Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026764 (multiple myeloma)
 36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antiserum was generated in rabbits to the RPMI 8226 tissue culture line of human myeloma cells, and its reactions with fixed smears of bone marrow aspirates from patients with multiple myeloma, macroglobulinemia, benign monoclonal gammopathy (BMG), leukemia, and nonneoplastic plasmacyosis was assessed by indirect immunofluorescence. After absorption with preparations of bone marrow from normal individuals, the antiserum reacted to a significantly higher titer with a specific subpopulation of plasma cells in smears from 81% of patients having multiple myeloma and 50% of patients having BMG than with cells in smears of bone marrow aspirates from normal individuals or patients having leukemia or nonneoplastic plasmacytosis, or than with cells in smears of peripheral blood from patients having Hodgkin's and non-Hodgkin's lymphoma. Absorption of the antiserum with RPMI 8226 cells or with a bone marrow preparation from a patient with multiple myeloma but not the Jijoye line of Burkitt's lymphoma reduced reactivity for cells in myeloma bone marrow. The antiserum reacted at a lower titer with the Jijoye and EB-3 lines of Burkitt's lymphoma, the RPMI 4098 cell line of normal human lymphocytes, and culture lines of human melanoma and osteogenic sarcoma than with the RPMI 8226 cells or bone marrow from certain patients having multiple myeloma. Approximately 50% of the cells reactive with antiserum to RPMI 8226 cells in the bone marrow of patients with multiple myeloma were not producing immunoglobulin, as assessed by double immunofluorescence assay. The data suggested that a subpopulation of plasma cells in the bone marrow of patients with multiple myeloma possesses a tumor-associated antigen.
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PMID:Tumor-associated antigens in human myeloma. 5 51

Cultured human myeloma cells (ARH-77, RPMI-8226 and U-266), like leukaemic B lymphoid cells, consistently exerted a strong stimulating capacity on allogeneic lymphocytes in the 'one-way' mixed lymphocyte reaction. An optimal stimulation was seen when a 1:1 ratio or 1:2 ratio of responding cell:stimulating cells of each cell line was utilized. The stimulating capacity of ARH-77 or RPMI-8226 cells was significantly diminished when a 1:4 ratio of responding cells:stimulating cells was utilized. Fresh bone marrow cells containing more than 80% plasma cells from a patient with multiple myeloma, on the other hand, failed to exert the stimulating capacity on two occasions. The striking difference between cultured myeloma cells and fresh plasma cells is that the Ia-like antigen is present on cultured myeloma cells, and this antigen is absent on fresh plasma cells. The relationship between the Ia-like antigen and the stimulating capacity in 'one-way' mixed lymphocyte reaction is discussed.
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PMID:Human myeloma cells and their strong stimulating capacity in 'one-way' mixed lymphocyte reaction: a comparative study with leukaemic B lymphoid cells. 15 62

Freshly explanted human myeloma cells formed colonies of monoclonal plasma cells in soft agar in the presence of medium conditioned by the adherent spleen cells of mineral oil-primed BALB/c mice. The medium showed peak activity at a dilution of 1:4. 2-mercaptoethanol or monothioglycerol was necessary for colony formation. Other thiols tested were ineffective in promoting colony growth. Colony-forming cells adhered to nylon wool, but not glass beads or plastic dishes. The presence of E-rosetting cells was not required for myeloma colony formation. Antibody prepared against a human myeloma cell line, RPMI 8226, reduced colony formation. These studies demonstrate the usefulness of this bioassay for determining functional properties of the myeloma colony-forming cell.
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PMID:The nature of cells generating human myeloma colonies in vitro. 42 63

