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)

Immunological factors are involved in all aspects of the lymphomas and leukaemias. The aetiology of these diseases is related at least in some cases to immunodeficiency, immunostimulation, autoimmunity and a dysregulation of the immune system. The majority of lymphomas and leukaemias are monoclonal proliferations of the B-lymphocyte series at different stages of maturation while some are derived from T lymphocytes and others have no recognisable B or T-cell markers. Each of the lymphoid malignancies has a characteristic and unique pattern of immunological deficiency, suggesting a unique aetiology. Hodgkin's disease and histiocytic lymphoma, the acute leukaemias and chronic myelogenous leukaemia have predominantly cell-mediated immune deficiencies, while lymphocytic lymphoma, chronic lymphocytic leukaemia, multiple myeloma, and the plasma cell dyscrasias have predominantly humoral immune deficiencies. There is a relationship between immunocompetence and prognosis and between immunocompetence and extent of disease in the lymphomas and leukaemias. Immunocompetent patients have a better prognosis and more limited disease than immunoincompetent patients. Therapy for these diseases profoundly suppresses host defence mechanisms, particularly those which are cell-mediated. Ability to resist or recover from this immunosuppression is also associated with an improved prognosis. Lymphoma and leukaemia also induce a tumour-specific immune response in the tumour-bearing host and this also correlates with prognosis. These factors form a rational basis for immunotherapy and indeed lymphomas and leukaemias respond to active nonspecific immunotherapy with BCG and active specific immunotherapy with tumor cells resulting in prolongation of remission duration and survival.
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PMID:Effect of haematological malignancies and their treatment on host defence factors. 78 32

Three monoclonal antibodies to mycobacterium tuberculosis were produced and designated Ra1, Ra2 and Ra3. The spleen cells of BALB/C mice were immunized with intact, ultrasonicated M. H37Ra and H37Ra culture filtrate and were fused with NS-1 myeloma cells. The monoclonal antibodies were IgG2a, IgM and IgM respectively. The monoclonal antibodies were characterized by ELISA on 14 mycobacterial species. It showed that they reacted with H37Ra and some of mycobacterial species but did not with BCG. McAb Ral was used to prepare immunoabsorbent, and Ag-Ra1 was isolated from unheated H37Ra culture filtrate by affinity chromatography with the absorbent. Ag-Ral was a glycoprotein with MW. of 66 KDa and produced DTH in guinea pigs.
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PMID:[Production and characterization of 3 mcAbs to Mycobacterium tuberculosis]. 180 31

The relationship between various diseases and immunisations and the risk of multiple myeloma was analysed using data from a hospital-based case-control study conducted in Northern Italy on 117 patients with multiple myeloma and 477 controls. Associations were observed for clinical history of scarlet fever (relative risk, RR = 2.0; 95% confidence interval, CI = 1.1-3.9), tuberculosis (RR = 2.3%; 95% CI = 0.9-5.7) and BCG immunisation (RR = 3.0; 95% CI = 1.4-6.4). The relative risk was 1.8 (95% CI = 0.9-3.5) for episodes of Herpes zoster infection, but most of the excess cases occurred within 10 years of diagnosis, suggesting that this might have been an early manifestation of the disease. No association emerged for common childhood viral infections or any other immunisation practice. When various classes of infectious or inflammatory diseases were grouped together according to their aetiology, there was a significant positive association with chronic bacterial illnesses (RR = 1.8; 95% CI = 1.1-2.8), and the relative risk estimates increased with the number of bacterial diseases. The trend in risk with number of diseases was significant (chi 21 = 4.5, P = 0.03). A negative association was found between allergic conditions and risk of multiple myeloma (RR = 0.6; 95% CI = 0.3-1.0).
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PMID:Medical history and the risk of multiple myeloma. 203 2

Three hybridomas which secrete antibodies to Mycobacterium avium were obtained by the fusion of p3u1 myeloma cells with spleen cells of mice immunized with M. avium culture sonicate. The reactivity of these monoclonal antibodies was determined in 16 species of mycobacteria by an enzyme-linked immunosorbent assay. An antibody, designated Avi-3, reacted only with M. avium and not with the reference strains of the other 15 species of mycobacteria tested, including M. intracellulare, M. paratuberculosis, and M. lepraemurium. Specificity of the antibody was confirmed by assay, using a specific DNA probe of M. avium complex in 29 M. avium complex isolates. An antigen was purified from M. avium culture sonicate on a monoclonal antibody Avi-3-coupled affinity column. The purified antigen gave a single band (molecular size, about 27 kilodaltons) upon sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The antigen Avi-3 showed strong skin test activity in guinea pig preimmunized with heat-killed M. avium but not in those sensitized with heat-killed M. intracellulare or M. bovis BCG. Purified protein derivative elicited positive skin reactions in all the immunized guinea pigs. When heat-killed M. avium was used as the immunogen, strong lymphoproliferative responses were observed in cultures stimulated with the antigen Avi-3. These results suggest that M. avium-specific antigen Avi-3 may facilitate the diagnosis of mycobacterial infections.
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PMID:Production of a monoclonal antibody specific for Mycobacterium avium and immunological activity of the affinity-purified antigen. 292 41

