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10X single-cell RNASeq profiling of immune infiltrate from mutant IDH1 ICC tumors treated with AG120 (mIDH1 inhibitor) or vehicle

ABSTRACT: 10X single-cell RNASeq profiling of immune infiltrate from mutant IDH1 ICC tumors treated with AG120 (mIDH1 inhibitor) or vehicle

PROVIDER: PRJNA726264 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14364103.fastq.gz	Fastqsanger.gz
	SRR14364104.fastq.gz	Fastqsanger.gz
	SRR14364105.fastq.gz	Fastqsanger.gz
	SRR14364106.fastq.gz	Fastqsanger.gz
	SRR14364107.fastq.gz	Fastqsanger.gz

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Sorted tumor RNA-seq of syngeneic murine mutant IDH1 ICC tumor model treated with IDH1 inhibitor against vehicle

Project description:IDH1 is the most commonly mutated metabolic gene across human cancers, with the highest mutational frequency observed in AML, glioma, chondrosarcoma, and intrahepatic cholangiocarcinoma. Mutations of the hot spot R132 codon alter the activity of the IDH1 enzyme, resulting in the NADPH-dependent conversion of alpha-ketoglutarate to (R)-2-hydroxyglutarate [(R)-2HG], which accumulates to mM levels within tumors. (R)-2HG competitively inhibits a range of enzymes that utilize alpha-ketoglutarate. Targets include the JmjC family histone demethylases and TET family DNA demethylases whose inhibition is linked to the altered epigenetic state characteristic of many mIDH tumors. To gain insight into the mechanisms underlying the anti-tumor efficacy of inhibition of mutant IDH1 we conducted RNA-sequencing (RNA-seq) analysis of purified tumor cells. For these studies, the immune-competent 2205 subcutaneous allograft model was treated with AG120 or vehicle for 6 days and non-tumor cells were removed by magnetic bead sorting (negative selection for CD45+ immune cells, CD31+ endothelial cells, TER119+ erythrocytes, and CD90.2+ fibroblasts).

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10X single-cell RNASeq profiling of immune infiltrate from mutant IDH1 ICC tumors treated with AG120 (mIDH1 inhibitor) or vehicle

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Transcriptional expression of ICC-DMP and ICC-MY in murine small intestine

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RNA sequencing data of differentially treated cancer associated fibroblast, myeloid-derived supression cells, and ICC tumor cells in ICC patient

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