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Genome wide analysis of mouse gastrointestinal stromal tumors (GIST) in a mouse model of spontaneous GIST.

ABSTRACT: Analysis of mouse GIST tumors at the gene expression level. The purpose of the study was to identify immunomodulatory genes in mouse GIST tumors after in vivo treatment with the specific tyrosine kinase inhibitor imatinib mesylate. Total RNA obtained from mouse GIST tumors after in vivo treatment with imatinib or vehicle control injected intraperitoneally.

ORGANISM(S): Mus musculus

SUBMITTER: Jeffrey Zhao

PROVIDER: E-GEOD-30416 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genome wide analysis of mouse gastrointestinal stromal tumors (GIST) in a mouse model of spontaneous GIST.

Project description:Analysis of mouse GIST tumors at the gene expression level. The purpose of the study was to identify immunomodulatory genes in mouse GIST tumors after in vivo treatment with the specific tyrosine kinase inhibitor imatinib mesylate.

2011-12-31 | GSE30416 | 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. Four GIST cell lines were split and cultured overnight. Cells were harvested for RNA extraction and hybridization on Affymetrix U133plus2 microarrays.

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

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

Expression Data from Gastrointestinal Stromal Tumor (GIST) Cell Lines

2015-01-08 | GSE64762 | GEO

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

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

2013-11-20 | GSE51698 | GEO

Unraveling the Mechanisms of Sensitivity to Anti-FGF Therapies in Imatinib-Resistant Gastrointestinal Stromal Tumors (GIST) Lacking Secondary KIT Mutations

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.

2023-11-09 | GSE247170 | GEO

Kinome Profiling of Gastrointestinal Stromal Tumors Using Multiplexed Inhibitor Beads and Mass Spectrometry Identifies Wee1 as a Candidate Therapeutic Target

Project description:Purpose: Management of gastrointestinal stromal tumor (GIST) has been revolutionized by the identification of activating mutations in KIT and PDGFRA and the clinical application of receptor tyrosine kinase (RTK) inhibitors in the advanced disease setting. Stratification of GIST into molecularly defined subsets provides insight into clinical behavior and response to approved targeted therapies. Although these RTK inhibitors are effective in the majority of GIST, resistance to these agents remains a significant clinical obstacle. Development of effective treatment strategies for refractory GIST requires identification of novel targets to provide additional therapeutic options. Global kinome profiling has the potential to identify critical signaling networks and reveal protein kinases that are essential in GIST. Experimental Design: Using Multiplexed Inhibitor Beads and Mass Spectrometry paired with a super-SILAC kinome standard, we explored the majority of the kinome in GIST specimens from three GIST subtypes (KIT-mutant, PDGFRA-mutant and succinate dehydrogenase-deficient GIST) to identify novel kinase targets. In vitro and in vivo studies were performed to evaluate the utility of targeting the identified kinases in GIST. Results: Kinome profiling revealed distinct signatures in three GIST subtypes. PDGFRA-mutant GIST had elevated tumor associated macrophage (TAM) kinases and immunohistochemical analysis confirmed increased TAMs present in these tumors. Kinome profiling with loss-of-function assays revealed a significant role for G2-M tyrosine kinase, Wee1, in GIST survival. In vitro and in vivo studies revealed significant efficacy of MK-1775 (Wee1 inhibitor) in combination with avapritinib in both KIT and PDGFRA-mutant GIST cell lines, as well as notable efficacy of MK-1775 as a single agent in the PDGFRA-mutant line. Conclusions: These studies provide strong preclinical justification for the use of MK-1775 in GIST.

2021-09-09 | PXD020720 | Pride

RNA-Seq of murine GIST-like tumors after Etv1 ablation

Project description:We used a mouse expressing three alleles 1) KitV558Delta/+ activating allele that develop GIST-like tumors in the cecum, 2) Etv1 flox/flox conditional knockout allele and 3) Rosa26-CreERT2 tamoxifen activated Cre allele. Mice were treated with either Tamoxifen (to delete Etv1) or corn oil (control). Cecal tumors were isolated for gene expression profiling by RNA-Seq. Expression profile mouse cecal GIST tumor with or without Etv1 ablation was generated by RNA-Seq

2015-01-01 | E-GEOD-64608 | 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

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