Exomic microRNA Profiling of Bone Marrow Aspirate Plasma and Comparison with mRNA Profiles Used in the Clinical Management of Multiple Myeloma

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 5681-5681
Author(s):  
Ryan K Van Laar ◽  
Rachel Flinchum ◽  
Brown Nathan ◽  
Joseph Ramsey ◽  
John Shaughnessy ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
Peripheral Blood ◽  
Bone Marrow Aspirate ◽  
Plasma Cells ◽  
Molecular Subtype ◽  
Gene Expression Signature ◽  
Disease Status ◽  
Hematologic Malignancies ◽  
Microrna Profiling

Abstract Exosome-mediated processes are increasingly being implicated in the pathobiology of many forms of solid tumors and hematologic malignancies. In the case of blood cancers, an oncogenic role for exosomes has been demonstrated for multiple myeloma (MM). An increased understanding of the abundance and disease association of extra-cellular microRNAs in particular, may lead to opportinities to improve early detection and management of MM and precursor conditions. We performed microRNA profiling of cell-free bone marrow aspirate plasma on a series of 100 patients with diagnoses of MGUS, active multiple myeloma or relapsed multiple myeloma. The microRNA profiles were compared between disease status groups and also individually with each patient’s routine MyPRS results (ie. GEP70 high/low risk and molecular subtype gene signatures), generated from their malignant CD138+ plasma cells1. MicroRNAs with patterns of expression associated with these clinically validated genomic (mRNA) signatures were investigated to determine if they (i) were known regulators of the genes used in MyPRS and (ii) in a cross-validated analysis, were able to predict the patients MyPRS risk group and molecular subtype. An additional series of paired peripheral blood and bone marrow aspirates (isolated CD138+ plasma cells) were also microRNA and MyPRS profiled, to further investigate the role and potential clinical utility of extracellular microRNAs in multiple myeloma. Results will be presented which describe the abundance of individual microRNA's in realtion to disease status, including microRNA's previously linked to the regulation of mRNA's contained in the GEP70 signature. The ability to predict MGUS progression risk or active myeloma prognosis using molecular signatures in peripheral blood may increase access to, and adoption of, genomic technologies in the diagnosis and management of these related conditions. Reference: [1] van Laar R, Flinchum R, Brown N, et al. Translating a gene expression signature for multiple myeloma prognosis into a robust high-throughput assay for clinical use. BMC Medical Genomics. 2014;7(1):25. Disclosures Van Laar: Signal Genetics: Employment, Equity Ownership. Flinchum:Signal Genetics: Employment. Nathan:Signal Genetics: Employment. Ramsey:Signal Genetics: Employment. Shaughnessy:Signal Genetics: Consultancy.

scholarly journals High-dose sequential chemoradiotherapy in multiple myeloma: residual tumor cells are detectable in bone marrow and peripheral blood cell harvests and after autografting

Blood ◽  
1995 ◽  
Vol 85 (6) ◽  
pp. 1596-1602 ◽  
Author(s):  
P Corradini ◽  
C Voena ◽  
M Astolfi ◽  
M Ladetto ◽  
C Tarella ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
B Cells ◽  
Peripheral Blood ◽  
Plasma Cells ◽  
Disease Status ◽  
Residual Tumor ◽  
High Dose ◽  
Myeloma Cells ◽  
Igh Genes

Based on preliminary encouraging results in terms of response rate and survival, high-dose chemoradiotherapy has gained considerable interest in the treatment of patients with multiple myeloma (MM). We have evaluated the presence of residual myeloma cells in 15 of 18 patients enrolled in a high-dose sequential (HDS) chemoradiotherapy program followed by autografting. Our analysis has been performed both on bone marrow (BM) and peripheral blood (PB) cell harvests and after autografting. As it has been recently shown that B cells clonally related to malignant plasma cells are detectable in MM patients, we have developed a polymerase chain reaction (PCR)-based strategy to detect both residual B cells and plasma cells using clone-specific sequences derived from the rearrangement of Ig heavy chain (IgH) genes. The complementarity-determining regions (CDR) of IgH genes have been used to generate tumor-specific primers and probes. The constant (C) region usage defined the differentiation stage of residual myeloma cells. We report that plasma cells were detectable in PB and BM cell harvests and after transplantation in all assessable patients, irrespective of disease status. B cells were detectable in a consistent proportion of BM and PB samples at diagnosis, but only in one case at the time of PB and BM cell harvests. These cells became sometimes detectable after transplantation. Whether residual myeloma cells are clonogenic and contribute to relapse is currently unknown, and further investigations are required.

