Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression signature predictive of rapid response to imatinib mesylate in Gastrointestinal Stromal Tumor (GIST)

ABSTRACT: Gene expression profiling using oligonucleotide microarrays performed on tumor samples obtained before and after imatinib mesylate (IM) therapy. Rapid responding (to IM) samples were compared to non-responding/stable disease samples as measured by CT scan measurements to identify a gene signature that can predict rapid response to IM.

ORGANISM(S): Homo sapiens

PROVIDER: GSE15966 | GEO | 2009/11/24

SECONDARY ACCESSION(S): PRJNA115541

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcription profiling of human gastrointestinal stromal tumour is predictive of rapid response to imatinib mesylate

Project description:Gene expression profiling using oligonucleotide microarrays performed on tumor samples obtained before and after imatinib mesylate (IM) therapy. Rapid responding (to IM) samples were compared to non-responding/stable disease samples as measured by CT scan measurements to identify a gene signature that can predict rapid response to IM. Experiment Overall Design: 54 samples, 29 pre-treatment biopsy samples, 25 post-treatment/post-surgery tumor samples from Gastrointestinal Stromal Tumors

2009-12-02 | E-GEOD-15966 | biostudies-arrayexpress

Zebrafish liver transcriptome in response to chronic treatment with environmentally relevant concentrations of imatinib mesylate

Project description:Imatinib mesylate (IM) a protein kinase inhibitor drug that selectively inhibits certain oncogenic mutant protein tyrosine kinases. After application, IM is via hospital and municipal waste water effluents released into the aquatic environment, where it can harm non-target organisms. The aim of this study was to evaluate changes in gene transcription in liver of adult F1 zebrafish (Danio rerio) continuously exposed to IM at environmentaly relevant concentrations of 0.01 µg/L and 1 µg/L.

2019-11-05 | GSE84394 | GEO

Imatinib Mesylate With or Without Surgery in Treating Patients With Metastatic Gastrointestinal Stromal Tumor That is Responding to Imatinib Mesylate

Project description:RATIONALE: Surgery may remove residual disease in patients with gastrointestinal stromal tumor that is responding to imatinib mesylate. It is not yet known whether surgery is more effective than continued imatinib mesylate in treating patients with metastatic gastrointestinal stromal tumor. PURPOSE: This randomized phase III trial is studying giving imatinib mesylate therapy together with surgery to see how well it works compared with imatinib mesylate alone in treating patients with metastatic gastrointestinal stromal tumor that is responding to imatinib mesylate.

| 2076430 | ecrin-mdr-crc

Claudin-1 contributes to gastrointestinal stromal tumors (GIST) resistance to imatinib mesylate (IM) via regulation of FGFR2-mediated signaling.

Project description:Acquired resistance of gastrointestinal stromal tumors (GISTs) to imatinib mesylate (IM) is one of the most critical challenges in GIST therapy. Here we show that a long-term culture of GIST T-1 cells with IM induces clonal heterogeneity resulting in the appearance of cancer cells exhibiting activation of the FGFR-signaling pathway which was associated with KIT loss. The first one was due to the overexpression of FGFR1/2 and increased production of FGF-2 ligand. These events maintained GIST resistance to IM and rendered these GIST cells highly sensitive to all types of pan-FGFR-inhibitors used in the current study. Knockout of FGFR2 in this GIST subclone significantly attenuated pro-apoptotic and anti-proliferative activities of infigratinib (BGJ 398) both in vitro and in vivo, thereby suggesting the activation of FGFR-signaling pathway via FGFR2-mediated axis as the predominant molecular mechanism in these GIST cells. Collectively, the extended inhibition of KIT-signaling in GISTs induces clonal heterogeneity of cancer cells and might change the tumor’s sensitivity to FGFR-inhibitors due to selection of cancer cells with an FGFR-overactivated pathway.

2025-08-26 | GSE296175 | GEO

Treatment of Patients With Everolimus and Imatinib Mesylate Who Have Progressive Gastro Intestinal Stromal Tumors (GIST) and Are Resistant to Imatinib Mesylate

Project description:The purpose of this multicenter, single-arm, Simon two-stage, phase II trial is to determine the efficacy and safety of everolimus in combination with Imatinib mesylate in patients with previously treated, histologically proven GIST whose disease has recurred or progressed while receiving 400 mg/day of Imatinib mesylate at any time during at least a 2 months’ treatment period.

