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The effect of imatinib therapy on tumor associated macrophages (TAMs) in murine gastrointestinal stromal tumor (GIST)

ABSTRACT: The gene expression profile of TAMs sorted from vehicle control tumors in GIST mice (Sommer et al, PNAS 2003) was compared to TAMs sorted from mice after 2 weeks of imatinib therapy The Affymetrix Mouse Genome 430A 2.0 platform was used

ORGANISM(S): Mus musculus

PROVIDER: GSE51698 | GEO | 2013/11/20

SECONDARY ACCESSION(S): PRJNA224582

REPOSITORIES: GEO

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The effect of imatinib therapy on tumor associated macrophages (TAMs) in murine gastrointestinal stromal tumor (GIST)

Project description:The gene expression profile of TAMs sorted from vehicle control tumors in GIST mice (Sommer et al, PNAS 2003) was compared to TAMs sorted from mice after 2 weeks of imatinib therapy The Affymetrix Mouse Genome 430A 2.0 platform was used Each treatment group had 8 mice. After 2 weeks of treatment, mice were sacrificed and tumors digested with collagenase. TAMs were then FACS sorted and pooled by group. Pooled groups were run in duplicate for the gene expression array.

2013-11-20 | E-GEOD-51698 | biostudies-arrayexpress

The effect of imatinib therapy on tumor associated macrophages (TAMs) in human gastrointestinal stromal tumor (GIST)

Project description:The gene expression profile of TAMs microbead isolated from freshly obtained human GISTs were compared in tumors that were untreated, responding to imatinib (sensitive), or resistant to imatinib (resistant) The Affymetrix Human Genome U133A 2.0 platform was used TAMs were microbead isolated from 12 untreated, 5 sensitive, and 4 resistant tumors. Tumors were obtained freshly from the operating room from consenting patients using an IRB approved protocol. Tumors were digested using collagenase and TAMs isolated using microbead negative selection for KIT, CD3, and CD56 followed by positive selection for CD14.

2013-11-20 | E-GEOD-51697 | biostudies-arrayexpress

The effect of imatinib therapy on tumor associated macrophages (TAMs) in human gastrointestinal stromal tumor (GIST)

2013-11-20 | GSE51697 | GEO

Gene expression analysis of imatinib-resistant GIST

Project description:To reveal mechanisms for acquired imatinib resistance in gastrointestinal stromal tumor (GIST), we have analyzed several cell lines with resistance to imatinib.

2016-12-27 | GSE69465 | GEO

Identification of transcriptional difference between Imatinib-sensitive and resistant patients with gastrointerstinal stromal tumor (GIST)

Project description:Purpose: The goals of this study are to characterize the transcriptional dysregulation of GIST. More importantly, the transcriptome differences betweeen Imatinib-sensitive and resistant patients are compared to identify RNAs that may impact Imatinib resistance. Methods: High-throughput RNA sequencing (RNA-seq) was employed to capture the transcriptional changes in GIST compared to normal samples. RSEM was used to quantify gene expression and DESeq2 was utilized to compared expression changes between different sample groups.

2021-07-29 | GSE155800 | GEO

Affymetrix human DMET Plus array in GIST patients treated with imatinib

Project description:To understand the contribution of germline DNA polymorphisms discriminating between imatinib clinical outcome and toxicity, 38 GIST patients (all with KIT exon 11 mutation) treated with imatinib were analyzed through Affymetrix human DMET Plus array.

2019-01-01 | GSE119558 | GEO

Expression Data from Gastrointestinal Stromal Tumor (GIST) Cell Lines

Project description:Activating mutations in either KIT or PDGFRA are present in approximately 90% of gastrointestinal stromal tumors (GISTs). Although treatment with the KIT and PDGFR inhibitor imatinib can control advanced disease in about 80% of GIST patients, the beneficial effect is not durable. Here, we report that ligands from the FGF family reduced the effectiveness of imatinib in GIST cells, and FGF2 and FGFR1 are highly expressed in all primary GIST samples examined. The combination of KIT and FGFR inhibition showed increased growth inhibition in imatinib-sensitive GIST cell lines in the presence or absence of added FGF2 in vitro, and delayed tumor regrowth in vivo. In addition, inhibition of mitogen-activated protein kinase (MAPK) signaling by imatinib was not sustained in GIST cells. An extracellular signal-regulated kinase (ERK) rebound occurred through activation of FGF signaling, and was repressed by FGFR1 inhibition. Downregultation of Sprouty proteins played a role in the imatinib-induced feedback activation of FGF signaling in GIST cells. We used micorarrays to quantify the gene expression levels in GIST cell lines.

2015-01-08 | GSE64762 | GEO

Expression Data from Gastrointestinal Stromal Tumor (GIST) Cell Lines

2015-01-08 | E-GEOD-64762 | biostudies-arrayexpress

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

Imatinib Treatment of GIST882

Project description:Gastrointestinal Stromal Tumor frequently harbor mutations in the KIT receptor tyrosine kinase and depend on its activity for growth. This underlies the efficacy of imatinib, a inhibitor of KIT activity, in GIST management. GIST882 is a patient derived GIST cell line that harbor a K640E exon 13 KIT mutation and is sensitive to imatinib treatment. To analyze the downstream effect of KIT inhibition, GIST882 cells were treated for 8 hours with 1μM Imatinib.

2010-10-13 | GSE22433 | GEO

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