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RNAseq of tumor samples from CT26 syngeneic mouse treated with a PI3Ka/d inhibitor (AZD8835)

ABSTRACT: RNAseq of tumor samples from CT26 syngeneic mouse treated with a PI3Ka/d inhibitor (AZD8835)

PROVIDER: PRJEB29676 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR2888650.fastq.gz	Fastqsanger.gz
	ERR2888660.fastq.gz	Fastqsanger.gz
	ERR2888651.fastq.gz	Fastqsanger.gz
	ERR2888661.fastq.gz	Fastqsanger.gz
	ERR2888652.fastq.gz	Fastqsanger.gz

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RNAseq of tumor samples from CT26 syngeneic mouse treated with a PI3Ka/d inhibitor (AZD8835)

Project description:PI3K inhibitors with differential selectivity to distinct PI3K isoforms have been tested extensively in clinical trials, largely to target tumor epithelial cells. PI3K signaling also regulates the immune system and inhibition of PI3Kdelta modulate the tumor immune microenvironment of pre-clinical mouse tumor models by relieving T-regs-mediated immunosuppression. While PI3K inhibitors as a class and PI3Ka/d specifically are associated with immune-related side effects. However, the impact of mixed PI3K inhibitors in tumor immunology is under-explored. Here we examine the differential effects of AZD8835 a dual PI3Ka/d inhibitor specifically on the tumor immune microenvironment using syngeneic CT26 mice. CT-26 (5x10^6 cells/mouse) tumor cells were implanted subcutaneously (s.c.) in the left flank of female Balb/c and C57/Bl6 mice, respectively. AZD8835 was dosed at 50mg/kg twice daily in at 2days on/ 5 days off schedule for times indicated in figures or 25mg/kg BID daily. At end of study tumor tissues were then transferred into the gentleMACS C Tube containing RPMI. Tumor samples were processed using the mouse tumor dissociation kit from Miltenyi Biotec. Cells were liberated from tumors for downstream application using a mouse tumor dissociation kit and octodissociator (Miltenyi) according to manufacturer’s instructions. For RNA sequencing, total RNA was extracted using the RNeasy 96 Qiacube HT Kit (Qiagen), quality validated using nanodrop and Quantit RNA Assay Kit (Thermo Fisher), and submitted for TrueSeq Stranded mRNA library preparation, following the manufacturer’s instructions (Illumina). Resulting libraries were sequenced on the HiSeq4000 System.

2019-01-08 | E-MTAB-7386 | biostudies-arrayexpress

RNAseq of tumor samples from CT26 syngeneic mouse treated with a PD-L1 and CTLA-4 immunotherapy combination

Project description:The ability to modulate immune-inhibitory pathways using checkpoint blockade antibodies such as PD-1, PD-L1, and CTLA-4 represents a significant breakthrough in cancer therapy in recent years. This has driven interest in identifying small-molecule-immunotherapy combinations to increase the proportion of responses. Murine syngeneic models, which have a functional immune system, represent an essential tool for pre-clinical evaluation of new immunotherapies. However, immune response varies widely between models and the translational relevance of each model is not fully understood, making selection of an appropriate pre-clinical model for drug target validation challenging. Utilizing RNAseq transcriptomic profiling, we have characterised the changes in gene regulatory pathways and immune populations in CT26 mice after treatment with the combination of anti-PD-L1 and anti-CTLA-4 antibodies. At day 7 post tumor implant, the pathways analysis of differentially expressed genes indicated an enrichment for migration of leukocytes in response to inflammation and communication between innate and adaptive immune cells. Similarly, analysis of upstream regulators suggested that lipopolysaccharide, IL-1B, TNF, IFNG, and NFKB1A pathways associated with inflammation were activated. At day 14, pathways related T-helper cell signalling pathways were upregulated. In addition, upstream regulators of the lipopolysaccharide and IFNG pathway, as well STAT1 and IL21 pathway were enriched, indicative of innate and adaptive immune response to inflammation.

2020-04-16 | E-MTAB-7777 | biostudies-arrayexpress

RNAseq of tumor samples from CT26 syngeneic mouse treated with a PD-L1 and CTLA-4 immunotherapy combination

Project description:RNAseq of tumor samples from CT26 syngeneic mouse treated with a PD-L1 and CTLA-4 immunotherapy combination

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The cecal contents of CT26 syngeneic mouse model

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the cecal contents of CT26 syngeneic mouse model

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Project description:the cecal contents of CT26 syngeneic mouse model Raw sequence reads part2

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TCR variable regions transcripts of CT26-shppp2r1a and CT26-scr samples

Project description:TCR variable regions transcripts of three CT26-shppp2r1a samples and three CT26-scr samples

2021-11-20 | GSE189092 | GEO

Multiome analysis (ATAC + Gene Expression (GEX)) of SUN1 knockout and control CT26 tumors grown in syngeneic mouse model

Project description:T cell infiltration is essential for immune checkpoint inhibitors to be effective in treating solid cancers. Through a bioinformatic pipeline, we identified a target gene SUN1 that might relate to modulating immune cell infiltration and immune response. Thus, we generated one Sun1_knockout CT26 cell line (Sun1_KO) using CRISPR-Cas9. By performing multiome single nuclei sequencing using tumors grown in syngeneic model, we set out to understand how mouse Sun1 can affect the regulatory network in tumor cells in vivo.

2024-03-29 | GSE262237 | GEO

RNA sequencing data of CT26-shppp2r1a and CT26-scr samples

Project description:Goal: Microsatellite-instable (MSI) tumors are one of the few cancers that respond to immune checkpoint blockade (ICB); however, the mechanism of MSI status development is unclear. Here, we report that protein phosphatase 2A (PP2A) deletion or inactivation converted cold microsatellite-stable (MSS) into MSI tumors. Objectives: Using RNA sequencing data of three CT26-shppp2r1a data and a CT26-scr data, we demonstrate that these intestinal tumors display differential core driver pathways.

2021-08-26 | GSE182571 | GEO

RNA-Seq analysis of SUN1 knockout and control CT26 cells and tumors

Project description:T cell infiltration is essential for immune checkpoint inhibitors to be effective in treating solid cancers. Through a bioinformatic pipeline, we identified a target gene SUN1 that might relate to modulating immune cell infiltration and immune response. Thus, we generated one Sun1_knockout CT26 cell line (Sun1_KO) and two control CT26 cell lines (Sun1_Control) using CRISPR-Cas9. By performing RNA-seq on cultured cells, tumors grown in syngeneic model, and purified tumor cells from tumors grown in syngeneic model, we set out to understand how mouse Sun1 can affect immune-related pathways and immune cell infiltration and anti-PD1 efficacy in BALB/c mice.

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