scholarly journals Mir-485-3p and Mir-654-3p Expression in Bone Marrow Mesenchymal Stromal Cells in Patients with Monoclonal Gammopathies Is Related to the Status of the Disease

Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 3155-3155
Author(s):  
Carlos Fernandez de Larrea ◽  
Tania Diaz ◽  
Alfons Navarro ◽  
Ester Lozano ◽  
Mari-Pau Mena ◽  
...  
Keyword(s):  
Gene Expression ◽  
Multiple Myeloma ◽  
Bone Marrow ◽  
Mesenchymal Stromal Cells ◽  
Mirna Expression ◽  
Stromal Cells ◽  
Plasma Cells ◽  
Differentially Expressed ◽  
Monoclonal Gammopathies ◽  
The Status

Abstract Background: Crosstalk between malignant plasma cells and surrounding cells in the bone marrow (BM), such as mesenchymal stromal cells (MSCs), endothelial cells and immune cells, is crucial for pathogenesis of multiple myeloma (MM) and in asymptomatic monoclonal gammopathies. In these diseases, microRNAs (miRNAs) could be useful as biomarkers for diagnosis, prognosis and evaluation of treatment response. miRNAs can be released to the serum and transferred among MM cells and BM-MSCs as cell-cell communication. Previously, we have showed a serum 14-miRNA signature associated with complete remission (CR) after autologous stem-cell transplantation (ASCT). In this sense, patients in CR with partial recovery of two normal serum miRNA levels, similar to those with monoclonal gammopathy of undetermined significance (MGUS), was associated with better prognosis. The aim of this study was to analyze the miRNAs profile in mesenchymal stromal cells derived from bone marrow of patients with multiple myeloma in different status of the disease, comparing with MGUS controls. Methods: We analyzed samples from 95 patients with MGUS (N=23), MM at diagnosis (N=14), relapsed/refractory MM (N=14), MM in partial response (PR) or very good partial response (VGPR) (N=15), MM in CR (N=24) and healthy donors (N=5). Mononuclear cells from BM samples were cultured in DMEM containing 10% FBS. After a week, non-adherent cells were removed, whereas BM-MSCs were selected by their adherence to the plastic and their phenotype was confirmed by multiparametric flow cytometry. In a first screening phase, we analyzed 670 microRNAs in 20 primary BM-MSC from patients with MGUS (N=4), symptomatic MM (N=8) and MM in CR (N=8). miRNAs differentially expressed were identified according to a supervised analysis using significance analysis of microarrays (SAM) and Student's t-test based on multivariate permutation (with random variance model). miRNAs differentially expressed between groups of patients were validated in the whole cohort of BM-MSC from patients. Paired malignant plasma cells (CD38+) miRNA expression from patients with symptomatic MM as well as miRNA in serum samples paired with BM-MSC samples were also compared. RmiR package was used to identify miRNA targets, cross-correlating the miRNA expression data from the present study with our findings on the gene expression signature (Affymetrix Human Genome U219 array) in 12 BM-MSCs from patients (4 MGUS, 4 symptomatic MM and 4 in CR), based on the predicted targets from TargetScan and miRBase databases. Results: In the screening phase, we identified a miRNA profile of 10 miRNAs (miR-663b, miR-654-3p, miR-206, miR-411*, miR-885-5p, miR-668, miR-638, miR-485-3p, miR-744* and miR-199a) differentially expressed between patients with symptomatic MM and MM in CR (adjusted p-value <0.0001). In the validation phase, miR-485-3p and miR-654-3p resulted differentially expressed in the three groups of patients: MGUS, symptomatic MM and patients in CR (ANOVA test: p=0.0101 and p=0.0228, respectively). The levels of these miRNAs were significantly decreased in patients with MM than in those with MGUS, and these levels seemed to recover when patients achieved CR. These two miRNAs (miR-485-3p and miR-654-3p) were also correlated with all degrees of response in MM and with asymptomatic gammopathies (ANOVA test: p=0.0154 and p=0.0487, respectively). Moreover, paired cross-correlation among these two miRNAs expression with our results in mRNA gene expression profile data showed 324 for miR-485-3p and 265 for miR-654-3p genes (correlation index < -0.8) (Figure 1A and 1B). miR-485-3p and miR-654-3p showed a higher expression in BM-MSC than in MM CD38+ cells, suggesting MSC as cell of origin for these miRNAs. Serum expression of these two miRNAs was concordant with the observed in BM-MSC, with higher in patients in CR and MGUS than in those with symptomatic MM (Figure 1C and 1D). miRNA expression in BM-MSC supernatant as well as the identification of the biological role and validation of the miRNA targets are ongoing. Conclusion: miR-485-3p and miR-654-3p expression in mesenchymal stromal cells from bone marrow in patients with multiple myeloma and asymptomatic monoclonal gammopathies is related to the status of the disease and the response to treatment. These miRNAs are also expressed in serum, resulting in potential biomarkers for disease activity and risk of progression. Disclosures Rosinol: Janssen, Celgene, Amgen, Takeda: Honoraria. Bladé:Janssen: Honoraria.

