Project description:To gain insight into the differential expressed genes in immune edited tumor cell lines, we performed genome-wide RNA-sequencing analysis (RNA-seq) in parental P0 (CaSki-P0) and immune edited P3 (CaSki-P3) cells.
Project description:The emergence of immune resistance variants during immunotherapy is poorly understood. We generated a highly immune resistant cell line (P3) from a susceptible cell line (P0) by subjecting it to 3 rounds of in vivo immune selection. Subsequently, microarray analysis of P0 and P3 was performed to identify genes that may contribute to the increase in immune resistance. Experiment Overall Design: Four experimental replicates were prepared for each cell line. P0 is the control cell line, and P3 is the experimental/resistant cell line.
Project description:The emergence of immune resistance variants during immunotherapy is poorly understood. We generated a highly immune resistant cell line (P3) from a susceptible cell line (P0) by subjecting it to 3 rounds of in vivo immune selection. Subsequently, microarray analysis of P0 and P3 was performed to identify genes that may contribute to the increase in immune resistance. Keywords: cell type comparison
Project description:Villar and intervillar epithelial cells were FACs isolated from P0, P3, P6, or P10 CD1 mouse medial small intestine. Three biological replicates were used for e ach population, and expression profiles were determined using Illumina HiSeq. Comparison of the sample groups allowed for identification of compartment-specific and stage-specific genes.
Project description:Investigation of differential gene expression array between primary and cultured human bone marrow MSCs as adherent cells (P0 and P3) or spheres (P0 and P3)
Project description:Our previous data obtained by using immunohistochemistry showed, that Fgf10+/- (50% Fgf10 expression compared to WT) in hyperoxic condition at postnatal day 3 (P3) compared to WT has less vessel count in the lung and less muscularization of small capillaries in the lung. Furthermore, Fgf10+/- showed a drastic increase in mortality upon hyperoxic lung injury. Main question to be answer by this experiment is as followed: Does Fgf10+/- mice after hyperoxia from P0-P3 show different expression profiles at P3 compared to WT? To adress this question we harvest lungs at P3 from WT and Fgf10+/- after hyperoxia treatment from P0-P3. For this the mice were sacrificed by Ketamin/ Dormitor ip, lungs were perfused transcardiac with PBS and directly frozen in liquid nitrogen.
Project description:Our previous data obtained by using immunohistochemistry showed, that Fgf10+/- (50% Fgf10 expression compared to WT) in hyperoxic condition at postnatal day 3 (P3) compared to WT has less vessel count in the lung and less muscularization of small capillaries in the lung. Furthermore, Fgf10+/- showed a drastic increase in mortality upon hyperoxic lung injury. Main question to be answer by this experiment is as followed: Does Fgf10+/- mice after hyperoxia from P0-P3 show different expression profiles at P3 compared to WT? To adress this question we harvest lungs at P3 from WT and Fgf10+/- after hyperoxia treatment from P0-P3. For this the mice were sacrificed by Ketamin/ Dormitor ip, lungs were perfused transcardiac with PBS and directly frozen in liquid nitrogen.
Project description:Expression arrays comparing Campylobacter jejuni 11168 before and after serial passage in C57 BL/6 IL-10 deficient mice. Gene expression was compared during exponential growth in Bolton broth. Unpassaged (p0) C. jejuni 11168 was compared to the same strain after 1 passage (p1) and after three passages (p3) through the mice. Biological replicates: 4 for p0 v. p1, 3 for p0 v. p3
Project description:This study aims to investigate the regulatory influence of the host microenvironment on tumor growth during the establishment of patient-derived xenograft (PDX) models of human lung cancer in athymic nude mice. By serially passaging tumor tissues from primary clinical specimens through generations P0 to P3, we examined how the immunodeficient but NK cell-competent microenvironment of athymic nude mice affects tumor adaptation and progression. Whole transcriptome (RNA-seq) profiling was used to identify changes in gene expression related to immune signaling and stromal interaction across passages. This project provides important insights into the role of the murine host microenvironment, particularly innate immune responses, in shaping the development and evolution of human lung cancer in PDX models, and supports future translational studies using PDX systems as clinically relevant tools for cancer research.
Project description:Tumor metabolic reprogramming profoundly shapes antitumor immunity, but the mechanisms linking glutamine metabolism to immune evasion in hepatocellular carcinoma (HCC) remain incompletely understood. Here, we identify the glutamine transporter SLC1A5 as a tumor-intrinsic regulator of HCC progression and antitumor immunity. Genetic deletion or pharmacological inhibition of SLC1A5 suppressed tumor growth across autochthonous, orthotopic, and subcutaneous tumor models and enhanced the efficacy of immune checkpoint blockade. Mechanistically, SLC1A5-dependent glutamine metabolism maintained cellular redox homeostasis and mitochondrial integrity, whereas SLC1A5 loss promoted mitochondrial stress and activation of type I interferon signaling, thereby enhancing antitumor CD8+ T-cell responses. Conversely, SLC1A5 overexpression promoted tumor progression and immune suppression. These findings establish SLC1A5-mediated glutamine metabolism as a metabolic mechanism of immune evasion and suggest SLC1A5 as a potential therapeutic target for improving immunotherapy responses in HCC.