all GBMs, FGFR3::TACC3 fusion-positive GBMs manifest recurrent morphological features that allow prediction of this subtype, possibly affecting trial eligibility and/or targeted therapies. However, we have previously shown that an identical histological pattern can be present in wildtype examples, and conversely, occasional FGFR3::TACC3 fusion-positive tumors lack this stereotypic morphology; thus, ultimately molecular characterization is required. We now report for the first time an adult with FGFR3::TACC3 fusion-positive GBM showing archetypal histological features who developed extracranial metastases to provide further insight into potential behavior of the GBM type.MethodsReport of a 70-year-old man with left parietal GBM who developed 2 subsequent metastases, all 3 of which were assessed by next-generation sequencing (NGS) and DNA methylation.ResultsBiopsy-proven dural metastases occurred at 8 months and cervical lymph node metastasis at 12-month post-diagnosis before the patient succumbed at 23 months. By NGS, all 3 tumors showed FGFR3::TACC3 fusion as well as an additional PDZD2::TERT fusion of uncertain significance. DNA methylation profiling demonstrated mesenchymal subtype in the initial biopsy and RTKII subtype in subsequent dural and lymph node metastases, indicating intratumor spatial heterogeneity or temporal evolution.ConclusionRarely, FGFR3::TACC3 fusion-positive GBM patients may develop dural and extracranial metastatic spread, the latter with subclass switching on epigenomic analysis.

| S-EPMC9476975 | biostudies-literature

The tumorigenic fusion FGFR3-TACC3 escapes miR-99a regulation in glioblastoma

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2012-12-01 | E-GEOD-42402 | biostudies-arrayexpress

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.

2022-05-16 | GSE200647 | GEO

Targeted Therapy with Anlotinib for a Patient with an Oncogenic FGFR3-TACC3 Fusion and Recurrent Glioblastoma.

Project description:We describe a case of recurrent glioblastoma treated with anlotinib in this report. The patient was administered anlotinib 12 mg p.o. once every day (days 1-14, with a 21-day cycle) (anlotinib clinical study NCT04004975) and oral temozolomide chemotherapy 100 mg/m2 (days 1-7, days 15-21, 28-day cycle; 12 cycles). After 2 months of therapy, the patient achieved a partial response that has been maintained for >17 months of follow-up. Molecular characterization confirmed the presence of a TERT promoter mutation, wild-type IDH1/2, an FGFR3-TACC3 fusion, and FGFR3 amplification in the patient. Anlotinib is a multitarget tyrosine kinase inhibitor that was originally designed to inhibit VEGFR2/3, FGFR1-4, PDGFR?/?, and c-Kit. Patients with TERT promoter mutations and high-grade IDH-wild-type glioma have shorter overall survival than patients with IDH-wild-type glioma without TERT promoter mutations. However, this patient had a favorable clinic outcome, and FGFR3-TACC3 fusion may be a new marker for treatment of glioma with anlotinib. KEY POINTS: This case study is believed to be the first report that FGFR3-TACC3 fusion could be a novel indication to treat recurrent glioblastoma with the drug anlotinib. This case exhibited an exceptional response (maintained partial response >17 months) after 2-month combined therapy of anlotinib and oral temozolomide chemotherapy. This case also underscores the importance of molecular diagnosis for clinically complex cases. Tumor tissue-based assessment of molecular biomarkers in brain tumors has been successfully translated into clinical application.

| S-EPMC7930428 | biostudies-literature

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