scholarly journals Multiple myeloma: circulating lymphocytes that express plasma cell antigens

Blood ◽  
1984 ◽  
Vol 64 (2) ◽  
pp. 352-356
Author(s):  
GJ Ruiz-Arguelles ◽  
JA Katzmann ◽  
PR Greipp ◽  
NJ Gonchoroff ◽  
JP Garton ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
Plasma Cell ◽  
Peripheral Blood ◽  
Plasma Cells ◽  
Peripheral Blood Lymphocytes ◽  
Tumor Burden ◽  
B Cell Differentiation ◽  
Blood Lymphocytes ◽  
Bone Marrow Plasma

The bone marrow and peripheral blood of 14 patients with multiple myeloma were studied with murine monoclonal antibodies that identify antigens on plasma cells (R1–3 and OKT10). Peripheral blood lymphocytes expressing plasma cell antigens were found in six cases. Five of these cases expressed the same antigens that were present on the plasma cells in the bone marrow. Patients that showed such peripheral blood involvement were found to have a larger tumor burden and higher bone marrow plasma cell proliferative activity. In some patients, antigens normally found at earlier stages of B cell differentiation (B1, B2, and J5) were expressed by peripheral blood lymphocytes and/or bone marrow plasma cells.

Adhesion molecule immunophenotype of bone marrow multiple myeloma plasma cells impacts the presence of malignant circulating plasma cells in peripheral blood

2020 ◽  
Author(s):  
Indrė Klimienė ◽  
Mantas Radzevičius ◽  
Rėda Matuzevičienė ◽  
Katažina Sinkevič‐Belliot ◽  
Zita Aušrelė Kučinskienė ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
Adhesion Molecule ◽  
Peripheral Blood ◽  
Plasma Cells

Spontaneous Tumoural Regression in a Patient with t(4;14) Translocation Multiple Myeloma. A Case Report.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 4777-4777
Author(s):  
Noemi Puig ◽  
Christine Chen ◽  
Joseph Mikhael ◽  
Donna Reece ◽  
Suzanne Trudel ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
Case Report ◽  
Bone Marrow Biopsy ◽  
Peripheral Blood ◽  
Low Dose ◽  
Plasma Cells ◽  
Protein Electrophoresis ◽  
Urine Collection ◽  
Normal Limits

Abstract INTRODUCTION Despite recent advances, multiple myeloma continues to be an incurable malignancy, with a median overall survival (OS) of 29–62 months. A shortened survival is seen in myeloma patients having a t(4;14) translocation either with standard or high-dose chemotherapy (median OS 26 and 33 months, respectively). CASE REPORT A 60 year-old female was found to have a high ESR (121mm/h) and low hemoglobin (113g/L) in December 2005. Further work-up led to the diagnosis of stage 1A (Durie-Salmon) multiple myeloma on the basis of the following investigations: a protein electrophoresis showed IgG 12.2g/L, IgA 23.4g/L and IgM 0.33g/L with an IgA-kappa paraprotein; a bone marrow biopsy revealed 20–30% infiltration with atypical plasma cells, kappa restricted; IGH-MMSET fusion transcripts were detected by RT-PCR, consistent with the presence of t(4;14) positive cells in the specimen; a metastatic survey showed generalized osteopenia throughout the axial skeleton and multiple subtle permeative lucencies in the proximal humeral diaphyses bilaterally. A 24-hour urine collection showed 0.05g/L proteinuria with no Bence-Jones proteins detected. Her peripheral blood counts were as follows: hemoglobin 118g/L (MCV 91fL), platelets 275 bil/L and white blood cells 6.6 bil/L with 3.9 neutrophils and 1.8 lymphocytes. Her electrolytes and calcium were within normal limits but she had a slightly elevated creatinine at 107umol/L (normal <99). Her b2-microglobulin, C-reactive protein and albumin were all normal at 219nmol/L (normal ≤219), 4mg/L (normal ≤12) and 36g/L (36–50) respectively. No active therapy was recommended apart from monthly PAMIDRONATE for permeative lucencies. Her past medical history was significant for an IgA cryoglobulinemia diagnosed in 1985 when she presented with arthritis, purpura and Raynaud’s phenomenon. Her cryocrit has been ranging from 0–25% over the years; most recently still at 5%. She did not require any treatment until 1989 when she was started on low dose-steroids. Her flares consist mainly of lower limbs arthritis and purpura and they have been treated with intermittent PREDNISONE 5–7.5mg per day. A progressive drop in her M-protein has been documented since June 2006 with her most recent protein electrophoresis revealing no paraprotein, quantitative IgG is 7.7g/L, IgA 2.23g/L and IgM 0.63g/L. A bone marrow biopsy has shown less than 5% plasma cells. Her peripheral blood counts and biochemistry remained within normal limits and her skeletal survey is unchanged. A 24-hour urine collection shows no significant proteinuria (0.07g/L). Her free light chains assay revealed kappa 13.8mg/L and lambda 11.0mg/L with a ratio kappa/lambda 1.3. CONCLUSIONS We have documented tumoural regression in a patient with IgA-kappa multiple myeloma and t(4;14) only receiving intermittent low dose PREDNISONE and monthly PAMIDRONATE. This exceptional phenomenon has been well described with other malignancies such as testicular germ cell tumours, hepatocellular carcinomas and neuroblastomas; however, to the best of our knowledge, only in 2 cases of multiple myeloma. The unusual nature of this finding is highlighted by the presence of the t(4;14) in the plasma cells, known to be associated with more aggressive disease. The underlying mechanisms, speculated to be immunological for most of the other cancers, remain completely unknown in this case.

