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

W3/25 antibody is the monoclonal product of a hybrid cell resulting from the fusion of a mouse myeloma cell line with spleen cells from a mouse immunized with rat thymocytes. Pure clones have been derived, and segregants free of parental myeloma chains have been isolated. Previous studies have shown that this antibody recognizes a subpopulation of T cells among rat thoracic duct lymphocytes. In the work reported here, three T-cell functions were assayed after separating rat thoracic duct lymphocytes on the fluorescence-activated cell sorter on the basis of labeling with W3/25 antibody. Two of the functional activities appeared to be completely segregated by this procedure. Thus, helper cell activity for an anti-hapten plaque-forming cell response was confined to the labeled population, whereas the allogeneic suppressive effect produced in a parental vector F1 adoptive transfer was mediated by cells in the unlabeled fraction. The third function, graft-versus-host activity, was almost entirely contained within the labeled subpopulation. It is concluded that the antigenic determinant recognized by the monoclonal antibody W3/25 is a differentiation marker for T-cell functional subpopulations.
J Exp Med 1978 Sep 01
PMID:T-lymphocyte heterogeneity in the rat: separation of functional subpopulations using a monoclonal antibody. 2 36

Described here is a 59 year old man with dermatomyositis and hypogammaglobulinemia. His muscle power improved after corticosteroid therapy, but extensive amyloidosis and repeated infections appeared. Bone marrow morphology suggested multiple myeloma, but treatment with cytotoxic drugs had no beneficial effect on the amyloidosis. Because of rapid progression of the amyloidosis and further infections, cytotoxic drug therapy was stopped, corticosteroid dosage was decreased, and supplementary immunoglobulin therapy was instituted. The infections occurred less frequently and the amyloidosis appeared to regress. This case suggests that immunosuppressive therapy may exacerbate amyloidosis. The literature is reviewed, and the possible role of humoral immunodeficiency in the pathogenesis of amyloidosis is discussed. It is suggested that supplementary immunoglobulin may be beneficial in amyloidosis.
Am J Med 1975 Sep
PMID:Amyloidosis associated with dermatomyositis and features of multiple myeloma. The progression of amyloidosis associated with corticosteroid and cytotoxic drug therapy. 5 87

Changes in rat mast cell cyclic adenosine 3',5' monophosphate (cAMP) concentrations during stimulation of histamine release by concanavalin A (con A) and anti-IgE were studied. Con A caused an increase in cAMP with a mean peak level at 20 sec of 232% of control (range 164% to 365%). Con A-stimulated cells demonstrated falls toward control levels after 20 sec, but generally remained above control for at least 5 min. By 10 min cAMP had returned to control values. The con A effect on cAMP occurred in the absence of phosphatidyl serine but was markedly inhibited by 5 mM alpha-methyl-D-mannose. Anti-IgE induced a less marked increase in cAMP (157% of control, range 110% to 540% of control) which reached a peak at 20 sec. Two monospecific goat anti-rat myeloma IgE antisera induced similar changes in cAMP whereas normal goat IgG had no effect. These peak values were followed by a rapid decrease in cAMP. Within 2 min the cAMP content of anti-IgE stimulated cells had fallen to levels well below control and remained below control levels from 45 sec to over 15 min. Histamine release in both systems began after the peak cAMP levels, during the period of rapid destruction of cAMP.
J Immunol 1976 Sep
PMID:Modulation of cyclic AMP in purified rat mast cells. III. Studies on the effects of concanavalin A and anti-IgE on cyclic AMP concentrations during histamine release. 6 Apr 47

Murine myeloma immunoglobulin (IgA, K) J539, which shows enhanced tryptophanyl fluorescence on ligand binding, and S10, which shows reverse-sign changes in tryptophanyl fluorescence on ligand binding (RLIF, see below), have been reduced, alkylated, and dissociated into their light (L) and heavy (H) chains. Two hybrid recombinants, H10L539 and H539L10, have been prepared and the 7S material has been isolated by chromatography. The binding behavior of these recombinants was studied with a number of ligands. Both recombinants showed activity with beta(1 leads to 6) linked galactose ligands comparable to the native immunoglobulins. The ligand-induced fluorescence changes of the recombinants paralleled those of the heavy chain donor. For the recombinant H10L539, two different galactose-ligands caused fluorescence changes in opposite directions. It was quantitatively shown that binding of these ligands, nevertheless, took place in the same combining region. The idiotype of each recombinant resembled that of the heavy chain donor.
J Immunol 1977 Sep
PMID:The formation of active hybrid immunoglobulins from the heavy and light chains of beta(1, 6) D-galactan binding murine myeloma IgA's S10 and J539. 7 Apr 73

