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Single cell RNA sequencing revealed a chemokine self-feeding of myeloma cells for extramedullary metastasis

ABSTRACT: To determine the mechanisms of the initial extramedullary translocation of myeloma cells from bone marrow into peripheral blood. We found that the clonal cPCs were more frequently detected by flowcytometry in extramedullary plasmacytoma patients and worsened their prognosis. It is technically much easier to collect single cPCs using FACS than it is to perform EMP biopsy. Combining imaging extramedullary plasmacytoma diagnosis and cPCs detection may be a promising strategy for prognostic stratification. Using single-cell transcriptome analysis, we found that CXCL12, a key molecule for the CXCR4-dependent cell retention mechanism in bone marrow, was abnormally up-regulated in cPCs and might initially enable cPCs evasion and translocation into blood.

ORGANISM(S): Homo sapiens

PROVIDER: GSE137545 | GEO | 2019/09/18

REPOSITORIES: GEO

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Project description:Primary extramedullary plasmacytoma

| PRJNA661244 | ENA

Clonal cytogenetics changes in progression of multiple myeloma to extramedullary relapse and plasmocellular leukemia – case report

Project description:Extramedullary relapse (EM) of multiple myeloma (MM) is defined as infiltration of plasma cells (PC) outside of the bone marrow. EM is an aggressive form of the disease with a dismal outcome. We present cytogenetic findings of a 52-year-old female patient who was diagnosed with MM in 2008 and progression of MM to EM and plasmocellular leukemia retrospective analysis of TP53 mutation status showed presence of 2 known missense mutations in exon 6 (c.632C>T) and exon 7 (c.700T>C). EM relapse of this patient was connected to a change of the entire genome profile. We suppose that the extramedullary lesion originated by an expansion of one clone of tumor plasma cells from the bone marrow, which was confirmed by identical genomic profile of both tested samples. Thus, change of ploidy status should be considered as potential hallmark of adverse course of the disease.

2015-10-06 | E-MTAB-3600 | biostudies-arrayexpress

Small RNA sequencing of plasma cells of multiple myeloma patients with extramedullary disease

Project description:Background: Extramedullary disease (EM) in multiple myeloma (MM) is defined by escape of malignant plasma cells out of the bone marrow. The mechanisms of extramedullary spread are not well understood. MicroRNAs (miRNA) were proven to be involved in the pathogenesis of MM; nevertheless, there is a lack of knowledge about their role in EM. Methods: Using NGS analysis, we identified ten differentially expressed miRNA in plasma cells of MM versus EM patients. We performed qPCR in validation phase, using TaqMan Advanced MiRNA Assays. Results: In this study, we identified 10 miRNAs differentially expressed between MM and EM patiens.

2022-12-14 | GSE129918 | GEO

Clonal cytogenetics changes in progression of multiple myeloma to extramedullary relapse and plasmocellular leukemia – case report

2015-10-10 | E-MTAB-3577 | biostudies-arrayexpress

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

Expression profiling of microRNAs enriched in small extracellular vesicles isolated from bone marrow plasma of patients with multiple myeloma, extramedullary disease, and plasma cell leukemia

Project description:Multiple myeloma is a plasma cell malignancy characterized by the abnormal increase of monoclonal immunoglobulins. Despite great treatment advances, there are still patients experiencing migration of tumor cells from the bone marrow and progression of the disease into its aggressive forms including extramedullary disease or plasma cell leukemia. Although the exact molecular mechanisms are not known, several studies have confirmed the involvement of small extracellular vesicles-enriched microRNAs in multiple myeloma progression. Thus, we have performed the expression profiling of these molecules in bone marrow plasma of patients with multiple myeloma, extramedullary disease, and plasma cell leukemia using next-generation sequencing with the aim to identify new molecules involved in the disease pathogenesis. In total, 42 microRNAs were wound to be significantly deregulated among analyzed subgroups. The independent validation by RT-qPCR confirmed the elevated levels of miR-155-5p, miR-140-3p, miR-584-5p, miR-191-5p, and miR-143-3p in patients with multiple myeloma compared to extramedullary disease and/or plasma cell leukemia. Subsequent statistical analysis proved several significant correlations between clinical characteristics or flow cytometry parameters of patients and microRNAs’ expression. In addition, low levels of miR 140 3p, miR-191-5p, miR-744-5p, and miR-143-3p were associated with worse overall survival. These results indicate that deregulation of microRNAs could contribute to multiple myeloma progression. Nevertheless, the exact mechanisms have yet to be clarified.

2024-04-30 | GSE262424 | GEO

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

CGH analysis of an extramedullary muletiple myeloma PDX

Project description:A patient derived orthotopic xenograft (PDOX) was generated from a patient with an aggressive EMM to study in-depth genetic and epigenetic events and drug responses related to extramedullary disease. One of these studies was the evaluation of genetic imbalances by Affymetrix Cytoscan 750K array. The PDOX was derived from a fresh punch of an extramedullary cutaneous lesion that was orthotopically implanted in a NSG mouse. The PDOX mimicked histologic and phenotypic features of patient’s tumor. Cytogenetic studies revealed a hyperploid genome with multiple genetic poor-prognosis alterations. Copy number alterations were detected in all chromosomes.

2021-06-18 | E-MTAB-10630 | biostudies-arrayexpress

Single cell RNA sequencing of multiple myeloma I

Project description:To understand molecular events associated with myeloma progression, we applied single-cell RNA sequencing to myeloma cells in the bone marrow and extramedullary sites. Transcriptome analysis, at single cell level, demonstrates that proliferation and alterations in antigen presentation are associated with myeloma progression whereas NF-kB pathway activation has an anti-correlation. While these alterations are prominent in most of the extramedullary myeloma cells, some myeloma cells in the bone marrow show gene expression signatures resembling extramedullary cells even when the myeloma cells were taken at stable disease. Altogether single-cell transcriptome analysis reveals both common transcriptional programs and heterogeneity turned on during myeloma progression.

2019-10-17 | GSE106218 | GEO

Extramedullary hematopoiesis and immune training drive systemic inflammation and associated organ damage in Systemic Lupus Erythematosus (RRBS)

Project description:Extramedullary hematopoiesis (EMH) is an emerging player in peripheral tissue injury in autoimmune disorders. Here, we use the NZBW/F1 lupus mouse model to explore the contribution of EMH to disease pathogenesis of SLE. We demonstrate that EMH takes place in the spleen of F1-L mice and show it is correlated with the activity of lupus nephritis (LN). Transcriptomic analysis demonstrated that splenic hematopoietic stem and progenitor cells (HSPC) carry a higher inflammatory potential than their bone marrow counterparts. Administration of β-glucan, an inducer of innate immunity, exacerbated splenic EMH, increased neutrophil production and worsened LN. Transcriptomic signatures of HSPCs in SLE patients with high disease activity show changes similar to the ones observed in the lupus-prone mouse model. Overall, EMH and trained immunity are ubiquitous in SLE, contributing to disease pathogenesis by sustaining and amplifying the inflammatory response and increasing the risk for flare of the disease.

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