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

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

PROVIDER: PRJEB48486 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR7198351_1.fastq.gz	Fastqsanger.gz
	ERR7198351_2.fastq.gz	Fastqsanger.gz
	ERR7198352_1.fastq.gz	Fastqsanger.gz
	ERR7198352_2.fastq.gz	Fastqsanger.gz
	ERR7198353_1.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).

2021-11-23 | E-MTAB-11112 | biostudies-arrayexpress

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

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

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

Project description:An interactive tumor microenvironment with different stromal cell types is necessary for supporting cancer stemness. Cancers with dense fibrotic stroma such as intrahepatic cholangiocarcinoma (ICC) are often highly aggressive and chemotherapy resistance. Here, we show that cancer associated fibroblasts (CAF) greatly enhances the capacity of blood CD33+ myeloid-derived suppressor cells (MDSCs) to promote stem-like properties in ICC cells and tumor growth via paracrine signaling. Mechanistically, CAF mediates hyperactivated 5-LO pathway in CD33+ MDSCs via secretion of IL-6 and IL-33, resulting in overproduction of LTB4, which acts on BLT2 to promote cancer stemness via Akt-mTOR signaling. hyperactivated 5-LO pathway are observed in tumor-infiltrating CD33+ MDSCs compared with blood counterparts from the same ICC patients. Moreover, BLT2 blockade augments chemotherapeutic efficacy in ICC PDX models. Thus, our study reveals a previously unrecognized stromal cell network in which CAF educate myeloid cells to shape the optimal supportive microenvironment for the aggressive nature of ICC.

2022-01-01 | GSE158755 | GEO

Mutant IDH1 regulates the tumor-associated immune system in gliomas

Project description:Gliomas harboring mutations in isocitrate dehydrogenase 1/2 (IDH1/2) have the CpG island methylator phenotype (CIMP) and significantly longer patient survival time than wild-type IDH1/2 tumors. Although there are many factors underlying the differences in survival between these two tumor types, immune-related differences in cell content are potentially important contributors. In order to investigate the role of IDH mutations in immune response, we created a syngeneic pair mouse model for mutated IDH1 (mutIDH1) and wild-type IDH1 (wtIDH1) gliomas and demonstrated that muIDH1 mice showed many molecular and clinical similarities to muIDH1 human gliomas, including a 100-fold higher concentration of 2-hydroxygluratate (2-HG), longer survival time, and higher CpG methylation compared to wtIDH1. Also, we showed that IDH1 mutations caused downregulation of leukocyte chemotaxis, resulting in repression of the tumor-associated immune system. Given that significant infiltration of immune cells such as macrophages, microglia, monocytes, and neutrophils is linked to poor prognosis in many cancer types, these reduced immune infiltrates in muIDH1 glioma tumors may contribute in part to the differences in aggressiveness of the two glioma types.

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

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Project description:The cell line-derived xenografts and patient derived xenografts have limited use in cancer immunotherapy evaluation because an immune compromised host is required for xenotransplantation. Syngeneic mouse models are derived by transplanting established mouse cell lines or tumor tissues to strain matched mouse hosts, which are better suited to study the interplay between immune and tumor cells. We investigated the differences as well as similarities of a panel of ten mouse syngeneic models to features of human tumors by proteomics, which will provide valuable information to assist experimental biologists in model selection.

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mRNA expression data of tumor samples with/without IDH1/2 mutations and of controls

Project description:We determined differentially expressed genes between tumor samples with and without IDH1/2 mutations, and between tumors with IDH1/2 mutations and controls. A total of 21 tumours which include 6 enchondromas and 10 chondrosarcomas (3 grade I, 7 grade II) of Ollier disease, as well as 1 enchondroma and 4 chondrosarcomas grade II of solitary tumors, and 6 controls (growth plate and cartilage) were selected for expression analysis. Sample preparation, RNA isolation, synthesis of cDNA, cRNA amplification, hybridization of cRNA onto the Illumina Human-6 v3.0 Expression BeadChips, microarray data preprocessing, quality control, and detection of differential expression were performed as described previously (PMID: 21372215, PMID: 21584901). We determined differential expression between tumor samples without detectable IDH1 or IDH2 mutation (n=3) and samples with IDH1 or IDH2 mutations (n=18), and between samples with IDH1 or IDH2 mutation and controls (n=6). Probes with Benjamini and Hochberg False discovery rate-adjusted P-values (adjP) < 0.05 and a log fold change (logFC) > 0.1 were considered to be significantly differentially expressed.

2011-11-05 | E-GEOD-30835 | biostudies-arrayexpress

Single cell sequencing of mouse syngeneic tumor models

Project description:Single cell sequencing of mouse syngeneic tumor models

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mRNA expression data of tumor samples with/without IDH1/2 mutations and of controls

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