The binding of human IgE myeloma proteins to 16 human cultured lymphoblastoid cell lines was studied by measuring specific uptake of radiolabeled deaggregated IgE myeloma proteins and/or E-IgE rosette formation. Eight lines, RPMI-8866, Wil-2WT, RPMI-6410, RPMI-1788, RPMI-4265, Clowers, COLO-59 and Victor, bound IgE as shown by at least one of these methods. The lines, RPMI-4098, SCRF-5004, NC-37, Daudi, Raji, P3JHR-1, RPMI-1301 and Molt-4 did not bind IgE. Of the positive cell lines, 58 to 98% of the cells formed E-IgE rosetts. The binding of IgE was Fc fragment specific. It could only be inhibited by human IgE and its Fc fragment but not by IgE Fab fragments and Ig of other classes. The binding of IgE also appeared to be species specific, since a rat IgE myeloma protein did neither bind to the cells nor inhibit the binding of human IgE. The binding of IgE was relatively temperature independent and was abolished by trypsin and pronase pretreatment of the cells. Most of the cell lines binding IgE did not bind IgG but had surface immunoglobulin and did not form spontaneous E rosettes. These data suggest that certain lymphoblastoid cells may have receptors for IgE.
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PMID:Binding of IgE myeloma proteins to human cultured lymphoblastoid cells. 79 32

The optimum composition of several serum-free media has been established for a long-term cultivation of hybridomas, lymphoid and erythroleukemic cells. The medium DME/F12 appeared to be the medium of choice. It is necessary to supplement the basic medium with lipid and iron transport proteins (bovine serum albumin, transferrin) and peptide hormone (insulin) for obtaining stable results. However, there are differences in successful growth of examined cell lines under serum-free conditions: some of them acquire saturation density comparable with that of the control medium (hybridomas derived from myeloma Sp2/0-Ag14, cell lines K-562, Raji) but other lines do not (hybridoma derived from myeloma NS0/1, cell lines Namalwa, RPMI 1788, Molt-4). Thus, these serum-free media are not universal, therefore each new hybridoma and cell line should be tested to determine the suitability for them of some proposed media. The high effectiveness of cultivation under serum-free conditions can be presumably achieved by optimization of both qualitative and quantitative composition of the serum replacement and of the basic medium.
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PMID:[The cultivation of mouse and human lymphoid cells on serum-free media]. 129 79

Glucocorticoid receptors and glucocorticoid receptor RNA (GR RNA) were measured in doxorubicin resistant myeloma cell lines to investigate the relationship between multi-drug resistance and glucocorticoid sensitivity. Glucocorticoid binding sites and GR RNA were found to be lowered in all the tested doxorubicin resistant cell lines: R10, R40 and R60 compared to the untreated wild type RPMI 8226 cells (Dalton, et al., 1984). The least resistant cell line, R10, maintained a down regulation of GR RNA after 48 hours of dexamethasone (10(-6) M) treatment of the cells. Interestingly, the R10 cell line has been reported to be very sensitive to dexamethasone treatment. However, the GR RNA levels increased in presence of dexamethasone in the most resistant cell line, R40, R60 by comparison to the wild type. Thus, the reduction of GR RNA by doxorubicin treatment appears to be overcome by dexamethasone in the most resistant cell lines. Steroids may be helpful in reversing resistance and maintaining drug sensitive human tumor populations that will continue to respond to cancer chemotherapeutic agents.
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PMID:Dexamethasone reverses glucocorticoid receptor RNA depression in multi-drug resistant (MDR) myeloma cell lines. 134 65

To clarify the components of cellular immunity responsible for defense against the clonal development of myeloma cells, we tested the capacity of human peripheral blood lymphocytes (PBLs) to inhibit the growth of 3 human myeloma cell lines (RPMI 8226, OPM-1, and OPM-2). RPMI 8226 was found to be sensitive to PBLs, showing almost complete growth arrest when cultured with PBLs for 72 h. Inhibition of the growth of RPMI 8226 cells required direct cell-to-cell contact but not presensitization of the PBLs to the target cells, and did not depend on the generation of soluble factors. CD3+, CD4-, CD8- and CD16- cells were found to be the major subset contributing to inhibition of the growth of RPMI 8226 cells, and this growth inhibition was cytostatic rather than cytotoxic. These characteristics distinguished it from growth inhibition mediated by the natural killer system. Impaired PBL-mediated growth inhibition of RPMI 8226 cells was found in patients with various hematologic diseases, including myeloma. It therefore appears that the CD3+, CD4-, CD8- and CD16- cell subset might be involved in tumor immunity in myeloma.
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PMID:Growth inhibition of RPMI 8226 human myeloma cells by peripheral blood lymphocytes. 135 Jan 58

