Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Glioneuronal tumor with ATRX alteration, kinase fusion and anaplastic features (GTAKA) with leptomeningeal dissemination and ZMIZ1::RET fusion [methylation array]

ABSTRACT: Glioneuronal tumor with ATRX alteration, kinase fusion and anaplastic features (GTAKA) with leptomeningeal dissemination and ZMIZ1::RET fusion [methylation array]

PROVIDER: PRJNA1066351 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Glioneuronal tumor with ATRX alteration, kinase fusion and anaplastic features (GTAKA) with leptomeningeal dissemination and ZMIZ1::RET fusion

Project description:Glioneuronal tumor with ATRX alteration, kinase fusion and anaplastic features (GTAKA) with leptomeningeal dissemination and ZMIZ1::RET fusion

| PRJNA1066350 | ENA

Glioneuronal tumor with ATRX alteration, kinase fusion and anaplastic features (GTAKA) with leptomeningeal dissemination and ZMIZ1::RET fusion [RNA-seq]

Project description:Glioneuronal tumor with ATRX alteration, kinase fusion and anaplastic features (GTAKA) with leptomeningeal dissemination and ZMIZ1::RET fusion [RNA-seq]

| PRJNA1066352 | ENA

Glioneuronal tumor with ATRX alteration, kinase fusion and anaplastic features (GTAKA) with leptomeningeal dissemination and ZMIZ1::RET fusion [RNA-seq]

Project description:Herein we describe a case with histological, immunohistochemical and molecular features of GTAKA showing widespread leptomeningeal dissemination.

2024-07-17 | GSE253610 | GEO

Glioneuronal tumor with ATRX alteration, kinase fusion and anaplastic features (GTAKA) with leptomeningeal dissemination and ZMIZ1::RET fusion [methylation array]

Project description:Herein we describe a case with histological, immunohistochemical and molecular features of GTAKA showing widespread leptomeningeal dissemination.

2024-07-17 | GSE253604 | GEO

Glioneuronal tumor with ATRX alteration, kinase fusion and anaplastic features (GTAKA) with leptomeningeal dissemination and ZMIZ1::RET fusion

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

2024-07-17 | GSE253611 | GEO

RET fusion genes, BCR-RET and FGFR1OP-RET, are associated with chronic myelomonocytic leukemia, display sensitivity to Sorafenib, an inhibitor of tyrosine-kinase activity and enhance monocytic differentiation

Project description:Myeloproliferative neoplasms are frequently associated with aberrant constitutive tyrosine kinase (TK) activity resulting from point mutations or chimaeric fusion genes, such as BCR ABL1 or JAK2 V617F. We report here for the first time in hematological malignancies, two novel fusion genes involving the TK RET, BCR-RET and FGFR1OP-RET, in chronic myelo monocytic leukemia (CMML) cases. The two RET fusion genes lead to the aberrant activation of RET, are able to transform hematopoietic cells and skew the hematopoietic differentiation program towards the monocytic/macrophage lineage. We also report that the BCR-RET fusion protein is insensitive to Imatinib but sensitive to Sorafenib in vivo. CMML is an hematopoietic malignancy associated with the frequent activation of the RAS pathway. The RET fusion genes seems to constitutively mimic the same signaling pathway than RAS mutations. Overall, the RET fusion genes behaviors in the monocytic lineage underlie the role of the normal RET TK activity during the physiological monocytic differentiation. We analysed BAF/3 cells infected by BCR-RET, FGFR1OP-RET or BCR-ABL1P210 fusion genes retroviruses and sorted out using EGFP fluorescence, with Affymetrix GeneChip MouseGene 1.0 ST platform.

2012-01-06 | E-GEOD-34900 | biostudies-arrayexpress

2012-01-06 | GSE34900 | GEO

RNA sequencing analysis of gene expression profiles of OLFM4-RET fusion in HEK293 cells

Project description:The purpose of this assay is to determine the gene expression profiles induced by OLFM4-RET fusion, therefore further understanding the molecular mechanim of oncognesis by OLFM4-RET

2020-09-18 | GSE158176 | GEO

Proteogenomics analysis unveils a novel TFG-RET gene fusion and druggable targets in papillary thyroid carcinomas

Project description:Papillary thyroid cancer (PTC) is the most common type of endocrine malignancy. From a set of PTC patients whose tumor did not harbour any BRAF or RAS mutations, a 35 years old male patient’s normal, primary tumor and lymph node (LN) metastatic tissues were subjected to genomics and proteomics analysis. By RNA-seq analysis, we identified a novel RET rearrangement involving exons 1-4 from the 5’ end of the Trk fused Gene (TFG) fused to the 3’ end of RET tyrosine kinase leading to a TFG-RET fusion which transforms immortalized human thyroid cells in a kinase-dependent manner. Further, TFG-RET oncogene oligomerises in a PB1 domain-dependent manner and consistently, mutation of the oligomerisation interface led to the inhibition of RET-mediated oncogenic transformation. Quantitative proteomic analysis of the same samples revealed the upregulation of proteins involved in the ubiquitination machinery including E3 Ubiquitin ligase HUWE1 and DUBs like USP9X and UBP7 in both tumor and LN metastatic lesions. We further identified that expression of TFG-RET led to the upregulation of HUWE1. Further, in a cohort of PTC patients, we observed higher expression of HUWE1, USP9X and USP7 in the tumor and metastatic lesions, when compared to the matched normal tissue. Transient knockdown of HUWE1, USP9X and USP7 affected viability and proliferation of TFG-RET transformed cells. Consistently, inhibition of RET, HUWE1 and DUBs by small molecule inhibitors significantly reduced RET-mediated oncogenesis. Apart from unveiling a novel oncogenic RET fusion in PTCs, our data may open a novel avenue of targeting ubiquitin signaling machinery in human PTCs.

2020-04-02 | PXD016828 | Pride

Proteogenomics analysis unveils a novel TFG-RET gene fusion and druggable targets in papillary thyroid carcinomas

Project description:Papillary thyroid cancer (PTC) is the most common type of endocrine malignancy. From a set of PTC patients whose tumor did not harbour any BRAF or RAS mutations, a 35 years old male patient’s normal, primary tumor and lymph node (LN) metastatic tissues was subjected to genomics and proteomics analysis. By RNA-seq analysis, we identified a novel RET rearrangement involving exons 1-4 from the 5’ end of the Trk fused Gene (TFG) fused to the 3’ end of RET tyrosine kinase leading to a TFG-RET fusion which transforms immortalized human thyroid cells in a kinase dependent manner. Further, TFG-RET oncogene oligomerises in a PB1 domain dependent manner and consistently, mutation of the oligomerisation interface led to the inhibition of RET-mediated oncogenic transformation. Quantitative proteomic analysis of the same samples revealed the upregulation of proteins involved in the ubiquitination machinery including HECT carrying E3 Ubiquitin ligase HUWE1 and DUBs like USP9X and UBP7 in the tumor and LN metastatic lesions. We further identify that expression of TFG-RET led to the upregulation of HUWE1. Further, in a cohort of PTC patients, we observed higher expression of HUWE1, USP9X and USP7 in the tumor and metastatic lesions, when compared to the matched normal tissue. Transient knockdown of HUWE1, USP9X and USP7 affected viability and proliferation of TFG-RET transformed cells. Consistently, inhibition of RET, HUWE1 and DUBs by small molecule inhibitors significantly reduced RET-mediated oncogenesis. Apart from unveiling a novel oncogenic RET fusion in PTCs, our data may open a novel avenue of targeting ubiquitin signaling machinery in human PTCs.

2020-04-02 | PXD016739 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data