Enrichment of functional CD8 memory T cells specific for MUC1 in bone marrow of patients with multiple myeloma

Blood ◽  
2005 ◽  
Vol 105 (5) ◽  
pp. 2132-2134 ◽  
Author(s):  
Carmen Choi ◽  
Mathias Witzens ◽  
Marianna Bucur ◽  
Markus Feuerer ◽  
Nora Sommerfeldt ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
T Cells ◽  
Cd8 T Cells ◽  
Peripheral Blood ◽  
Hematologic Malignancies ◽  
Myeloma Cell ◽  
Interferon Γ ◽  
Multiple Myeloma Cell ◽  
Healthy Donors

AbstractMultiple myeloma (MM) is one of the most common hematologic malignancies. Despite extensive therapeutical approaches, cures remain rare exceptions. An important issue for future immunologic treatments is the characterization of appropriate tumor-associated antigens. Recently, a highly glycosylated mucin MUC1 was detected on a majority of multiple myeloma cell lines. We analyzed bone marrow and peripheral blood of 68 patients with HLA-A2–positive myeloma for the presence and functional activity of CD8 T cells specific for the MUC1-derived peptide LLLLTVLTV. Forty-four percent of the patients with MM contained elevated frequencies of MUC1-specific CD8 T cells in freshly isolated samples from peripheral blood (PB) or bone marrow (BM) compared with corresponding samples from healthy donors. BM-residing T cells possessed a higher functional capacity upon specific reactivation than PB-derived T cells with regard to interferon γ (IFN-γ) secretion, perforin production, and cytotoxicity.

Combination Therapy with Lenalidomide, Bortezomib, Liposomal Doxorubicin and Dexamethasone (LBlipDD) May Overcome Resistance to Prior Treatment with Doxorubicin, Lenalidomide, and Bortezomib in High-Risk Multiple Myeloma (MM).

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 4838-4838
Author(s):  
Reinhard Ruckser ◽  
Georg Tatzreiter ◽  
Elvira Kitzweger ◽  
Karin Strecker ◽  
Stefan Hraby ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
High Risk ◽  
Combination Therapy ◽  
Liposomal Doxorubicin ◽  
Bone Marrow Aspirate ◽  
Plasma Cells ◽  
Who Grade ◽  
Normal Value ◽  
Serum Igg

