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YFP+PDGFRa+ and YFP+PDGFRa– stromal cells isolated from the small intestine of LTBRfloxedPDGFRa/YFP mice

ABSTRACT: YFP+PDGFRa+ and YFP+PDGFRa– stromal cells isolated from the small intestine of LTBRfloxedPDGFRa/YFP mice

PROVIDER: PRJNA824320 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18926049.fastq.gz	Fastqsanger.gz
	SRR18926050.fastq.gz	Fastqsanger.gz
	SRR18926051.fastq.gz	Fastqsanger.gz
	SRR18926052.fastq.gz	Fastqsanger.gz
	SRR18926053.fastq.gz	Fastqsanger.gz

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YFP+PDGFRa+ and YFP+PDGFRa– stromal cells isolated from the small intestine of LTBRfloxedPDGFRa/YFP mice

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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.

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