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)

Fusion between P3 x 63 Ag8 mouse myeloma cells and spleen cells from BALB/c mice immunized with influenza type A or B or parainfluenza type 1 virus generated reproducibly antiviral antibody-producing somatic cell hybrids (hybridomas). Eleven hybridomas derived from spleen cells of mice immunized with influenza type A virus were directed against the viral hemagglutinin, one reacted with a host component derived from chickens, and one expressed a specificity not further characterized. The hybridoma antibodies tended to be highly specific for the hemagglutinin of the immunizing virus and seemed to express the same repertoire of strain-specific antibody reactivities as splenic precursor B cells, they did not express any of the frequently occurring crossreactive anti-hemagglutinin specificities. Hybridomas producing crossreactive antibodies against hemagglutinin could be obtained if priming and boosting virus were heterologous.
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PMID:Repertoire of antiviral antibodies expressed by somatic cell hybrids. 20 3

We have produced somatic cell hybrids between mouse myeloma cells and spleen cells derived from a BALB/c mouse immunized with purified influenza virus. The hybrid cells were found to produce large amounts of antibodies specific for the hemagglutinin of the virus and were able to induce tumor formation when injected into BALB/c mice.
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PMID:Production of antibodies against influenza virus by somatic cell hybrids between mouse myeloma and primed spleen cells. 26 47

Fifty-eight patients with a variety of haematological lymphoproliferative or myeloproliferative disorders were given bivalent subunit influenza virus vaccine, and their antibody responses after vaccination were compared with those of a normal control group. Although geometric mean titres of the patient group showed lower initial antibody levels, smaller increments, and lower final titres, after vaccination 83% of this group achieved satisfactory antibody levels to the A/Pt Chalmers strain, and 57% to the B/Hong Kong strain. The lowest antibody levels and smallest responses occurred in patients with non-Hodgkin's lymphoma, Hodgkin's disease, and multiple myeloma. Four of seven patients who showed low antibody levels, and no response to the first injection, responded to a second dose.
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PMID:Immunization with influenza vaccine in patients with haematological malignant disease. 85 89

The epitope corresponding to amino acid residues 147-161 of the nucleoprotein (NP) of influenza A virus is recognized by CTL in association with H-2Kd class I Ag. Herein, we engineered an Ig molecule carrying this CTL epitope by replacing the diversity gene segment of the H chain V region of an anti-arsonate antibody with an oligonucleotide that encodes the CTL epitope. The chimeric H chain gene was expressed either alone or together with the parental L chain in the nonsecreting BALB/c myeloma B cell line, SP2/0. The Ig produced by cells transfected with both the chimeric H chain and parental L chains genes expressed the NP epitope but lost the original arsonate binding activity. In addition, SP2/0 cells expressing the chimeric H chain either alone or together with the parental L chain were lysed by class I restricted NP-epitope specific CTL. By contrast, SP2/0 cells pulsed with soluble chimeric Ig molecules were not lysed by the specific CTL. These observations indicate that: 1) this particular CTL epitope can be expressed on Ig molecules without altering the H and L chain pairing; 2) this CTL epitope can be generated from this chimeric Ig in which it is surrounded by flanking regions distinct from those of the viral NP; and 3) the generation of this CTL epitope from the Ig molecule requires the endogenous pathway as do viral proteins.
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PMID:Cells expressing an H chain Ig gene carrying a viral T cell epitope are lysed by specific cytolytic T cells. 137 50

Studies were carried out to determine the optimum conditions for the production of equine monoclonal antibodies (MAbs). Lymphocytes from ponies immunised with influenza A equine 2 virus, isolate A/Equine/Newmarket/79 (H3N8) were fused with mouse myeloma (NSO) cells and with horse-mouse heterohybridomas made aminopterin-sensitive by selective growth in 8-azaguanine. Although all fusions initially resulted in heterohybridoma colonies that secreted equine immunoglobulin, many of these were unable to maintain secretion for longer than a few weeks. Increasing the time between immunisation and the booster injection of Newmarket/79 virus, the inclusion of Freund's incomplete adjuvant and the use of an aminopterin-sensitive primary heterohybridoma as the fusion partner, improved the production of HIg-secreting heterohybridomas. After two clonings eight cell lines were established which maintained anti-Newmarket/79 antibody secretion for over a year. FACS analysis of the cell lines provided a useful means of predicting breakdown of MAb secretion by the cell lines, thus enabling re-cloning to be carried out in time.
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PMID:The production of equine monoclonal immunoglobulins by horse-mouse heterohybridomas. 163 74