Continuous monitoring of fluorescence (CMF) has been used to examine doxorubicin efflux from intact human myeloma cells. The time resolution of these measurements has enabled detailed comparison of the initial rates of efflux for the drug-sensitive myeloma line RPMI 8226 and a series of sequentially derived multidrug-resistant (MDR) lines expressing different amounts of human MDR protein (P-glycoprotein). Cells that are 3-, 10-, 60-, or 120-fold resistant to doxorubicin export approximately 10, 20, 30, or 33% more doxorubicin than the parental sensitive cells, respectively, when all are preloaded to the same level of total intracellular drug. Remarkably, however, when cells are loaded to the same level of exchangeable drug the initial rates of efflux are found to be virtually identical. This agreement between rates is apparently not dependent on the drug concentration. Approximately 50% of the increase in the steady-state level of doxorubicin efflux for the resistant cells is abolished upon glucose starvation. However, surprisingly, the apparent initial rates of efflux from the treated and untreated cells are found to be virtually the same. Pretreatment of the resistant cells with verapamil reduces the steady-state level of efflux but increases the apparent initial rate at some concentrations. Conversely, vincristine does not alter steady state but slows the initial rate of efflux from both sensitive and resistant cells by approximately the same extent. Finally, quite interestingly, a nearly linear relationship between pHi and relative steady state of efflux is found for the series of cell lines. These data are interpreted in terms of existing models for MDR.
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PMID:Analysis of the steady-state and initial rate of doxorubicin efflux from a series of multidrug-resistant cells expressing different levels of P-glycoprotein. 136 58

Multiple myeloma cell lines and patient tumor samples with and without the expression of the classical multidrug resistance (MDR) phenotype were investigated in vitro for drug induced cytotoxicity and modulation of drug resistance. Overall there was a good correlation in the cell lines between MDR expression, as measured by immunocytochemistry with monoclonal antibodies against P-glycoprotein 170 (Pgp), and in vitro resistance to doxorubicin (dox) and vincristin (vcr). Drug resistance in the cell line RPMI 8226 dox 40, expressing a high level of Pgp, was almost completely reversed by the novel non-immunosuppressive cyclosporin A (CsA) analog SDZ PSC-833 (PSC), while the chemosensitizers verapamil, CsA and quinine, in clinically achievable concentrations, were much less effective. In cell lines with low Pgp expression, PSC and the other chemosensitizers seem equally effective. The patient tumor samples were selected to represent different combinations of Pgp expression, drug resistance and effects of chemosensitizers. PSC and CsA appeared equally potent and resistance modulation was detected not only in Pgp positive, but also in Pgp negative tumor samples. Furthermore, in one case of a Pgp expression myeloma, chemosensitizers were without effect. These findings indicate the need to incorporate in vitro chemosensitivity assays with Pgp determination when the effects of MDR modulating chemosensitizers are to be studied in the clinic.
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PMID:SDZ PSC-833--a novel potent in vitro chemosensitizer in multiple myeloma. 136 99

A monoclonal antibody (mAb) specific to low-affinity receptor for IgE (FceRII/CD23) was established by the fusion of spleen cells of BALB/c mice immunized with the FceRII+ human B lymphoblastoid cell line (RPMI 8866) with mouse myeloma P3U1. Four mAbs, 10/3 (IgG1), 11/4 (IgG1), 12/2 (IgG2b) and 15/6 (IgM), almost completely inhibited the IgE binding to FceRII+ cells but not to FceRII- cells. More directly, they were demonstrated to react only with 43-kD component/FceRII of the cell lysate of RPMI 8866 cells by sodium dodecyl sulfate polyacrylamide gel electrophoresis and Western blot analysis. Since they have a different epitope specificity, a solid-phase radioimmunoassay (RIA) for the measurement of IgE-binding factor (IgE-BF) was established. It was found that the RIA with the use of 10/3 and 125I-labeled 11/4 or 12/2 gave good results in the detection of IgE-BF derived from B cells and monocytes as well as of T-cell-derived IgE-BF. More importantly, serum IgE-BF was also quantitatively measured by this RIA. Although increased serum levels of IgE-BF were observed in atopic patients, serum IgE-BF was decreased rather than increased in patients with very high serum IgE. This phenomenon may be explained by the decreased ability of the patients' B cells to spontaneously release IgE-BF in vitro.
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PMID:Establishment of a sensitive radioimmunoassay for the detection of human IgE-binding factor (soluble CD23). 138 43


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