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CD7 promotes extramedullary involvement of the B-cell acute lymphoblastic leukemia line Tanoue by enhancing integrin beta2-dependent cell adhesiveness

ABSTRACT: The Tanoue expressing firefly-luciferase gene, Luc-Tanoue, was transplanted into non-obese diabetic/severe combined immunodeficient mice, and cells infiltrated in the brain were cultured ex vivo. This process was repeated 4 times to obtain the highly invasive line Luc-Tanoue-F4. Comparison of the global gene expression signatures of Luc-Tanoue-F4 and Luc-Tanoue indicated that the CD7 gene showed the largest increase in expression among EMI-related genes in Luc-Tanoue-F4.

ORGANISM(S): Homo sapiens

PROVIDER: GSE53651 | GEO | 2013/12/27

SECONDARY ACCESSION(S): PRJNA232584

REPOSITORIES: GEO

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CD7 promotes extramedullary involvement of the B-cell acute lymphoblastic leukemia line Tanoue by enhancing integrin beta2-dependent cell adhesiveness

Project description:The Tanoue expressing firefly-luciferase gene, Luc-Tanoue, was transplanted into non-obese diabetic/severe combined immunodeficient mice, and cells infiltrated in the brain were cultured ex vivo. This process was repeated 4 times to obtain the highly invasive line Luc-Tanoue-F4. Comparison of the global gene expression signatures of Luc-Tanoue-F4 and Luc-Tanoue indicated that the CD7 gene showed the largest increase in expression among EMI-related genes in Luc-Tanoue-F4. Tanoue expressing firefly-luciferase gene, Luc-Tanoue, was transplanted into non-obese diabetic/severe combined immunodeficient mice, and cells infiltrated in the brain were cultured ex vivo. This process was repeated 4 times to obtain the highly invasive line Luc-Tanoue-F4.

2013-12-27 | E-GEOD-53651 | biostudies-arrayexpress

RNA sequencing for AML patients with and without extramedullary infiltration

Project description:Extramedullary infiltration (EMI) is a concomitant manifestation indicating poor prognosis of acute myeloid leukemia (AML), yet the underlying mechanism remains poorly understood and therapeutic options are limited. Here, we employed single-cell RNA sequencing on bone marrow (BM) and EMI samples from an AML patient presenting pervasive leukemia cutis. A complement C1Q+ macrophage-like leukemia subset which is enriched within cutis and existed in BM prior to EMI manifestations was identified and further verified in multiple AML patients. RNA-sequencing and quantitative proteomics profiling revealed adverse prognosis of patients bearing C1Q+ population. C1Q expression endowed leukemia cells with tissue-infiltration ability which could establish prominent cutaneous or gastrointestinal EMI nodules in patient-derived xenograft (PDX) and CDX models. Fibroblasts attracted migration of the C1Q+ leukemia cells through surface C1Q-gC1QR recognition and subsequent stimulation of MAFB5 TGF-β signaling. Thus, C1Q orchestrates cancer infiltration pathways through communicating with fibroblasts and represents a compelling therapeutic target for EMI.

2023-04-07 | GSE213584 | GEO

Gene expression profiling of tumor cells and M2 macrophages from WT mice and mice with deletion of integrin beta3 in macrophage lineage cells (b3KOM)

Project description:To better understand the impact of integrin beta3 signaling in myeloid cells on the tumor microenvironment, we compared the gene expression profiles of FACS isolated GFP+ PyMT-BO1 MFP tumor cells and also M2 TAMs (CD11b+Gr1-F4/80+CD206+) from tumor tissue of WT mice and b3ÎÎÎ mice. PyMT-BO1-GFP-Luc tumor cells (100,000) were injected into mammary fat pad (MFP) tissue from WT and b3KOM mice. PyMT-BO1-GFP-Luc cells and CD206hi tumor-associated macrophages (TAMs) were FACS-sorted from day 10 MFP tumor tissue. FACS-sorted cells directly used for RNA extraction and hybridization on Affymetrix microarrays.

