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Testing the Anti-cancer Drug, Rogaratinib (BAY 1163877), for Treatment of Advanced Sarcoma With Alteration in Fibroblast Growth Factor Receptor (FGFR 1-4), and in Patients With SDH-deficient Gastrointestinal Stromal Tumor (GIST)

ABSTRACT: This phase II trial studies the effect of rogaratinib in treating patients with sarcoma with a change in a group of proteins called fibroblast growth factor receptors (FGFRs) or SDH-deficient gastrointestinal stromal tumor (GIST). Rogaratinib may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth.

DISEASE(S): Stage Iii Small Intestinal, Esophageal, Colorectal, Mesenteric, And Peritoneal Gastrointestinal Stromal Tumor Ajcc V8,Stage Iv Gastric And Omental Gastrointestinal Stromal Tumor Ajcc V8,Locally Advanced Gastrointestinal Stromal Tumor,Sarcoma,Locally Advanced Sarcoma,Metastatic Sarcoma,Stage Iii Gastric And Omental Gastrointestinal Stromal Tumor Ajcc V8,Stage Iv Small Intestinal, Esophageal, Colorectal, Mesenteric, And Peritoneal Gastrointestinal Stromal Tumor Ajcc V8,Metastatic Gastrointestinal Stromal Tumor,Neoplasms,Gastrointestinal Stromal Tumors

PROVIDER: 2355161 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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Expression Data from Gastrointestinal Stromal Tumor (GIST) Cell Lines

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2015-01-08 | GSE64762 | GEO

Expression Data from Gastrointestinal Stromal Tumor (GIST) Cell Lines

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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

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mRNA profiles in gastrointestinal stromal tumor (GIST) cell lines and GIST-associated fibroblast

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mRNA profiles in gastrointestinal stromal tumor (GIST) cell lines and GIST-associated fibroblast

Project description:To identify mRNA profiles in GIST and CAFs, we performed RNA sequencing analysis (RNA-seq) using GIST cell lines, GIST-T1 and GIST882, and CAFs.

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GIST proteome dataset(Proteomic Maps of Human Gastrointestinal Stromal Tumor Subgroups)

Project description:Gastrointestinal stromal tumor (GIST) is a common sarcoma of gastrointestinal tract (GIT) with high metastatic and recurrence rates, but the proteomic features are still less understood. Here we performed systematic quantitative proteome profiling of GIST from 13 patients classified into very low/low, intermediate and high risk subgroups. An extended cohort of GIST (n = 131) was used for immunohistochemical validation of proteins of interest. In total, 10064 proteins were quantified, covering 61% of the GIT transcriptome from The Human Protein Altas. Out of the 10064 quantified proteins, 4938 proteins were observed in all 13 cases with 518 proteins upregulated and 190 proteins downregulated in tumorous tissues independent of risk rating. Pathway analysis showed that the downregulated proteins were mostly enriched in metabolic pathway, while the upregulated proteins mainly belonged to spliceosome pathway. In addition, 131 proteins showed differentially expressed patterns among GIST subgroups with statistical significance. The 13 GIST cases were classified into 3 subgroups perfectly based on the expression of these proteins. The molecular phenotypes of oncoproteins, tumor suppressors, phosphatase and kinases were summarized, and some important molecules were observed. Immunohistochemical analysis of two phosphatases PTPN1 (n = 117) and PPP2CB (n=113) revealed that the GIST patients with high PTPN1 had low chances of developing metastasis, and the expression of PPP2CB was likely to be associated with GIST risk. Collectively, this work provides valuable information for understanding the inherent biology and evolution of GIST.

2019-01-29 | PXD011299 |

MiRNAs array after SH3BP2 silencing in Gastrointestinal stromal tumor cells

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miRNA expression profile in GIST (gastrointestinal stromal tumor)

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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.

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