Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA profiling of IL-34 overexpressing acute myeloid leukemia (AML) cells

ABSTRACT: Acute myeloid leukemia (AML) is a highly heterogeneous disease. In our study, we found that overexpressing IL-34 in AML cells accelerates the AML progression and shorten the mice survival, which is medicated by LSC level. We used one of the LSC markers, c-Kit, to divide AML cells. The goals of this study aim to reveal the mechanism mediated by IL-34 overexpression, we performed the RNAseq profiling of MA9-c-kit-, MA9-c-kit+ and MA9-IL-34 AML cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE213201 | GEO | 2022/09/16

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

RNA profiling of IRF7 knockout acute myeloid leukemia (AML) cells

Project description:Acute myeloid leukemia (AML) is an aggressive hematopoietic malignant. In our study, we found that knockout of IRF7 in AML cells accelerates the AML progression and shorten the mice survival, which is medicated by LSC level. The goals of this study aim to reveal the mechanism mediated by IRF7 knockout, we performed the RNAseq profiling of WT c-kit-, WT c-kit+ and IRF7-/- c-kit+ AML cells

2021-06-30 | GSE178560 | GEO

Gene expression profiles of AML derived stem cells: similarity to hematopoietic stem cells

Project description:Tumors contain a fraction of cancer stem cells that maintain the propagation of the disease. The CD34‏CD38_ cells, isolated from acute myeloid leukemia (AML), were shown to be enriched leukemic stem cells (LSC). We isolated the CD34‏CD38_ cell fraction from AML and compared their gene expression profiles to the CD34‏CD38‏ cell fraction, using microarrays. We found 409 genes that were at least twofold over- or underexpressed between the two cell populations. These include underexpression of DNA repair, signal transduction and cell cycle genes, consistent with the relative quiescence of stem cells, and chromosomal aberrations and mutations of leukemic cells. Comparison of the LSC expression data to that of normal hematopoietic stem cells (HSC) revealed that 34% of the modulated genes are shared by both LSC and HSC, supporting the suggestion that the LSC originated within the HSC progenitors. We focused on the Notch pathway since Jagged-2, a Notch ligand was found to be overexpressed in the LSC samples. We show that DAPT, an inhibitor of gamma-secretase, a protease that is involved in Jagged and Notch signaling, inhibits LSC growth in colony formation assays. Identification of additional genes that regulate LSC self-renewal may provide new targets for therapy. Microarrays were used to compare the gene expression patterns between AML CD34+CD38- cells and AML CD34+CD38+

2011-12-01 | E-GEOD-34044 | biostudies-arrayexpress

RNA-seq analysis of αPD-1 treatment outcomes in IL-34 expressing or not expressing CT26 cell line

Project description:Interleukin-34 (IL-34) is an alternative ligand to colony-stimulating factor-1 (CSF-1) for the CSF-1 receptor that acts as a key regulator of monocyte/macrophage lineage. In this study, we show that cancer cells-derived IL-34 mediates resistance to immune checkpoint blockade regardless of CSF-1 existence. In a therapeutic study of a programmed death-1 and cytotoxic T-lymphocyte-associated antigen-4 blocking monoclonal antibody, the expression of IL-34 in tumors was accompanied with limited benefits compared to IL-34 non-expressing tumors in various murine cancer models. Consistent with its immunosuppressive characteristics, the expression of IL-34 in tumors correlates with decreased frequencies of cellular (such as CD8+ and CD4+ T cells) and molecular (including various cytokines and chemokines) effectors at the tumor microenvironment. In addition, IL-34 blockade expands the M1-macrophage population. Then, a neutralizing antibody against IL-34 helped to reverse these effects and improved the therapeutic effects of the immune checkpoint blockade in combinatorial therapeutic models, including a patient-derived xenograft model of primary lung adenocarcinoma. Collectively, we revealed that tumor-derived IL-34 inhibits the efficacy of immune checkpoint blockade and proposed the utility of IL-34 blockade as a new strategy for cancer therapy.

2020-09-30 | GSE157602 | GEO

RNA profiling of Suv39h1 overexpressed MLL-AF9 induced acute myeloid leukemia (AML) cells

Project description:Acute myeloid leukemias (AMLs) with rearrangement of the mixed-lineage leukemia (MLL) gene are the most aggressive hematopoietic malignancies. By analyzing the clinical data, we found the expression of SUV39H1 was significantly decreased in AML patients and MLL-AF9 (MA9) induced AML mice, in comparison with controls. Remarkably, when overexpress Suv39h1 in MA9 AML mice, the survival of AML mice was significantly prolonged.To examined the mechanism mediated by Suv39h1 overexpression (SUV-OE), we performed the RNAseq profiling of SUV-OE MA9 AML cells and control cells.

2020-12-22 | GSE115549 | GEO

Burkholderia thailandensis 34 strain:34

Project description:Burkholderia thailandensis 34 strain:34 Genome sequencing

| PRJNA178704 | ENA

IL-34-differenciated CD14+CD115+ monocytes expand and potentiate IL-34+ Tregs to control human transplant rejection

Project description:IL-34-differenciated CD14+CD115+ monocytes expand and potentiate IL-34+ Tregs to control human transplant rejection

| PRJEB37095 | ENA

Transcription profiling of human MLL-AF10 myeloid leukemia cellular subsets

Project description:Leukemia cells from mice with MLL-AF10 AML were fractionated into separate sub-populations on the basis of c-kit expression, which correlates with MLL LSC frequency (Somervaille and Cleary, 2006). The sorted AML sub-populations exhibited substantial differences in their frequencies of AML CFCs/LSCs (mean 14-fold) and morphologic features, consistent with a leukemia cell hierarchy with maturation through to terminally differentiated neutrophils. Experiment Overall Design: Leukemic splenocytes from four mice with MLL-AF10 AML were sub-fractionated in to c-kit high and c-kit negative sub-populations by FACS.

2009-02-21 | E-GEOD-13692 | biostudies-arrayexpress

Integrative epigenomic analysis in MLL-AF9 acute myeloid leukemia (AML) and B-acute lymphoblastic leukemia (B-ALL)

Project description:Next generation DNA sequencing of acute myeloid leukemia (AML) patient samples has revealed novel recurrent mutations while at the same time highlighting the genetic heterogeneity of the disease. These observations suggest that an extraordinarily large number of combinations of mutations can contribute to leukemogenesis. In order to address the question of the contribution of patient genetic background to AML we have developed a model system to generate multiple human leukemias in a single donorâs genetic background. Stepwise RNA-seq data from this model shows that in the context of AML driven by the MLL-AF9 (MA9) oncogene, the genetic background of the donor does not have a detectable effect. Comparison of these model leukemias from multiple single donors to AML patient samples containing MA9 translocations revealed conserved gene expression patterns not previously highlighted in this genetic sub-type. We further demonstrate that the expression of one of these genes, RET, is essential both in vivo and in vitro growth of MA9 AMLs . study of methylome during the development of MLL-AF9 AML

2017-05-02 | E-GEOD-70755 | biostudies-arrayexpress

Integrated analysis of MLL-AF9 AML patients and model leukemias highlights RET and other novel therapeutic targets (Leukemia Cell Bank)

2017-05-02 | E-GEOD-72061 | biostudies-arrayexpress

Integrated analysis of MLL-AF9 AML patients and model leukemias highlights RET and other novel therapeutic targets [RNA-Seq_AML]

2017-05-02 | E-GEOD-71686 | biostudies-arrayexpress