Characterization of Mesenchymal Stem Cells Abnormalities in Multiple Myeloma.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 511-511 ◽  
Author(s):  
Philippe Bourin ◽  
Jill Corre ◽  
Karène Mahtouk ◽  
Mélanie Gadelorge ◽  
Patrick Laharrague ◽  
...  
Keyword(s):  
Gene Expression ◽  
Stem Cells ◽  
Multiple Myeloma ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Plasma Cells ◽  
Osteoblastic Differentiation ◽  
Differentially Expressed ◽  
Matrix Mineralization ◽  
Protein Levels

Abstract Introduction: The bone marrow microenvironnement (BMMe) play a significant role in the physiopathology of the multiple myeloma (MM). However, its abnormality still remains controversial. To address this question, we studied bone marrow mesenchymal stem cells (MSCs), the only long-lived cells of the BMMe. We compared, at a genomic and functional level, the MSCs isolated from patients with MM, to MSCs isolated from healthy subjects and those with monoclonal gammopathy of unknown significance (MGUS). Material and methods : Bone marrow samples from 26 MM patients, 7 MGUS patients and 11 healthy individuals were compared. The MSCs were selected by their adherence on plastic and were cultured in alpha-MEM medium + 10% SVF and antibiotics during 2 passages (primo-culture = P0 and first passage = P1). The gene expression profiling was carried out by Affymetrix GeneChip microarrays (U133 plus 2.0). The expression of interesting differentially expressed genes was validated by ELISA or qRT-PCR. The phenotype was studied by flow cytometry (CD45, CD90, CD73, CD13, CD14). The CFU-F frequencies in BM samples and in cell suspensions after P0 and P1 were studied as well as the cell productions after P0 and P1. The osteoblastic differentiation was evaluated both by alkaline phosphatase dosing and matrix mineralization quantification. We also carried out co-cultures of the MSCs with CD34+ cells to quantify their hematopoietic supportive potential. Finally XG1 and Molp-6, respectively stroma independent and stroma dependent cell lines, were co-cultured with MSCs to check the capacity of the MSCs to support malignant plasma cell growth. Results: Gene expression profile independently classified the MSCs in a normal and in a MM group. MGUS MSCs were interspersed between those 2 groups. 145 distinct genes were differentially expressed in MM and normal MSCs. Among them, 46% could be involved in tumor-microenvironment cross-talk. Known soluble factors involved in MM physiopathologic features, such as IL-6, IL-1ß, DKK1 and amphiregulin, were identified and new ones found. In particular growth and differentiation factor-15 (GDF-15), already described as a accurate biomarker of numerous tumours, was significantly overexpressed (p&lt;0.001) in MM MSCs both at mRNA and protein levels (183.5 ± 64.9 vs 749 ± 90.9 for mRNA, 1 10−4 pg/cell ± 1.9 10−5 pg/cell vs 4.3 10−4 pg/cell ± 1.4 10−4 pg/cell for protein respectively for normal and MM MSCs). It was also able to induce dose-dependant growth of Molp-6, in the absence of a supportive stroma. The phenotype and the CFU-F frequencies and the cell productions were similar in the 3 groups of MSCs and their hematopoietic supportive capacity was maintained. The MM MSCs complete differentiation towards the osteoblastic lineage, evaluated quantitatively, was faded. And very importantly, MM MSCs constituted a better supportive feeder layer for the Molp-6 cell line as compared to normal MSCs (cell expansion after 7 days : 2.1 ± 0.3 vs 3.3 ± 0.4, p = 0.04, respectively for normal and MM MSCs). On the other hand, the growth of XG1 was not influence by the subject origin of the MSCs. Conclusion: Our results show that the MSCs, like the malignant plasma cells, are abnormal in MM. This confirms the place of microenvironnement in the physiopathology of the MM and makes it possible to identify new potential therapeutic targets.

