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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Breakpoint analysis of transcriptional and genomic profiles uncovers novel gene fusions spanning multiple human cancer types (exon expression)

ABSTRACT: Custom Agilent 8 x 15K microarray interrogating exon level expression of a set of genes previously known to be involved in oncogenic rearrangements. The goal of this study was to discover novel gene fusions by screening for exonic expression transitions within individual genes. Sixteen cancer samples and cell lines, including eight positive controls with known gene fusions and eight sarcoma specimens, where gene fusions have yet to be discovered, were hybridized against a common reference mRNA control (pooled from 11 diverse cell lines)

ORGANISM(S): Homo sapiens

SUBMITTER: Craig Giacomini

PROVIDER: E-GEOD-39287 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Breakpoint analysis of transcriptional and genomic profiles uncovers novel gene fusions spanning multiple human cancer types (exon expression)

Project description:Custom Agilent 8 x 15K microarray interrogating exon level expression of a set of genes previously known to be involved in oncogenic rearrangements. The goal of this study was to discover novel gene fusions by screening for exonic expression transitions within individual genes.

2013-05-31 | GSE39287 | GEO

Breakpoint analysis of transcriptional and genomic profiles uncovers novel gene fusions spanning multiple human cancer types (RNA-seq)

Project description:We report the design and implementation of a "breakpoint analysis" pipeline to discover novel gene fusions by tell-tale transcript level or genomic DNA copy number transitions occurring within genes. We use this method to prioritize candidate rearrangements from high density array CGH datasets as well as exon-resolution expression microarrays. We mine both publicly available data as well as datasets generated in our laboratory. Several gene fusion candidates were chosen for further characterization, and corresponding samples were profiled using paired end RNA sequencing to discover the identity of the gene fusion. Using this approach, we report the discovery and characterization of novel gene fusions spanning multiple cancer subtypes including angiosarcoma, pancreatic cancer, anaplastic astrocytoma, melanoma, breast cancer, and T-cell acute lymphoblastic leukemia. Taken together, this study provides a robust approach for gene fusion discovery, and our results highlight a more widespread role of fusion genes in cancer pathogenesis. Breakpoint analysis for the discovery of novel gene fusions across human cancers

2013-05-31 | E-GEOD-45133 | biostudies-arrayexpress

Breakpoint analysis of transcriptional and genomic profiles uncovers novel gene fusions spanning multiple human cancer types (RNA-seq)

2013-05-31 | GSE45133 | GEO

Breakpoint analysis of transcriptional and genomic profiles uncovers novel gene fusions spanning multiple human cancer types.

Project description: Not available

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Breakpoint analysis of transcriptional and genomic profiles uncovers novel gene fusions spanning multiple human cancer types (RNA-seq)

Project description: Not available

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Breakpoint analysis of transcriptional and genomic profiles uncovers novel gene fusions spanning multiple human cancer types

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

2013-05-31 | GSE45137 | GEO

Breakpoint analysis of transcriptional and genomic profiles uncovers novel gene fusions spanning multiple human cancer types

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

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Fusion partners influence cellular and molecular phenotypes of oncogenic BRAF fusions

Project description:Fusion genes can be oncogenic drivers in a variety of cancer types and represent potential targets for targeted therapy. The BRAF gene is frequently involved in oncogenic fusions, with fusion frequencies of 0.2-3% throughout different cancers. However, BRAF fusions rarely occur in the same gene configuration, potentially challenging personalized therapy design. In particular, the influence that is imposed by the wide variety of fusion partners on the oncogenic role of BRAF during tumor growth and drug response is unknown. Here, we used patient-derived colorectal cancer organoids to functionally characterize and cross-compare previously identified BRAF fusions containing various partner genes (AGAP3, DLG1 and TRIM24) with respect to cellular behaviour, downstream signaling activation and response to targeted therapies. We demonstrate that 5’ partner choice of BRAF fusions affects their subcellular localization and intracellular signaling capacity. In particular the DLG1-BRAF fusion protein showed distinct localization to the plasma membrane and exhibited increased activation of downstream MAPK signaling under unperturbed conditions. Moreover, phosphoproteomics and RNA sequencing identified distinct subsets of affected signaling pathways and altered gene expression of BRAF fusions. The different BRAF fusions exhibited varying sensitivities to simultaneous targeted inhibition of MEK and the EGF receptor family. However, all BRAF fusions conveyed resistance to targeted monotherapy against the EGF receptor family, suggesting that BRAF fusions should be screened alongside other MAPK pathway alterations to identify mCRC patients to exclude from cetuximab treatment

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ChIP-seq of TALE fusions

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ChIP-seq of TALE fusions

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