Browse
Submit Data
Databases
API
Help

Dataset Information

4 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Masitinib in First Line Treatment of Gastro-Intestinal Stromal Tumor (GIST)

ABSTRACT: Masitinib in First Line Treatment of Gastro-Intestinal Stromal Tumor (GIST)

DISEASE(S): Gastrointestinal Stromal Tumour,Gastro-intestinal Stromal Tumour,Gastrointestinal Stromal Tumors

PROVIDER: 2065554 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

ACCESS DATA

Json Xml

Similar Datasets

Masitinib in Patients With Gastro-Intestinal Stromal Tumour Resistant to Imatinib

Project description:The objective is to compare efficacy and safety of masitinib at 12 mg/kg/day to sunitinib at 50 mg/day in treatment of patients with gastro-intestinal stromal tumor resistant to imatinib.

| 2118321 | ecrin-mdr-crc

Methylome of a low-grade invasive GIST

Project description:A low-grade invasive gastro-intestinal stromal tumour (GIST) was subjected to whole-genome sequencing as well as methylation profiling using Illumina 450K BeadChip array, in order to determine the minimal set of genomic and epigenomic alterations necessary to trigger the formation of invasive GIST.

2014-08-01 | GSE55521 | GEO

Methylome of a low-grade invasive GIST

2014-08-01 | E-GEOD-55521 | biostudies-arrayexpress

Masitinib in Locally Advanced/Metastatic Gastro-intestinal Stromal Tumour (GIST)

Project description:The objective is to evaluate the efficacy and safety of AB1010 at 7.5 mg/kg/day in the treatment of non pre-treated, inoperable patients with locally advanced/metastatic GIST.

| 2079658 | ecrin-mdr-crc

The Biological Activity of Cediranib (AZD2171) in Gastro-Intestinal Stromal Tumours(GIST).

Project description:To determine the anti-tumour activity and biological effects of cediranib (AZD2171) at a dose of 45mg, primarily in Gastrointestinal Stromal Tumour (GIST) patients who are resistant to imatinib mesylate (current standard therapy) and also in patients with metastatic Soft Tissue Sarcoma (STS) resistant to standard therapy.

| 2033358 | ecrin-mdr-crc

Masitinib in Patients With Localized, Primary GIST After Complete Surgery and With High Risk of Recurrence

Project description:The objective is to compare the efficacy and safety of masitinib at 4.5 mg/kg/day to placebo in the treatment of patients with localized, primary gastrointestinal stromal tumor (GIST) after complete surgery and with high risk of recurrence.

| 2156727 | ecrin-mdr-crc

Broiler gastro-intestinal microbiome

Project description:Broiler gastro-intestinal microbiome Raw sequence reads

| PRJNA836733 | ENA

Gastrointestinal stromal tumor GIST: gene expresssion and ChIP analyses

Project description:This SuperSeries is composed of the following subset Series: GSE19396: ETV1 knockdown in GIST cell lines GSE22433: Imatinib Treatment of GIST882 GSE22441: Mapping of ETV1 genomic binding sites in gastrointestinal stromal tumor (GIST). Refer to individual Series

2010-10-14 | E-GEOD-22852 | biostudies-arrayexpress

Identification of common features proffered by KIT and PDGFRA mutations in gastro-intestinal stromal tumors

Project description:Mutations in KIT proto-oncogene receptor tyrosine kinase (KIT) or platelet derived growth factor receptor alpha (PDGFRA) are responsible for more than 85% of the gastrointestinal stromal tumors (GIST). The introduction of imatinib in the therapy scheme of GIST revolutionized the patient outcome. Unfortunately, the therapy allows a disease stabilization rather than curation. Resistance to the inhibitor arises in most cases within the two first years of therapy. The identification of new targets to treat GIST is now essential. We propose a thorough investigation of the activating mechanisms derived from the main PDGFRA and KIT mutants encountered in the GIST landscape. We identified striking differences among the different KIT mutants while PDGFRA mutants delivered a very uniform picture. KIT Exon 11 deletion mutant exhibited the highest intrinsic kinase activity and all KIT mutants were, in addition to their constitutive activation, responsive to stem cell factor (SCF) stimulation. This highlights the importance of evaluating the SCF expression profile in GIST patients. In contrast, PDGFRA mutants were not responsive to their ligand, PDGFAA, and displayed a very high intrinsic kinase activity. At the transcriptomic level, the mitogen-activated protein kinase (MAPK) pathway was established as the most prominent activated pathway, commonly up-regulated by all PDGFRA and KIT mutants. Inhibition of this pathway using the MEK inhibitor PD0325901 reduced the proliferation of GIST primary cells in the nanomolar range. This demonstrates the high value of MEK inhibitors for combination therapy in GIST treatment. This experiment contains expression data from HEK-293 cells expressing wild-type and mutant KIT. The mutants included in the study correspond to the main mutations found in GIST, mainly KIT Ex9 exhibits a duplication of AY502-503 and KIT Ex11 a deletion of residues 553 to 557.

2017-07-05 | E-MTAB-4548 | biostudies-arrayexpress

CeRNA Expression Profiling Identifies KIT Related circRNAs-miRNA-mRNA Networks in Gastro-intestinal Stromal Tumors

Project description:Gastrointestinal stromal tumors (GISTs) are the most common human sarcomas and typically locate in the stomach or small intestine. circular RNAs (circRNAs) were identified to plays vital roles in tumor oncogenesis and progression. To investigate the involvement of differentially expressing genes and circRNAs in GIST , transcriptomic analyses of differential expression genes and circRNAs were performed for discrimination of GISTs from normal tissues. The RNA samples were extracted from three GIST samples and three adjacent mucosa for microarray profiling and performed in Agilent-078298 human ceRNA array for gene and circRNAs expression profiling analysis. On average, we detected expression of 17,000 transcripts.Under the criteria fold change > 2 or < 0.5, we obtained a total of 5770 circRNAs and 1815 mRNAs were differentially expressed in GISTs. Hierarchy cluster analysis also indicated that the 6 samples were distributed into two clusters, 3 GIST samples in one cluster and 3 normal samples in another cluster. Then,qRT-PCR validation of the DEGs in GIST tissue and adjacent tissues.The results revealed that grouping was reasonable and the data can be directly applied to further analysis.

2019-05-21 | GSE131481 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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