Project description:CD84 can be expressed on stromal cells in CLL, its target gene in these cells have yet to be identified. This experiment aimed at determining the CD84 regulated genes on stroma.
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare CD84 activated to control treated primary human M-MDSCs from multiple myeloma patients transcriptome profiling (RNA-seq) to understand the role of CD84 on these cells Methods: mRNA profiles from sorted M-MDSCs from patient bone marrow samples were generated by deep sequencing, in triplicate, using a bulk adaptation of the MARS-Seq protocol.
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare CD84 activated to control treated primary human G-MDSCs from multiple myeloma patients transcriptome profiling (RNA-seq) to understand the role of CD84 on these cells Methods: mRNA profiles from sorted G-MDSCs from patient bone marrow samples were generated by deep sequencing, in triplicate, using a bulk adaptation of the MARS-Seq protocol.
Project description:Acute myeloid leukemia (AML) is an aggressive and often deadly malignancy associated with proliferative immature myeloid blasts. Here, we identified CD84 as a critical survival regulator in AML. High levels of CD84 expression provide survival advantage to leukemia cells, whereas CD84 downregulation disrupts their proliferation, clonogenicity and engraftment capabilities in both human cell lines and patient derived xenograft cells. Critically, loss of CD84 also markedly blocks leukemia engraftment and clonogenicity in MLL-AF9 and inv(16) AML mouse models, highlighting its pivotal role as survival factor across species. Mechanistically, CD84 regulates leukemia cells’ energy metabolism and mitochondrial dynamics. Depletion of CD84 alters mitochondrial ultra-structure and function of leukemia cells, and it caused down-modulation of both oxidative phosphorylation and fatty acid oxidation pathways. CD84 knockdown induced a block of Akt phosphorylation and down-modulation of nuclear factor erythroid 2-related factor 2 (NRF2) impairing AML antioxidant defense. Conversely, CD84 over-expression stabilizes NRF2 and promotes its transcriptional activation, thereby supporting redox homeostasis and mitochondrial function in AML. Collectively, our findings indicate that AML cells depend on CD84 to support antioxidant pro-survival pathways, highlighting a previously unexplored therapeutic vulnerability of leukemia cells.
Project description:CD84 is a key marker of PMN-MDSCs in multiple mouse models and patients tumor samples. Increased CD84 expression levels were found in pathophysiological conditions associated with thrombo-inflammation
Project description:compare gene expression profiles between normal and anergic T cells and identify upregulated genes in anergic T cells Experiment Overall Design: RNA from normal Th1 T cell clone and anergic Th1 T cell clone made anergic by plate-bound anti-CD3 antibody were isolated and amplified for microarray analysis
Project description:SAGE and MPSS libraries were produced from the same RNA sample extracted from an activated CD4+ T cell clone in order to compare the ability of these techniques to indentify the full range of genes expressed in a single cell type. Keywords: Technical comparison of tag-based technologies SAGE and MPSS
Project description:This study was a phase I/II trial initiated by the investigator to evaluate the safety and tolerability of anti-programmed cell death protein 1 (anti-PD1) antibody-activated autologous tumor-infiltrating lymphocytes (TILs) combined with adjuvant chemotherapy in participants with stage III colon cancer. Twenty participants were enrolled and anti-PD1 antibody-activated TILs was infused into participants after the final of adjuvant chemotherapy to assess the safety and 3-year disease-free survival.