| 2042769 | ecrin-mdr-crc

Gene expression profile induced by Imatinib

Project description:Activation-induced cytidine deaminase (AID) is essential for class switch recombination (CSR) and somatic hypermutation (SHM). Its deregulated expression acts as a genomic mutator that can contribute to the development of various malignancies. During treatment with imatinib mesylate (IM), patients with chronic myeloid leukemia (CML) often develop hypogammaglobulinemia, the mechanism of which has not yet been clarified. Here, we provide evidence that CSR upon B cell activation is apparently inhibited by IM through downregulation of AID. Furthermore, expression of E2A, a key transcription factor for AID induction, was markedly suppressed by IM. These results elucidate not only the underlying mechanism of IM-induced hypogammaglobulinemia but also its potential efficacy as an AID suppressor. We investigated that class switch recombination(CSR) upon B cell activation is apparently inhibited by imatinib mesylate(IM) through downregulation of activation-induced cytidine deaminase(AID). Furthermore, expression of E2A was markedly suppressed by IM. To elucidate the more detailed pathway, we performed the microarray analysis. Microarray analysis was performed on splenocytes cultured for 72 h in the presence or absence of 10 µM Imatinib. The mouse splenocytes were cultured for 72 h with or without 10 µM Imatinib (IM) in conditioning medium containing IL-4 and LPS. RNA from 1X10^6 splenocytes used for microarray analysis was isolated using the RNeasy Mini Kit (50) (Qiagen, Hilden, Germany).　Gene expression microarray analysis was performed using one-color microarray-based gene-expression analysis (Agilent Technologies, Santa Clara, CA, USA) according to the manufacturer’s instructions. After scanning, expression values for the genes were determined using GeneSpringGX software.

2012-02-08 | E-GEOD-35559 | biostudies-arrayexpress

Identification of copy number alterations by array comparative genomic hybridization in patients with late chronic or accelerated phase chronic myeloid leukemia treated with imatinib mesylate

Project description:The outcome of treating chronic myeloid leukemia (CML) with imatinib mesylate (IM) is inferior when therapy is commenced in late chronic or accelerated phase as compared to early chronic phase. This may be attributed to additional genomic alterations that accumulate during disease progression. We sought to identify such lesions in patients showing suboptimal response to IM by performing array-CGH analysis on 39 sequential samples from 15 CML patients. Seventy-four cumulative copy number alterations (CNAs) consisting of 35 losses and 39 gains were identified. Alterations flanking the ABL1 and BCR genes on chromosomes 9 and 22, respectively, were the most common identified lesions with 5 patients losing variable portions of 9q34.11 proximal to ABL1. Losses involving 1p36, 5q31, 17q25, Y and gains of 3q21, 8q24, 22q11, Xp11 were among other recurrent lesions identified. Aberrations were also observed in individual patients, involving regions containing known leukemia-associated genes; CDKN2A/2B, IKZF1, RB1, TLX1, AFF4. CML patients in late stages of their disease, harbor pre-existing and evolving sub-microscopic CNAs that may influence disease progression and IM response.

2011-03-15 | GSE23946 | GEO

Gene expression profile induced by Imatinib

2012-02-08 | GSE35559 | GEO

Claudin-1 contributes to gastrointestinal stromal tumors (GIST) resistance to imatinib mesylate (IM) via regulation of FGFR2-mediated signaling.

Project description:Claudin-1 contributes to gastrointestinal stromal tumors (GIST) resistance to imatinib mesylate (IM) via regulation of FGFR2-mediated signaling.

| PRJNA1258085 | ENA

BA/BE study of Imatinib Mesylate 400 mg Tablets

Project description:Intervention1: Imatinib Mesylate 400mg Manufactured by Eugia Pharma Specialities Limited, India: This study will consists of two periods and is multiple dose study. Eligible patients will be administered with test (Imatinib Mesylate 400mg ) or reference (GleevecÂ (Imatinib Mesylate) Tablets 400 mg;)for 7 consecutive days in each period crossed over without washout. Control Intervention1: Gleevec(R) -Imatinib Mesylate 400mg Distributed by Novartis Pharmaceuticals Corporation, USA.: This study will consists of two periods and is multiple dose study. Eligible patients will be administered with test (Imatinib Mesylate 400mg ) or reference (GleevecÂ (Imatinib Mesylate) Tablets 400 mg;)for 7 consecutive days in each period crossed over without washout. Primary outcome(s): AUC0-ï?´ -: Area under the plasma concentration time curve over the steady state dosing interval. Cmax-ss: Maximum concentration over the steady state dosing interval. Timepoint: Day 1, 5, 6, 8, 12 and 13: Venous blood samples will be withdrawn 5 minutes prior to morning dosing to confirm steady state condition. ( 3 days/ 12 mL/ period) Day 7 and 14: Venous blood samples will be withdrawn at 0.00 (pre-dose) and 0.50, 1.00, 1.50, 2.00, 2.50, 3.00, 3.50, 4.00, 4.50, 5.00, 6.00, 8.00, 12.00, 18.00 and 24.00 hours of post dose in each period. Study Design: Randomized, Crossover Trial Method of generating randomization sequence:Computer generated randomization Method of allocation concealment:Centralized Blinding and masking:Open Label

| 2577939 | ecrin-mdr-crc

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