Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Probing downstream effects of ALK and ROS1 fusion oncogenes in Glioma using proteomics

ABSTRACT: To identify targets of aberrantly expressed RTK-fusion oncogenes, serine/threonine and tyrosine phosphorylation signatures in transgenic cells lines expressing different RTK-fusion oncogenes were compared with their respective kinasedead mutant counterparts. Comparing the differentially phosphorylated proteins between the different RTK fusions were used to identify commonly deregulated pathways as well as pathways specifically targeted by individual RTK-fusions.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture

DISEASE(S): Brain Glioma

SUBMITTER: Ana Sofia Guerreiro Stücklin

LAB HEAD: Ana Sofia

PROVIDER: PXD059984 | Pride | 2026-01-22

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	20220225_002_S362862_TMT18_f1_P.raw	Raw
	20220225_003_S362862_TMT18_f2_P.raw	Raw
	20220225_004_S362862_TMT18_f3_P.raw	Raw
	20220225_005_S362862_TMT18_f4_P.raw	Raw
	20220225_006_S362862_TMT18_f5_P.raw	Raw

Items per page:

1 - 5 of 74

Similar Datasets

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

2020-01-16 | PXD013461 | Pride

First Generation Tools for the Modeling of Capicua-Family Fusion Oncoprotein-Driven Cancers (April 2023 Dataset)

Project description:The rearrangement of separate genes into neomorphic fusion oncogenes can occur after chromosomal damage and repair, causing cancer. In the case of sarcomas, several tumor types are driven by fusion oncogenes comprised of various partner genes. We study fusions involving capicua (CIC), a developmental transcriptional repressor whose fusion to 3' partner genes including DUX4, NUTM1, and LEUTX drives devastating tumors of the soft tissue, central nervous system, and spine. Here we develop the first tools to investigate previously understudied fusions of CIC and ATXN1 and express them in 293T cells to uncover convergent/divergent biology between various CIC-family fusions depending on what the specific partner genes are.

2025-05-13 | GSE295624 | GEO

First Generation Tools for the Modeling of Capicua-Family Fusion Oncoprotein-Driven Cancers (February 2025 Dataset)

2025-05-13 | GSE295625 | GEO

First Generation Tools for the Modeling of Capicua-Family Fusion Oncoprotein-Driven Cancers (May 2024 Dataset)

2025-05-13 | GSE295623 | GEO

Identification of PP1-fusion phosphatase substrates

Project description:This experiments was designed to identify substrates of holophosphatase complexes of PP1 and its specificity-determining regulator proteins. We generated fusions of Flag-tagged Protein Phosphatase 1 fusions with Phactr1-4, Neurabin, Spinophilin, PPPR15A, PPP1R15B, and PNUTS, in each case including known protein interaction domains immediately C-terminal to the PP1-binding sequences. Each fusion protein was stably expressed in 293 Flp-In TRex cells using a tetracycline inducible vector. To investigate the substrate specificities of the PP1-fusion proteins, we performed Tandem-Mass-Tag (TMT) phosphoproteomics. Fractionated peptides were measured in both MS2 and MS3 modes for maximal identification and quantification. Expression of the PP1-fusions revealed numerous phosphorylation sites that were specifically depleted compared with cells expressing PP1 alone.

2025-05-28 | PXD055166 | Pride

Fusion genes in EGFR mutant lung cancer

Project description:The clinical significance of gene fusions detected by DNA-based next generation sequencing remains unclear as resistance mechanisms to EGFR tyrosine kinase inhibitors (TKIs) in EGFR mutant non-small cell lung cancer (NSCLC). Through comprehensive evaluation of potential drug resistance-imparting fusion oncogenes in EGFR mutant lung cancers, we selected candidate samples to be further validated by confirmatory assay. Here, we performed RNA sequencing as an unbiased genome-wide method to identify novel oncogenic fusions. In 11 samples from 10 patients, 3 different fusion callers consistently detected only the DLG1-BRAF fusion in sample 6. None of other putative fusions detected by DNA-based hybrid capture sequencing were validated.We concluded that only a subset of putative fusion was validated by RNA-seq.

2022-08-08 | GSE182323 | GEO

Novel kinase fusion oncogenes in post-Chernobyl radiation-induced pediatric thyroid cancers

Project description:Exposure to ionizing radiation during childhood markedly increases the risk of developing papillary thyroid cancer. We identified non-overlapping somatic driver mutations in all 26 cases of post-Chernobyl thyroid cancers we studied through candidate gene assays and next generation RNA-sequencing. We found that 22/26 harbored fusion oncogenes arising primarily through intrachromosomal rearrangements. Altogether 23/26 of the oncogenic drivers identified in this cohort aberrantly activate MAPK signaling, including the two novel somatic rearrangements ETV6-NTRK3 and AGK-BRAF. Two other tumors harbored distinct fusions leading to overexpression of the nuclear receptor PPARγ. A lower prevalence of fusion oncogenes was found in a cohort of pediatric thyroid cancers from children from the same geographical regions that were not exposed to radiation. Radiation-induced thyroid cancers are a paradigm of tumorigenesis driven by fusion oncogenes that activate MAPK signaling or, less frequently, a PPARγ-driven transcriptional program. Examination of transcriptome profiles and genetic somatic changes in thyroid cancer.

2013-10-25 | E-GEOD-48850 | biostudies-arrayexpress

Population LEAF Expression profiling experiment

Project description:Transcription profiling by array of leaf samples of 94 genotypes deriving from a segregating diploid potato population

2011-12-31 | E-MTAB-808 | biostudies-arrayexpress

Whole-genome sequencing of SARS-CoV-2 samples in Sweden during early 2022

Project description:We developed an extraction-free qPCR assay to identify Omicron BA.1 cases and verified lineage by sequencing. We find that BA.2 variants show almost twice the viral load (Ct) compared to both BA.1 as well as Delta variants.

2022-05-25 | E-MTAB-11650 | biostudies-arrayexpress

Novel kinase fusion oncogenes in post-Chernobyl radiation-induced pediatric thyroid cancers

2013-10-25 | GSE48850 | GEO