2015-12-11 | E-GEOD-75882 | biostudies-arrayexpress

C1Q labels a highly aggressive macrophage-like leukemia population indicating extramedullary infiltration and relapse

Project description:Extramedullary infiltration (EMI) is a concomitant manifestation indicating poor prognosis of acute myeloid leukemia (AML), yet the underlying mechanism remains poorly understood and therapeutic options are limited. Here, we employed single-cell RNA sequencing on bone marrow (BM) and EMI samples from an AML patient presenting pervasive leukemia cutis. A complement C1Q + macrophage-like leukemia subset which is enriched within cutis and existed in BM prior to EMI manifestations was identified and further verified in multiple AML patients. RNA-sequencing and quantitative proteomics profiling revealed adverse prognosis of patients bearing C1Q + population. C1Q expression endowed leukemia cells with tissue-infiltration ability which could establish prominent cutaneous or gastrointestinal EMI nodules in patient-derived xenograft (PDX) and CDX models. Fibroblasts attracted migration of the C1Q + leukemia cells through surface C1Q-gC1QR recognition and subsequent stimulation of MAFB-TGF-β signaling. Thus, C1Q orchestrates cancer infiltration pathways through communicating with fibroblasts and represents a compelling therapeutic target for EMI.

2022-08-03 | PXD035784 | iProX

Expression data of circRNA from new diagnostic AML patients (with or without EMI) and healthy volunteers

Project description:CircRNA microarray was conducted to further explore the underlying circRNA expression alterations in extramedullary infiltration (EMI) of AML. 4 matched samples from EMI, non-EMI AML patients and healthy volunteers were selected. Mononuclear cells from 12 bone marrow samples were separated according to protocols. RNA was then extracted and hybridization for further microarray analysis.

2018-07-04 | GSE116617 | GEO

Expression data of whole genome from new diagnostic AML patients (with or without EMI) and healthy volunteers

Project description:Whole Genome microarray was conducted to further explore the underlying gene expression alterations in extramedullary infiltration (EMI) of AML. 4 matched samples from EMI, non-EMI AML patients and healthy volunteers were selected. Mononuclear cells from 12 bone marrow samples were separated according to protocols. RNA was then extracted and hybridization for further microarray analysis.

2018-07-04 | GSE116616 | GEO

MMP-9 sheds the beta2 integrin subunit (CD18) from macrophages.

Project description: Not available

| S-EPMC2689762 | biostudies-literature

Carfilzomib and dexamethasone for extramedullary myeloma with pleuropericardial involvement.

Project description: Not available

| S-EPMC5538069 | biostudies-other

Intratumor Heterogeneity of MIF Expression Correlates With Extramedullary Involvement of Multiple Myeloma.

Project description: Not available

| S-EPMC8276700 | biostudies-literature

Intratumor Heterogeneity of MIF Expression Correlates with Extramedullary Involvement of Multiple Myeloma

Project description:Macrophage migration inhibitory factor (MIF) has been shown to promote disease progression in many malignancies, including multiple myeloma (MM). We previously reported that MIF regulates MM bone marrow homing and knockdown of MIF favors the extramedullary myeloma formation in mice. Here, based on MIF immunostaining of myeloma cells in paired intramedullary and extramedullary biopsies from 17 patients, we found lower MIF intensity in extramedullary MM (EMM) versus intramedullary MM (IMM). Flow cytometry and histology analysis in ARD cell line-derived xenograft models showed a portion of inoculated human MM cells lost their MIF expression (MIFLow) in vivo. Of note, IMM had dominantly MIFHigh cells, while EMM showed a significantly increased ratio of MIFLow cells. We harvested the extramedullary human MM cells from a mouse and generated single-cell transcriptomic data. The developmental trajectories of MM cells from the MIFHigh to MIFLow state were indicated. The MIFHigh cells featured higher proliferation. The MIFLow ones were more quiescent and harbored abundant ribosomal protein genes. Our findings identified in vivo differential regulation of MIF expression in MM and suggested a potential pathogenic role of MIF in the extramedullary spread of disease.

2021-07-20 | GSE175660 | GEO

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