Hybridomas have been prepared from active B cells in lymphoid tissue draining lesions of Crohn's disease (CD) and ulcerative colitis (UC), by fusion of fresh mesenteric lymph node suspensions with the murine JK myeloma. Two hundred and fifty nine immunoglobulin secreting hybridomas have been obtained from nine patients. The antibodies have been screened for binding to food antigens, sections of human gut, and bacteria including two unidentified acid fast isolates from CD lymph nodes. Autoantibodies, and antibodies to food antigens implicated by others in the aetiology of CD were rare, comprising 1.2%, and 2.5% respectively. Most donors yielded none of these. Thus neither food antigens nor autoantigens are major antigenic stimuli in nodes draining inflammatory bowel disease. On the other hand between 19% and 83% of supernatants from different donors bound to one or more bacterial genus. The mycobacteria and the CD isolates were amongst the genera to which most antibodies bound, though binding to E coli was more frequent. Significantly more CD than UC derived supernatants bound to BCG. As mycobacteria are not though to be part of the normal bowel flora, the high percentage of hybridomas secreting antibodies which bind to this genus is surprising.
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PMID:Specificity of antibodies secreted by hybridomas generated from activated B cells in the mesenteric lymph nodes of patients with inflammatory bowel disease. 325 42

A hybridoma clone secreting rat monoclonal antibody (MAB) designated as 3F3.5F and which reacted with a population of activated tumoricidal mouse peritoneal macrophage (M phi) was produced by the fusion of mouse myeloma cells with rat spleen cells immunized against adherent BCG-activated mouse peritoneal exudate cells (adherent BCG-PEC). The antibody was cytotoxic and of the rat IgM class. The specific reactivity of the antibody with mouse primary cells and cell lines was examined by complement-dependent cytotoxicity and indirect immunofluorescence flow cytometry analysis. The antibody was found to bind to about 40% of the adherent BCG-PEC activated in vivo and elicited peritoneal macrophages activated in vitro by lymphokine and lipopolysaccharide (LPS), to about 35% of polymorphonuclear neutrophils (PMN) 15 hr after intraperitoneal injection of BCG, to about 30% of bone marrow cells from BCG-infected mice, to about 10% of P815 mastocytoma cells and to thioglycollate-induced PEC to some degree. It did not bind to other cells tested including BCG-induced peritoneal lymphocytes, non-tumoricidal PEC, thymocytes, spleen cells, resting bone marrow cells from normal mice, lymphomas, myelomas, fibroblasts, or macrophage-cell lines. Pretreatment of adherent BCG-PEC with MAB 3F3.5F and rabbit complement caused a considerable decrease in tumor cytotoxicity toward P815 cells, but the same pretreatment of non-adherent BCG-PEC had no inhibitory effect on natural killer activity for YAC-1 cells.
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PMID:A novel rat monoclonal antibody directed against a population of activated mouse peritoneal macrophages. 374 66

The present AML protocol which only applies one anthracycline associated with arabinosyl-cytosine gives a first remission plateau of 65% and a 75% survival plateau at five years. Contrary to other teams, we do not apply the allogenic bone marrow graft at the first remission but at the second one. The new protocol comprises application of two anthracyclines, adriamycin and aclacinomycin, a possible autologous bone marrow graft at first remission upon reinforcement, a combination of methotrexate and thioguanine as maintenance chemotherapy and immunotherapy with bestatine. The two protocols respectively applied to the ALL good prognosis and reserved prognosis, give 85% global survival. The autologous bone marrow graft is added at first remission to B or T forms or voluminous CALLA + types. The advantage of CNS radiotherapy is compared with its disadvantages. Bestatine is employed in immunotherapy. The immunoprevention protocol applied to CML blastic crisis (vaccination with a pool of CB blasts) from the second year has prolonged survival of patients suffering from this affection and also treated by splenectomy and hydroxyurea. Allogeneic or autologous bone marrow graft is added to the protocol. The same protocol is applied to not very aggressive LLC and LNH (lymphocytic and centrofollicular with small cleaved nucleus cells) and includes maximum remission induced by chemotherapy followed by immunotherapy (by thymuline and then, if immunity disorders are not corrected, by zinc, then bestatine and finally tuftsin). A similar sequence was applied to the myeloma, comprising MLP-PDN-CPM chemotherapy to induce remission, combination of MLP-PDN and CPM and, if there is resistance, CLB, 6-TG, PDN and TNP. Interferon is appropriate with certain cytopenic forms. A protocol comprising VCR, ADM, PDN, CPM and TNP is applied to centrofollicular NHL with small non cleaved nucleus cells or large cells. As Hoerni and Jones have obtained significant benefits with BCG, its terminal application is compared with that of bestatine. Finally a less mutagenic protocol than MOPP and/or ABVD is proposed for Hodgkin's disease. In this protocol, two cycles alternate, and they combine: a) firstly VCR, PDN, THP-ADM and VPS, and b) secondly VLB, DXM, ACM and TNP with alternatively BLM and PPM between the cycles. This chemotherapy is followed by the same immunorestoration protocol as that applied to LLC and myeloma.
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PMID:[Protocols for the treatment of leukemia and lymphoma: toward escalation or toward reduction of degree?]. 638 Jun 5