Abstract Introduction: Lenalidomide (Revlimid®) plus dexamethasone therapy and single-agent bortezomib therapy are approved for the treatment of relapsed/refractory multiple myeloma (MM) patients. A recent phase II trial has shown activity of lenalidomide/bortezomib/dexamethasone in patients with relapsed/refractory MM (Richardson, IMW 2007). Here, we present a case report on the efficacy of combination therapy with lenalidomide, bortezomib, liposomal doxorubicin, and dexamethasone in a patient who was refractory to prior treatments with bortezomib, lenalidomide, and doxorubicin. Methods and Results: A male patient (58 years) presented with IgG-lambda MM in June 2006. Laboratory tests at diagnosis showed total protein of 123g/L (normal value, 66–87 g/L) and a serum IgG of 87.3g/l (normal value, 7–16 g/L). The patient had t(11;14)(q13;q32) translocation and a del13q14, and bone marrow aspirate showed >90% plasma cells. From July 2006 to March 2007, the patient received 3 different chemotherapy treatment regimens (VAD: vincristine, Adriamycin® [doxorubicin], dexamethasone; VDD: Velcade® [bortezomib], doxorubicin, dexamethasone; and LD: lenalidomide, dexamethasone). He showed primary resistance to VAD treatment and developed resistance after 3 and 5 cycles of VDD and LD, respectively. At that point, the patient’s free light chain (fLCh) concentration was 2,320 mg/L (normal value, 5.7–26.3 mg/L). We changed the patient’s treatment regimen to the 4-fold combination of lenalidomide plus bortezomib plus liposomal doxorubicin (lipD) plus dexamethasone (LBlipDD), (lenalidomide 25 mg day 1–21, bortezomib 1mg/m2 day 1+4+8+11, lipD 50 mg/m2 day 4, dexamethasone 40 mg day 1+2+4+5+8+9+11+12; q28 days). The patient received 3 cycles of LBlipDD from May 2007 to July 2007. This treatment combination was well tolerated with no WHO grade 3 or 4 adverse events. The patient was reassessed after 3 treatment cycles. FISH showed a complete eradication of the former cytogenetic abnormalities, bone marrow aspirate showed <5% plasma cells and serum analysis demonstrated a normalized serum IgG value, and a decrease in the fLCh from 2,320 to 173 mg/L. The patient is for the first time transfusion independent and in very good clinical condition. High-dose melphalan with autologous stem cell support is currently planned. Conclusion: Treatment with LBlipDD leads to a good remission in a VAD-, VDD- and LD-resistant patient. The present observation suggests that the use of 4-fold combination of lenalidomide, bortezomib, liposomal doxorubicin, and dexamethasone can be effective in high-risk MM patients and warrants further investigation.

Expression of JAZ in Multiple Myeloma and Its Potential Role as A Novel Molecular Target.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 2862-2862
Author(s):  
Mingli Yang ◽  
Jingxin Qiu ◽  
Ying Li ◽  
David Ostrov ◽  
Jinghua Jia ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
Cell Death ◽  
Small Molecules ◽  
Normal Tissue ◽  
Potential Role ◽  
Plasma Cells ◽  
Hematologic Malignancies ◽  
Molecular Target ◽  
P53 Activation

