Project description:The aim of this work was to evaluate modifications of transriptomal landscape of tumors after treatment with anti-GARP:TGFb mAb combined or not with anti-PD1 mAb.
Project description:To investigate which factors might be driving the cachectic muscle wasting observed in our larval models bearing RasV12, scrib1 tumors, we performed RNA sequencing (RNAseq) on the cuticles of wild type and RasV12, scrib1 tumour-bearing larvae. Pathway and gene ontology analysis revealed significant deregulation of stress and starvation response genes, metabolic genes, and inflammation and immune regulatory genes within cachectic muscle of tumour bearing larvae.
Project description:CT26 tumors were implanted subcutaneously into syngeneic BALB/C mice and allowed to grow for 15-25 days. Tumors were collected, mechanically dissociated, and immune cells enriched using Percoll gradient. Cells were then stained with viability dye, CD45, CD3, and NKp46 to FACS sort for T cells (Live/CD45+/CD3+/NKp46-) and NK cells (Live/CD45+/CD3-/NKp46+). Isolated tumor infiltrating NK and T cells were then processed for RNA sequencing analysis.
Project description:Myeloid-derived suppressor cells (MDSC) are major negative regulators of immune responses in cancer and chronic infections. It remains unclear if regulation of MDSC activity at different conditions is controlled by similar mechanisms. In order to compare MDSC in mice with cancer and lymphocytic choriomeningitis virus (LCMV) infection, we would like to perform gene profiling and comparison of M-MDSCs in tumor bearing and LCMV infected mice using total RNAseq:
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.
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.
Project description:CT26 cells expressing lentiviral Cas9 and sgRNAs targeting either control or Gna13 were transplanted into immunocompetent BALB/c mice. Tumors were harvested and processed for RNA-seq
Project description:A majority of effector Treg cells (eTregs) that are abundant in many types of tumors are marked by the expression of Blimp1. However, the specific impact of Blimp1+ eTregs on, and mechanisms of action within, tumors remain unknown. To better understand the role of Blimp1 in the regulation of eTreg function in the tumor immunity, we profiled the differential gene expression in Blimp1-deficient eTregs compared to WT control eTregs from tumor-bearing mice.
Project description:The DNA exonuclease TREX1 degrades endogenous cytosolic DNA. Cytosolic DNA triggers the cGAS/STING pathway which increases type I interferon. To investigate the physiological significance of TREX1 loss on in vivo tumor growth, we implanted control and TREX1-deficient CT26 tumor cells into immunocompetent BALB/c hosts.Tumor cells were collected 7 days after tumors reached around 200mm3.
Project description:Combinatio of DSP-0509, small molecule TLR7 agonist, with anti PD-1 antibody enhanced anti-tumor inflammatory tumor microenvironment in CT26 tumor.