miRNA Expression in Multiple Myeloma as Predictive Model of Response to Bortezomib.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 4918-4918 ◽  
Author(s):  
Paola Neri ◽  
Kathy Gratton ◽  
Li Ren ◽  
Adnan Mansoor ◽  
Peter Duggan ◽  
...  
Keyword(s):  
Gene Expression ◽  
Multiple Myeloma ◽  
Bone Marrow ◽  
Cell Lines ◽  
Mirna Expression ◽  
Response To Therapy ◽  
Differentially Expressed ◽  
Mirna Signature ◽  
Prediction Of Response ◽  
Mirna Profiling

Abstract Abstract 4918 Background Bortezomib therapeutic efficacy is well established in multiple myeloma (MM) however response to this therapy remains difficult to predict with resistant disease observed in nearly 20% of MM patients. Through DNA microarrays, predictive models of response to stem cell transplant and Bortezomib were reported correlating mRNA expression data with disease outcomes and response to therapy. MicroRNAs (miRNAs) are a key class of small, non-coding RNA molecules that modulate post-transcriptional regulation of gene expression and were recently described to be involved in deregulation of gene expression in many cancers including MM. Little evidence however is available concerning the role of miRNA expression in the prediction of response to Bortezomib in MM. We aimed to assess the expression of miRNAs in a panel of Bortezomib highly sensitive and relatively resistant MM cell lines as well as primary MM cells and identify miRNA expression patterns that are associated with response to Bortezomib. Methods We have used miRNA microarrays (Affymetrix miRNA GeneChip) as well as liquid phase Luminex microbead miRNA profiling (Flexmir, Luminex) to profile miRNA expression in MM cell lines (MM1S, KMS11, INA6, U266) and sorted CD138+ bone marrow PCs from MM patients prior to treatment with Bortezomib (n=5; 3 sensitive and 2 resistant) and PCs from a healthy normal donor (n=1). The MM cell lines included in this analysis were classified as sensitive (S) or resistant (R) based on their Bortezomib IC50 at 48 hours (IC50 for MM1S and KMS11 ∼ 5 nM versus INA6 and U266 ∼ 20nM). For the microarray studies the hybridization signal values for the multiple probes for each miRNA were obtained and normalized with the use of miRNA QC tool (Affymetrix) and analyzed using Partek Genomics Suite software. Thereafter, filters were applied to identify the miRNA probes whose normalized signal were at least 2 folds differentially expressed between sensitive (MM1S) and resistant (INA6) cell lines with a P value < 0.05 (ANOVA) and a FDR of 0.05. Bortezomib sensitive (n=3) and resistant (n=2) primary MM samples were subjected to the same miRNA array analysis and filtering. Liquid phase Luminex microbead miRNA profiling (FlexmiR) was used for the confirmation (MM1S and INA6) and validation of the array results in other MM cell lines KMS11 (IC50 5nM) and U266 (IC50 20nM). Results Using Affymetrix miRNA GeneChip we identified 22 differentially expressed miRNA with overexpression of miR-155, miR-342-3p, miR-181a and b, miR-128, miR-20b and downregulation miR-let-7b, miR-let-7i, miR-let-7d, miR-let-7c, miR-222, miR-221, miR-23a, miR-27a and miR-29a in bortezomib relatively resistant (INA6) versus sensitive (MM1S) cell line. These results were confirmed in INA6 and MM1S cells with the use of Luminex microbead miRNA profiling and validated to be similarly differentially expressed between KMS11 (sensitive) and relatively U266 (resistant) cell lines. Furthermore, TargetScan algorithms and Ingenuity Pathway Analysis software were used to identify predicted miRNAs-targeted mRNAs or potentially regulated networks and included genes involved in cell cycle regulation, cell growth, apoptosis and ubiquitin-conjugation pathways. Lastly to further investigate the clinical relevance of miRNAs in MM in terms of prediction of response and outcome to Bortezomib, we correlated miRNA expression profile of sorted CD138+ bone marrow PCs from Bortezomib sensitive (n=3) and resistant (n=2) MM patients with their response to therapy. Unsupervised analysis of the data revealed that the Bortezomib sensitive MM patients clustered with MM1S cell line while resistant patients segregated into the INA6 cluster. Conclusion In summary, we have described a MM miRNA signature, which includes miRNAs that modulate the expression of proteins critical to myeloma pathogenesis and is predictive of response to Bortezomib. Further validation of this miRNA signature in a larger cohort of Bortezomib-treated MM patients is ongoing. Disclosures Stewart: Glaxo-Smith-Kline: Research Funding.