Recombinant Interleukin 4 was administered by subcutaneous injection at daily doses of 0.5, 1.0 or 5.0 micrograms kg-1 to nine patients as part of a Phase I Dose Toxicity Study. Dose limiting toxicity was reached at 5 micrograms kg-1 day-1. Symptoms of toxicity included fatigue, 'flu like symptoms and elevated liver enzymes. Modest but significant elevations of neutrophil and platelet counts occurred. No clear evidence of antitumour effects emerged although pain in metastatic lymph nodes and a small fall in myeloma paraprotein levels during dosing were observed. In vitro and murine in vivo studies indicate that patients with lymphoproliferative disease should be selected for Phase II trials.
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PMID:Recombinant human interleukin 4 (IL-4) given as daily subcutaneous injections--a phase I dose toxicity trial. 163 69

Great numbers of CD5+ B lymphocytes were detected in the peripheral blood of patients with B-CLL. To study the antibody repertoire of this immune cell subpopulation on a monoclonal level, we fused the lymphocytes derived from five different donors to a highly efficient HAT-sensitive heteromyeloma line (CB-F7). A fusion frequency of up to 10(-5) allowed us to analyse hundreds of initial hybridoma lines per fusion. In all culture supernatants in three out of five fusions IgM lambda antibodies were detected, in two experiments only IgM kappa was measured, suggesting monoclonality of the primary hybridoma cell lines. The later fusions resulted in hybridomas producing multi-specific antibodies against both an autoantigen and an infectious agent: (i) dsDNA/influenza virus haemagglutinin; (ii) dsDNA/class V outer membrane protein type C from Neisseria meningitidis. However, no antibodies of the described specificity were detected in blood sera of patients, indicating a 'switch-on' of the immunoglobulin secretion capacity of malignant B cells during fusion to a myeloma partner. We discuss the results as further evidence for the natural multi-reactive antibody repertoire of CD5+ B cells.
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PMID:Human hybridomas derived from CD5+ B lymphocytes of patients with chronic lymphocytic leukemia (B-CLL) produce multi-specific natural IgM (kappa) antibodies. 170 36

Three patients with multiple myeloma were treated with recombinant alpha-interferon (r IFN-alpha 2b Intron AR) along with combination chemotherapy i.e. melphelan and prednisolone. In one case it was given as an initial therapy, while the other two patients had refractory and relapsing disease respectively. IFN-alpha 2b was given in the dose of 2 x 10(6) Mu/m2 by subcutaneous injection thrice in a week for six months in two patients and for three months in one patient. All three patients experienced improvement in bone pains; partial response with reduction in the paraprotein level was seen in one patient; while there was no radiological, biochemical or haematological improvement in two patients. Side effects noted were flu like syndrome in all three patients and urticaria in one patient. They were treated symptomatically and did not require cessation of interferon therapy.
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PMID:Recombinant alpha-interferon therapy in multiple myeloma. 209 May 74

Three patients with symptomatic multiple myeloma who had achieved an objective response after conventional induction chemotherapy were treated with alpha-2b-interferon plus intermittent high-dose dexamethasone as consolidation therapy. This treatment included three mega units of alpha-2b-interferon three times a week, plus 4 days pulsed high-dose dexamethasone every 28 days for 6 months. Toxicity was limited to a mild flu-like syndrome. A further and significant M-component reduction (50%), obtained after conventional chemotherapy, suggests the value of intermittent high-dose dexamethasone plus interferon as consolidation therapy.
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PMID:Consolidation treatment with dexamethasone and alpha-2B recombinant interferon further reduces the M-component level in multiple myeloma patients responding to conventional induction chemotherapy. 209 2

The use of interferon for the induction treatment of multiple myeloma has been shown to be effective in about 20 percent of patients. We studied its effects on long-term survival when it was used for maintenance treatment. Between April 1985 and May 1988, 101 patients with symptomatic multiple myeloma who had had a substantial objective response or a lesser objective response with disappearance of symptoms ("disease stabilization") after 12 courses of induction chemotherapy were randomly assigned to receive recombinant interferon alfa-2b as maintenance therapy (n = 50) or to receive no treatment (n = 51). As of December 1989, 66 of the 101 patients have relapsed (25 given interferon and 41 not treated). The median duration of response (from the time of randomization) was 26 months in the patients given interferon and 14 months in the untreated patients (P = 0.0002). A total of 37 patients have died (14 given interferon and 23 not treated). The median duration of survival (from randomization) was 52 months in the interferon group and 39 months in the control group (P = 0.0526). Among the patients who had had a substantial objective response to induction chemotherapy, the difference in survival time was statistically significant (P = 0.03526). Interferon had to be stopped because of toxic effects in 3 of 12 patients initially treated with 10 MU (megaunits) per square meter of body-surface area. After the dose was reduced to 3 MU per square meter, the only toxic effect was a mild influenza-like syndrome lasting two to three weeks. We conclude that maintenance treatment with interferon prolongs response and survival in patients with multiple myeloma who have responded to conventional induction chemotherapy.
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PMID:Maintenance treatment with recombinant interferon alfa-2b in patients with multiple myeloma responding to conventional induction chemotherapy. 218 56


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