Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA316722 | ENA |
REPOSITORIES: ENA
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Project description:The aim of the study was to get insights into transcriptional alterations in bone marrow mesenchymal stromal cells derived from acute myeloid leukemia patients We compared the global gene expression profile from AML BM-MSC (n=19) to healthy donor (HD) controls (HD BM-MSC n=4) AML BM-MSC and HD BM-MSC were isolated from bone marrow aspirates (see below) and hybridized on an Affymetrix HG-U133 Plus 2.0 GeneChip
2016-07-27 | E-GEOD-84881 | biostudies-arrayexpress
Project description:The aim of the study was to get insights into transcriptional alterations in bone marrow mesenchymal stromal cells derived from acute myeloid leukemia patients We compared the global gene expression profile from AML BM-MSC (n=19) to healthy donor (HD) controls (HD BM-MSC n=4)
2016-07-27 | GSE84881 | GEO
Project description:We found that cells of acute myeloid leukemia (AML) affect the transcriptome of mesenchymal stromal cells (MSC) in bone marrow (BM) involved by AML. Gene expression in BM-MSC of AML-bearing mice differed from that in BM-MSC of control mice; some gene changes were the same across different types of AML produced by well-known fusion oncogenes, while others were specific to certain genotypes. There were notable differences between the effects of tp53 WT and tp53-/- AML with the same oncogene (MLL&FLT3-ITD); these were supported by in vitro experiments in which normal BM-derived MSC were cultured with the same tp53 WT and tp53-/- pair of AML cells.
2017-06-14 | GSE97194 | GEO
Project description:Transcriptional Alterations in Bone Marrow Mesenchymal Stromal Cells derived from Acute Myeloid Leukemia patients (AML BM-MSC)
| PRJNA335429 | ENA
Project description:Bone marrow (BM) mesenchymal stromal cells (BM-MSC) upregulate their NF-κB signaling to protect leukemia cells from chemotherapy-induced apoptosis.
2014-05-19 | GSE55533 | GEO
Project description:Heterogeneity and variable survival outcomes of Acute Myeloid Leukemia (AML), suggest that yet undiscovered genes and pathways contribute to AML. Mesenchymal stem cells (MSC), an important component of bone marrow/ stromal microenvironment has been shown to contribute to development and progression of various cancers. Current study was aimed at characterizing MSC from AML bone marrow (BM) and evaluate their therapeutic potential in controlling survival of AML leukemic blasts. MSCs were isolated and cultured from BM of high-risk AML patients. MSC were also obtained from BM of bi-lineage leukemia (ETP-ALL) patients as control MSC from precursor stage of leukemia. MSC derived from uninvolved BM (UnBM) of lymphoma patients were used as normal MSC control. Leukemic blasts were derived from BM of AML and ETP-ALL patients. Patient derived AML-MSC exhibited characteristic profile of MSC Type-II CD90+CD45lo expressing high percent of TLR3 than TLR4 receptors, indicating pro-tumorigenic nature. Gene expression profiles of freshly derived leukemia blasts, AML cell line and AML MSC exhibited deregulated and overactivated Aurora Kinase pathway and inflammasome innate immune pathway. These two pathways are known to be upregulated in many solid and hematological cancers. Further we observed few tumor suppressor genes were downregulated in these groups. In vitro, AML MSC supported survival of leukemic blasts and increased chemoresistance to standard anticancer drugs. Hence AML MSC and ETP-ALL MSC were treated with immunomodulatory drug cocktail (IMiD) containing TLR3 antibody, TLR4 ligand and CXCR4 antagonist peptide (Gift from Kyoto University, Japan), designated as MSC-IMiD. It was observed that MSC-IMiD reduced chemoresistance of leukemic blasts to certain extent in vitro. Further we evaluated if leukemia BM derived MSC, MSC culture supernatant or MSC-IMiD can provide therapeutic benefit to control growth of AML xenograft in mouse model. Human gene expression profile was mapped in human-mouse xenograft made as subcutaneous tumor in immunodeficient NOD-SCID mice model from AML cell line KG1. Comparison was done of all treated groups with tumor bearing control gene expression data. It was interesting to note that MSC and MSC-IMiD could reduce tumor growth in 50% of mice tested. Mice treated with MSC culture supernatant exhibited reduction in tumor growth at par with that seen in Adriamycin treated positive control group. Deregulation of Aurora kinase pathway, inflammasome pathway genes and tumor suppressor genes was found to be reversed in residual tumor tissue of mice treated with MSC and MSC culture supernatant. This gene expression profiling study has helped understanding pathways involved in chemoresistance and immune suppression observed in AML. Moreover, this study has provided leads that MSC or its conditioned media can be explored further to control abnormal myelopoiesis in AML and develop targeted therapy. Funding source: Grant ID: 53/13/2013/CMB/BMS. Grantee: Jyoti Kode Grant title: Understanding the cross-talk between mesenchymal stromal cells and leukemic stem cells in Acute Myeloid Leukemia: Implications in disease biology and therapy. Name of the funding source: Indian Council of Medical Research, Government of India, India.