Thirty-two monoclonal antibodies (MoAb) to Mycobacterium tuberculosis H37Rv, M. bovis BCG and M. leprae were produced. The spleen cells of BALB/c mice immunized with sonicated or intact bacilli were fused with Sp2/0-Ag-14 myeloma cells. Many more antibody producing hybridomas were found when M. tuberculosis, rather than M. leprae, was used as the immunogen. The MoAb were characterized by an enzyme immunoassay and immunofluorescence on 16 mycobacterial species. The sodium dodecylsulphate polyacrylamide gel electrophoresis immunoperoxidase assay was used to determine the molecular weight of the antigens detected by the MoAb. Antigens of high, low and intermediate molecular weight were found. Some of the antigens were proteinaceous, others of a glycolipid nature. The immunofluorescence assay proved to be essential for the selection of MoAb since some MoAb reacted only in this assay and not in the enzyme immunoassay. The most specific clones were found in the fusions with spleen cells of mice immunized with intact rather than sonicated bacteria. One MoAb (F29-29) reacted only with M. tuberculosis H37Rv; one (F41-3) only with M. leprae and another (F29-45) reacted with M. tuberculosis and M. gastrii. Several MoAb only reacted with three mycobacterial species: M. tuberculosis, M. kansasii and M. gastrii. Others showed unique patterns of reactivity by enzyme immuno- and immunofluorescence assay. The potential use of the MoAb for the identification of mycobacteria and mycobacterial antigens is discussed.
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PMID:Production and characterization of monoclonal antibodies to Mycobacterium tuberculosis, M. bovis (BCG) and M. leprae. 643 49

A conventionally produced antibody specific for hamster lung macrophages was prepared by immunizing guinea pigs with lung macrophages from LSH (inbred) hamsters. Specificity was achieved by absorbing the resulting serum with hamster blood cells and peritoneal macrophages. This antibody was used to precipitate antigen from detergent lysates of hamster lung macrophages. To produce monoclonal antibodies, F1 hybrids of Balb C X C57Bl6 mice were immunized with these immunoprecipitates. Fusion of splenic lymphocytes from these mice with NS-1 myeloma cells produced 4 hybrid cell lines. Subcloning yielded 18 lines producing antibody reacting only with lung macrophages, and 2 lines secreting nonreactive antibody. Screening used lung and peritoneal macrophages and an ELISA assay. Using gel electrophoresis and lysates of 125I-labeled lung macrophages, all 18 lines reacted with the same antigen, a protein of 102,000 daltons. Subclasses of these monoclonal antibodies included IgG2b kappa and IgG1 kappa. Quantitative ELISA assays showed that the antibody reacted with lung macrophages of LSH and LVG (outbred) hamsters, but not with hamster resident peritoneal macrophages, spleen cells, or bone marrow cells. The antibody did not cross-react with lung or resident peritoneal macrophages from mice, rats, or guinea pigs. By flow cytometry, no reaction was detected with resident, thioglycollate-elicited, or BCG-stimulated peritoneal macrophages. When frozen sections of lung and other organs were examined by indirect immunofluorescence and immunoperoxidase methods, only alveolar macrophages were stained.
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PMID:Monoclonal antibody to an alveolar macrophage surface antigen in hamsters. 646 78

The effect of chemoimmunotherapy consolidation treatment using alternating courses of alkylating agents and BCG was studied in 105 responding patients with multiple myeloma. The survival time of these patients was similar to that of responding patients treated on previous maintenance programs, indicating no apparent value from BCG for myeloma. The duration of unmaintained remission was longest in those with low numbers of residual plasma cells, and relapse usually developed within one year in patients with persistent serum myeloma peaks. Disease recontrol was achieved in 50% of relapsing patients whose median survival from retreatment was 20 months. Patient follow-up without chemotherapy until relapse was justified mainly for those responding patients with disappearance of myeloma proteins.
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PMID:Chemoimmunotherapy for multiple myeloma. 722 87


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