scholarly journals Gene Expression Profile of Circulating Myeloma Cells Reveals CD44 and CD97 (ADGRE5) Overexpression

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 5639-5639
Author(s):  
Tereza Sevcikova ◽  
Fedor Kryukov ◽  
Lucie Brozova ◽  
Jana Filipova ◽  
Zuzana Kufova ◽  
...  
Keyword(s):  
Gene Expression ◽  
Multiple Myeloma ◽  
Bone Marrow ◽  
Peripheral Blood ◽  
Research Funding ◽  
Plasma Cells ◽  
Flow Cytometric Analysis ◽  
Differentially Expressed ◽  
Paired Samples ◽  
Flow Cytometric

Abstract Introduction: Release of the aberrant plasma cells (PC) from the bone marrow (BM) and their presence in the peripheral blood (PB) is a maker of disease progression and worse survival in multiple myeloma (MM) (Nowakowski et al., 2005). Circulating plasma cells (cPCs) are able to survive without homing microenvironment, evade the original tumor and colonize other bone marrow niche. Detailed analysis of various surface proteins showed that cPCs display decreased levels of integrins, adhesion molecules N-CAM (CD56) and the stem cell factor receptor (Paiva et al., 2013). Comprehensive analysis of the genome-wide gene expression profiling that could provide deeper insight into the expression patterns of cPCs of MM is still lacking. Aims: To identify differentially expressed genes in paired samples of aberrant plasma cells from BM and PB and to describe potential biomarkers of cPCs in MM. Material and methods: Ten patients with multiple myeloma (seven new diagnoses and three relapses) have been included in the study after signing the informed consent form. Paired samples of aberrant plasma cells from bone marrow and peripheral blood were obtained from each patient. Aberrant plasma cells (aPCs) were sorted according to the immunophenotype as CD45dim/CD38+/CD19-/CD56-/+ cells. Gene expression profiling (GEP) was performed on paired samples using Affymetrix GeneChip Human Gene ST 1.0 array. RMA normalized data at gene level were analyzed using Wilcoxon paired test with Benjamini-Hochberg multiple testing correction. Results: The median infiltration of aberrant PC in the BM was 27.5% (range 1.1 - 93%) and 1.2% (range 0.19 - 2.8%) for cPCs in the PB. The median level of M-protein was 32.35 g/l (range 18.6 - 62.2 g/l). GEP analysis of paired BM and PB samples revealed 1001 significantly changed genes in cPCs (adjusted p-value<0.05). Gene ontology analysis did not reveal any significantly affected pathways. Nevertheless, two genes upregulated in cPCs, ADGRE5 and CD44, can be suggested as biologically relevant potential biomarkers of cPCs (Figure 1). Conclusion: The infiltration of aPCs in the bone marrow does not correlate with the amount of cPCs (p=0.16). Among differentially expressed genes, two surface markers upregulated in cPCs are of particular interest: CD44 and ADGRE5 (CD97). The CD44 antigen is a cell-surface glycoprotein involved in cell-cell interactions, cell adhesion and migration. Moreover, CD44 contribute to lenalidomide resistance in multiple myeloma (Bjorklund et al., 2014). CD97 is encoded by ADGRE5 gene and belongs to the EGF-TM7 subgroup of adhesion G-protein-coupled receptors. The expression of CD97 has been linked to invasive behavior in thyroid and colorectal cancer. Moreover, higher CD97 expression levels have been detected in 54% (208/385) of primary AML samples based on flow cytometric analysis (Wobus et al., 2015). Nevertheless, neither ADGRE5 nor CD97 expression were described in plasma cell dyscrasia previously. Thus, despite non-systemic changes of gene expression at the whole transcriptome level, cPCs in MM likely represent distinct biological entity with specific expression profile underlying advanced PC malignant transformation. To confirm the results, flow cytometric analysis on the bigger cohort will be performed. Acknowledgment: This study was supported by Institutional Development Plan of University of Ostrava (IRP201550) and The Ministry of Education, Youth and Sports (Specific university research of the Faculty of Medicine, University of Ostrava) project no. SGS03/LF/2015-2016, Ministry of Health Czech Republic RVO-FNOs/2014/17P and RVO-FNOs/2016/21. Figure 1 Genes of interest differentially expressed in the bone marrow (BM) versus peripheral blood (PB) aberrant plasma cells. Figure 1. Genes of interest differentially expressed in the bone marrow (BM) versus peripheral blood (PB) aberrant plasma cells. Disclosures Hajek: BMS: Honoraria; Onyx: Consultancy; Novartis: Research Funding; Amgen: Consultancy, Honoraria, Research Funding; Takeda: Consultancy, Honoraria, Research Funding.