2023-05-02 | GSE150070 | GEO
Project description:Acute myeloid leukemia (AML) is a heterogeneous clonal disorder of hematopoietic stem/progenitor cells characterized by excessive proliferation and subsequent accumulation of immature myeloid blasts, leading to impaired hematopoiesis in the bone marrow (BM). The progression of AML is closely linked to the crosstalk between leukemic cells and the BM microenvironment, in particular the mesenchymal stromal cells (MSCs). We compared the mRNA expression profile of BM-MSCs from newly diagnosed AML patients (n=3), relapsed AML patients (n=3) and healthy donor controls (n=3)
2021-11-26 | GSE122917 | GEO
Project description:Acute myeloid leukemia (AML) cells release abundant exosomal miR-7977 that transfer into bone marrow (BM) mesenchymal stromal cells (MSCs). We have shown that exosomal miR-7977 was highly released from AML cells and was transferred into BM MSCs. It has been well known that a microRNA has multiple targets. In fact, miRDB predicted 633 targets. Based on these findings, control and miR-7977mimic were transferred into BM MSCs. Subsequently, alteration of transcriptome was analyzed to gain insight into the role of miR-7977 in bone marrow micro environment.
2019-03-18 | GSE108186 | GEO
Project description:Acute myeloid leukemia (AML) cells can shape their niche to their own advantage, perturbing bone marrow stromal and immune landscape. Indeed, AML cells provide the signals, among which inflammatory mediators are crucial, since they are able to subvert mesenchymal stromal cell (MSC) funtions. In particular, IFN-γhigh AML cells hold an inflammatory/immune modulating signature distinct from IFN-γlow cases. We analyzed changes in the gene expression profile of MSCs induced by co-culture with AML cells in vitro. IFN-γhigh but not IFN-γlow AML cells profoundly subverted the MSC transcriptome by inducing immune-modulating pathways, which, intriguingly, included IFN-γ-dependent genes related to regulatory T cell (Treg) differentiation and immune suppression.
2022-07-31 | GSE155441 | GEO
Project description:While extensive efforts have been on understanding bone marrow (BM) niche contribution to normal and malignant hematopoiesis, the role of extramedullary niches has been largely ignored. Evidence suggests a BM mesenchymal stem cell (MSC) counterpart exists in skin. However, their native identity and role in hematopoiesis remain unexplored. Here, we demonstrated that mouse skin harbors MSC subsets that are phenotypically and molecularly similar to BM MSCs, including a primitive MSC population marked by Early B-cell Factor 2 (Ebf2) and downstream MSCs lacking Ebf2. Functionally, skin MSCs not only support acute myeloid leukemia (AML) stem cells but also protect them from chemotherapy. This persistence of AML cells in skin were further amplified in AML-promoting microenvironment lacking Lama4. Our study demonstrated the features of extramedullary niches in skin and their previously unrecognized role in supporting AML stem cells during chemotherapy, opening a new path for understanding the extramedullary manifestation of AML in patients.
2023-07-16 | GSE167562 | GEO