Abstract Abstract 2862 Poster Board II-838 Multiple myeloma (MM) is an incurable hematologic tumor caused by malignant transformation of plasma cells. JAZ (just another zinc finger protein) was previously identified in our laboratory as a unique ZFP that preferentially binds to double-stranded (ds) RNA rather than dsDNA. The JAZ gene is localized to the human chromosome 5q35-ter, which is a specific chromosomal region at which deletions and translocations occur in different hematologic malignancies including multiple myeloma. The NCI Cancer Genome Anatomy Project data base search reveals that a validated SNP (single nucleotide polymorphism) exists for JAZ at an evolutionarily conserved, 3'-untranslated, regulatory region of JAZ mRNA. This specific SNP exists only in the bone marrow cancer but not in the normal tissue, suggesting a potential role for JAZ in hematologic malignancies. Importantly, we recently discovered JAZ as a novel direct, positive regulator of p53 transcriptional activity. The mechanism involves direct binding to p53's C-terminal (negative) regulatory domain to activate “latent” p53 in response to non-genotoxic stress signals. Moreover, we found that interleukin-3 growth factor withdrawal upregulates JAZ expression in factor-dependent hematopoietic cells in association with activation of the p53 tumor suppressor and induction of apoptotic cell death, indicating that the expression of JAZ is important in the stress response. Thus, to examine the role of JAZ expression in hematologic malignancies, we carried out an immunohistochemistry (IHC) study of JAZ expression in murine and human bone marrow cells and in normal and malignant hematologic tissues and cell lines. The affinity-purified rabbit polyclonal antibody JAZ111 was used and its specificity was verified by the peptide inhibition and also using a commercially available monoclonal antibody against JAZ. Results reveal that JAZ is differentially expressed in different types or stages of hematopoietic cells. For instance, morphologically, JAZ appears to be (relatively) abundantly expressed in plasma cells in normal bone marrow samples and such observation was verified by co-staining with a CD38 antibody. Interestingly, results of JAZ111 staining of an MM tissue microarray (24 cases/48 cores, 13 MM and 11 normal tissues) reveal that in ∼50 % of the MM samples the expression of JAZ is substantially down-regulated compared to the normal tissue controls. This supports the notion that JAZ may play a tumor suppressor role. However, there are exceptions that JAZ was found to be highly or over-expressed in some MM samples on the microarray and other regular individual sample slides, suggesting that JAZ may be latent or inactivated in these cases. Co-staining of the MM samples with a p53 antibody shows that expression of p53 is low, which agrees with the notion that p53 expressed in the MM samples is usually the wild type but in a latent state since the p53 gene has been reported to be rarely mutated and the p53 pathway remains intact in multiple myeloma. Thus, we hypothesize that activation or reactivation of JAZ in the MM cells which express abundant but latent JAZ may induce p53 activation to arrest or kill MM cells. We have explored JAZ as a potentially novel molecular target in multiple myeloma by identifying small molecules that bind and activate JAZ. Using a high-throughput, “molecular docking” strategy, we have screened approximately 240,000 small molecules for their ability to interact with JAZ. Based on the Lipinski Rules for Drug Likeness (molecular characteristics favorable for absorption and permeability), we identified ∼70 putative “drug-like” binding molecules with high scores and obtained ∼40 of them from the NCI Developmental Therapeutics Program. We performed the cell viability study, flow cytometry and Western blot analysis to test their effect on the MM cell lines. Results demonstrate that several of the “candidate” JAZ-targeting compounds can potently induce growth arrest and/or cell death in association with p53 activation. Therefore, while further in vitro and in vivo characterization remains to be carried out, the JAZ-“targeting” compounds point the way to develop a potentially novel therapeutic strategy targeting JAZ to treat multiple myeloma. Disclosures: No relevant conflicts of interest to declare.

Single Cell RNA-Seq Reveals Clonal Consistency and Differential Malignancy in Extramedullary Plasmacytoma of Multiple Myeloma

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 4808-4808
Author(s):  
Shuang Geng ◽  
Jing Wang ◽  
Mingyi Chen ◽  
Wenming Wang ◽  
Yuhong Pang ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
Single Cell ◽  
Plasma Cell ◽  
Peripheral Blood ◽  
Plasma Cells ◽  
Conflicts Of Interest ◽  
Extramedullary Plasmacytoma ◽  
Rna Seq ◽  
Malignant Plasma Cell

Abstract Extramedullary Plasmacytoma (EMP) is a minor yet devastating metastatic form of Multiple Myeloma (MM), shortening patients' survival from 10 years to 6 months on average. Genetic cause of EMP in MM is yet to be defined. Transcriptome difference between EMP+ patients and EMP- patients is studied here on single cell level by RNA Sequencing (RNA-Seq). We sorted CD38+CD138+ malignant plasma cells from bone marrow and peripheral blood samples by flow cytometry, then picked up single malignant plasma cell and performed single cell RNA-Seq with SmartSeq2 protocol followed by Tn5-based library preparation from bone marrow, peripheral blood and extramedullary tissue of EMP patients. From the single cell RNA-Seq results, in bone marrow we found differential gene expression between EMP+ and EMP- samples, such as CTAG2, STMN1 and RRM2. By comparing circulating malignant plasma cells in PBMC and malignant plasma cell from the sample EMP+ patient, we observed metastatic clone in blood with the same VDJ immunoglobulin heavy chain as in bone marrow. Several genes' expression of these metastatic cells are down-regulated than in bone marrow, such as PAGE2, GTSF1, DICER1. These genes may correlate with egress capability of MM cells into peripheral to become circulating plasma cells (cPCs), and EMP eventually. Disclosures No relevant conflicts of interest to declare.