scholarly journals Bone Marrow Mesenchymal Stromal Cells in Multiple Myeloma: Their Role as Active Contributors to Myeloma Progression

Cancers ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 2542
Author(s):  
Patricia Maiso ◽  
Pedro Mogollón ◽  
Enrique M. Ocio ◽  
Mercedes Garayoa
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
Mesenchymal Stromal Cells ◽  
Stromal Cells ◽  
Plasma Cells ◽  
Myeloma Cells ◽  
Growth And Survival ◽  
Myeloma Bone Disease ◽  
Healthy Donors ◽  
Immunosuppressive Microenvironment

Multiple myeloma (MM) is a hematological malignancy of plasma cells that proliferate and accumulate within the bone marrow (BM). Work from many groups has made evident that the complex microenvironment of the BM plays a crucial role in myeloma progression and response to therapeutic agents. Within the cellular components of the BM, we will specifically focus on mesenchymal stromal cells (MSCs), which are known to interact with myeloma cells and the other components of the BM through cell to cell, soluble factors and, as more recently evidenced, through extracellular vesicles. Multiple structural and functional abnormalities have been found when characterizing MSCs derived from myeloma patients (MM-MSCs) and comparing them to those from healthy donors (HD-MSCs). Other studies have identified differences in genomic, mRNA, microRNA, histone modification, and DNA methylation profiles. We discuss these distinctive features shaping MM-MSCs and propose a model for the transition from HD-MSCs to MM-MSCs as a consequence of the interaction with myeloma cells. Finally, we review the contribution of MM-MSCs to several aspects of myeloma pathology, specifically to myeloma growth and survival, drug resistance, dissemination and homing, myeloma bone disease, and the induction of a pro-inflammatory and immunosuppressive microenvironment.

scholarly journals Effects of bone marrow-derived mesenchymal stromal cells on gene expression in human alveolar type II cells exposed to TNF-α , IL-1β , and IFN-γ

2018 ◽  
Vol 6 (16) ◽  
pp. e13831 ◽  
Author(s):  
Matthew Schwede ◽  
Erin M. Wilfong ◽  
Rachel L. Zemans ◽  
Patty J. Lee ◽  
Claudia dos Santos ◽  
...  
Keyword(s):  
Gene Expression ◽  
Bone Marrow ◽  
Mesenchymal Stromal Cells ◽  
Stromal Cells ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Tnf Α ◽  
Ifn Γ

Mesenchymal Stromal Cells From Myelodysplastic Syndrome Patients Show Lower DICER1 and DROSHA Expression, as Well as Decreased Mir-155 and Mir-181a MicroRNA Expression, When Compared with Healthy Controls

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 397-397
Author(s):  
Carlos Santamaría ◽  
Olga López-VIllar ◽  
Sandra Muntión ◽  
Belén Blanco ◽  
Soraya Carrancio ◽  
...  
Keyword(s):  
Gene Expression ◽  
Bone Marrow ◽  
Protein Expression ◽  
Myelodysplastic Syndrome ◽  
Western Blot ◽  
Mesenchymal Stromal Cells ◽  
Stromal Cells ◽  
Microrna Expression ◽  
Healthy Controls ◽  
Lower Expression