Validation of the Nextseq 500 and Development of a High-Throughput NGS Pipeline for Identifying Clinically-Relevant Gene Variants in Multiple Myeloma Specimens

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 5346-5346
Author(s):  
Agnieszka K. Zielinska ◽  
Kenton Leigh ◽  
Horacio Gomez ◽  
Ryan K Van Laar
Keyword(s):  
Gene Expression ◽  
Multiple Myeloma ◽  
Bone Marrow ◽  
High Throughput ◽  
Bone Marrow Aspirate ◽  
Relative Effectiveness ◽  
Gene Expression Signature ◽  
Molecular Profiling ◽  
Clinical Use ◽  
Dna And Rna

Abstract As molecular profiling technologies have evolved, our understanding of multiple myeloma heterogeneity and the relative effectiveness of treatment options have increased dramatically. Most recently, next generation sequencing (NGS) studies have provided a new degree of molecular resolution into this disease, however it remains a challenge to translate these methodologies and insights from research tools to widely-available clinical assays which can be performed as part of routine patient care. MyPRS® is a clinically and scientifically validated high-throughput gene-expression (Affymetrix) based assay available in all 50 US states. The CLIA and CAP-accredited laboratory workflow is able to isolate sufficient RNA from small amounts of fresh bone marrow aspirate, up to 72 hours post collection[1]. In order to expand the content of the MyPRS assay to include DNA-sequencing based variant, copy number and mutation detection, we have validated highly-scalable methods for isolating RNA and DNA separately and in parallel from individual patient specimens of varying quality and quantity. Yet another challenge of translational NGS profiling is performing complex laboratory procedures, developed primarily for research use only, with the requisite reproducibility and accuracy required for submission to regulatory agencies and ultimately for clinical use. Coupled with the protocols we developed for isolation of both DNA and RNA from small amounts of patient bone marrow aspirate, we performed an investigation of the Illumina NextSeq 500 and "on-site" BaseSpace data processing server. With the multiplexing and parallel processing capability of this platform we estimate being able to sequence, align and variant-call up to 150 myeloma-relevant genes at 1000x coverage per run. Results from our MM cell-line-, normal human- and NIST reference-DNA whole-exome-profiling studies show extremely high levels of technical reproducibility and agreement with results generated from 3rd party laboratories. In addition, we describe associations between the (RNA-expression based) prognostic, molecular subtyping and virtual karyotyping currently included in the MyPRS assay, with results from DNA-based exome profiling, performed on matched specimens. We believe findings underscore the need for comprehensive DNA and RNA based molecular profiling in order to make the most informed patient management decisions. 1. van Laar R, Flinchum R, Brown N, Ramsey J, Riccitelli S, Heuck C, Barlogie B, Shaughnessy Jr J: Translating a gene expression signature for multiple myeloma prognosis into a robust high-throughput assay for clinical use. BMC Medical Genomics 2014, 7 (1):25. Disclosures Zielinska: Signal Genetics: Employment. Leigh:Signal Genetics: Employment. Gomez:Signal Genetics: Employment. Van Laar:Signal Genetics: Employment.

scholarly journals Multiple myeloma: circulating lymphocytes that express plasma cell antigens

Blood ◽  
1984 ◽  
Vol 64 (2) ◽  
pp. 352-356 ◽  
Author(s):  
GJ Ruiz-Arguelles ◽  
JA Katzmann ◽  
PR Greipp ◽  
NJ Gonchoroff ◽  
JP Garton ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Bone Marrow ◽  
Plasma Cell ◽  
Peripheral Blood ◽  
Plasma Cells ◽  
Peripheral Blood Lymphocytes ◽  
Tumor Burden ◽  
B Cell Differentiation ◽  
Blood Lymphocytes ◽  
Bone Marrow Plasma

Abstract The bone marrow and peripheral blood of 14 patients with multiple myeloma were studied with murine monoclonal antibodies that identify antigens on plasma cells (R1–3 and OKT10). Peripheral blood lymphocytes expressing plasma cell antigens were found in six cases. Five of these cases expressed the same antigens that were present on the plasma cells in the bone marrow. Patients that showed such peripheral blood involvement were found to have a larger tumor burden and higher bone marrow plasma cell proliferative activity. In some patients, antigens normally found at earlier stages of B cell differentiation (B1, B2, and J5) were expressed by peripheral blood lymphocytes and/or bone marrow plasma cells.

Sign in / Sign up

Export Citation Format

Share Document