Abstract Abstract 397 Mesenchymal stromal cells (MSC) are closely related to the regulation of hematopoietic stem cell niche. Recently, Raaijmakers et al (Nature, 2010), published that deletion of Dicer1, a RNase III enzyme involved in microRNA biogenesis, in murine MSC-derived osteoprogenitors triggered peripherical blood cytopenias, myelodysplasia and subsequent AML, showing that molecular alterations in bone marrow microenvironment could result in clonal impaired haematopoiesis. Here, we have investigated whether MSC from myelodysplastic syndrome (MDS) patients show differences in DICER1 and DROSHA, another RNA III endonuclease, in comparison to healthy MSC. In addition, we have analyzed several hematopoietic-related microRNAs in these same samples. Bone marrow MSC from MDS patients (n=35; 10 5q- syndrome, 4 RA, 5 RARS, 10 RCMD, 3 RAEB, 2 MDS-U and 1 hypocellular MDS) and healthy donors (HD, n=20) were isolated and in vitro expanded following standard procedures until the third passage. Additionally, paired mononuclear cells (MNC) from 13 MDS and 8 HD were obtained. Total RNA was isolated using TRIzol reagent (Invitrogen). DICER1 and DROSHA relative gene expressions were assessed by quantitative PCR (Q-PCR) using commercial TaqMan® assay (Applied Biosystems®) with GAPDH as control gene. DICER1 and DROSHA (Abcam) protein expression were evaluated in whole cell lysates by western blot, using calnexin (Stressgen) as control. Several microRNAs with known role in hematopoiesis and immune system regulation were analyzed in 25 MDS and 12 HD by Q-PCR using commercial TaqMan® MicroRNA assay (Applied Biosystems®) with RNU43 as control microRNA. MSC from MDS showed significant lower DICER1 (0.0035±0.0020 vs. 0.0076±0.0092; p=0.044) and DROSHA (0.0070±0.0028 vs. 0.0135±0.0176; p=0.019) gene expression levels than healthy controls. Moreover, MSC from MDS showed lower protein expression of both DICER1 and DROSHA by western blot analysis, confirming Q-PCR findings. By contrast, no difference in either DICER1 (0.0197±0.0151 vs. 0.0173±0.0112; p=0.9) or DROSHA (0.0089±0.0023 vs. 0.0067±0.0037; p=0.09) gene expression were observed between MNC from MDS and HD. As far as microRNA expression, we observed a lower expression of mir-155 (0.63±0.92 vs. 0.94±0.49; p=0.007) and mir-181a (1.30±0.95 vs. 2.02±1.05; p=0.041) in MSC from MDS in comparison to healthy controls. Mir-155 and mir-181a are involved in T-cell and B-cell differentiation, while mir-155 are also related to erythroid and megakarycytic differentiation. We conclude that MSC from MDS patients show lower expression of DICER and DROSHA, two relevant RNA-III endonucleases involved in the microRNA biogenesis, confirming recent findings in murine models. Moreover, the expression of some microRNA is impaired in these cells, raising the possibility that these microenvironmental alterations could be involved in the MDS pathophysiology. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Bone Marrow Microenvironment in Multiple Myeloma Progression

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
S. Manier ◽  
A. Sacco ◽  
X. Leleu ◽  
I. M. Ghobrial ◽  
A. M. Roccaro
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
Stromal Cells ◽  
Plasma Cells ◽  
Cellular Compartment ◽  
Cell Homing ◽  
Premetastatic Niche ◽  
Bm Niche ◽  
Malignant Plasma Cell ◽  
Made In

Substantial advances have been made in understanding the biology of multiple myeloma (MM) through the study of the bone marrow (BM) microenvironment. Indeed, the BM niche appears to play an important role in differentiation, migration, proliferation, survival, and drug resistance of the malignant plasma cells. The BM niche is composed of a cellular compartment (stromal cells, osteoblasts, osteoclasts, endothelial cells, and immune cells) and a noncellular compartment including the extracellular matrix (ECM) and the liquid milieu (cytokines, growth factors, and chemokines). In this paper we discuss how the interaction between the malignant plasma cell and the BM microenvironment allowed myeloma progression through cell homing and the new concept of premetastatic niche.

Comparison of chemokine and receptor gene expression between Wharton's jelly and bone marrow-derived mesenchymal stromal cells

Cytotherapy ◽  
2012 ◽  
Vol 14 (1) ◽  
pp. 26-33 ◽  
Author(s):  
Sudha Balasubramanian ◽  
Parvathy Venugopal ◽  
Swathi Sundarraj ◽  
Zubaidah Zakaria ◽  
Anish Sen Majumdar ◽  
...  
Keyword(s):  
Gene Expression ◽  
Bone Marrow ◽  
Mesenchymal Stromal Cells ◽  
Stromal Cells ◽  
Receptor Gene ◽  
Wharton’S Jelly ◽  
Wharton's Jelly ◽  
Receptor Gene Expression
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