BALB/c mice were immunized against the idiotype of BALB/c myeloma J55,. Syngeneic, specific anti-idiotypic antibodies against this germ line idiotype were shown by the isoelectric focusing technique to be markedly heterogeneous. In fact, the heterogeneity of isogeneic anti-idiotypic sera appeared to be comparable to those of allogeneic anti-J558 sera, raised in A/J and CB20 mice. As a rule, individual mice exhibit different clonal spectra. By spleen cell transfer experiments, each individual spectrum of clones could be expanded in order to arrive at an estimate of the size of anti-idiotypic repertoires. These were found to be of the order of 7-16 different anti-idiotypic clones for an individual BALB/c mouse. From the infrequency of clonal repetition we conclude that the repertoire of the BALB/c strain must be well in excess of one hundred anti-idiotypic molecular species.
Eur J Immunol 1977 Sep
PMID:Characterization of syngeneic anti-idiotypic antibody against the idiotype fo BALB/c myeloma protein J558. 7 73

Twenty-seven patients with far-advanced multiple myeloma, resistant to standard agents, were treated with either adriamycin (eight patients) or bleomycin (19 patients). Adriamycin was given iv at a dose of 60 mg/m2 every 3 weeks and bleomycin was administered im at a dose of 15 mg/m2 weekly. Drug toxicity was modest. One partial response was seen with each agent, both occurring in "good-risk" patients.
Cancer Treat Rep 1978 Sep
PMID:Phase II study of adriamycin and bleomycin in patients with multiple myeloma. 8 Feb 75

Previous studies demonstrated that: i) the TNP-binding myeloma MOPC-315 differentiated during in vivo growth in diffusion chambers (DC) implanted i.p. into normal BALB/c mice, and ii) the myeloma cell differentiation was regulatable by carrier-specific presentation of TNP to MOPC-315 cells in carrier-primed mice. In those studies, promotion and suppression of MOPC-315 differentiation occurred in the presence of carrier-specific helper and suppressor activities, respectively. In the present studies, we demonstrate that carrier-specific regulation of MOPC-315 differentiation can be adoptively transferred to normal mice with carrier-primed T lymphocytes. In addition, the induced regulation of MOPC-315 differentiation is abrogated when macrophages are not present with MOPC-315 cells in the DC. These studies establish the immunologic basis of myeloma cell regulation and suggest that soluble, carrier-specific helper and suppressor factors of T cell origin regulate MOPC-315 differentiation directly or in collaboration with macrophages.
J Immunol 1978 Sep
PMID:Antigen-specific regulation of myeloma cell differentiation in vivo by carrier-specific T cell factors and macrophages. 8 Apr 22

A model of unresponsiveness to human gamma-globulin (HGG) which is maintained in the absence of demonstrable suppressor cells has been described. A/J mice were tolerized with deaggregated HGG purified from a variety of sources. The spleen cells from these tolerized mice were assessed for their ability to suppress the response of normal spleen cells to HGG when transferred into lethally irradiated mice. All of the HGG preparations obtained from commercial sources as Cohn fraction II of pooled, outdated plasma induced suppressor cells to HGG, although not of equal magnitude. However, suppressor cells could not be demonstrated in the spleens of mice tolerized with deaggregated HGG purified from the plasma of a healthy individual. This inability to detect suppression was independent of the method of purification of the HGG and of the time of assessment of the putative suppressor cells after tolerization. Similarly, deaggregated HGG isolated from an IgG1 lambda-myeloma protein induced unresponsiveness to HGG but did not stimulate demonstrable suppressor cells. These data suggest that suppressor T cells are not involved in the maintenance of tolerance to this antigen, although they may play a regulatory role in the immune response to HGG. Support for this concept was obtained by assessing the duration of unresponsiveness in the T and B lymphocytes of mice tolerized with the various HGG preparations. Mice tolerized with the HGG preparations that stimulated little or no suppression were among the last to recover responsiveness. Indeed, there was no consistent correlation between the level of suppressor cell activity and the degree of unresponsiveness in either the splenic T or B lymphocytes. Thus, although certain HGG preparations may provide a tool for the generation of antigen-specific suppressor T cells, the utilization of these suppressive preparations may be inappropriate for the investigation of the mechanisms of the induction and maintenance of the unresponsive state.
J Exp Med 1978 Sep 01
PMID:Induction and mode of action of suppressor cells generated against human gamma globulin. I. An immunologic unresponsive state devoid of demonstrable suppressor cells. 8 Dec 57

Type C particles released from cultured murine myeloma MOPC-315 cells were significantly protected when the purification steps were all conducted in the presence of 10% chicken egg yolk fluid. The yolk fluid also slowed down the inactivation of viral particles during incubation at 37 degrees C and enabled full recovery of viral particles through several cycles of freezing and thawing. The purification of viral particles in the presence of yolk fluid did not affect the capability of the viral DNA polymerase to reverse-transcribe the virion RNA in vitro, nor that of the viral RNA to act as a functional template.
Appl Environ Microbiol 1978 Sep
PMID:Chicken egg yolk stabilizes the reverse transcriptase activity in type C particles produced by cultured MOPC-315 murine myeloma cells. 8 22

145 Determinations of beta2-microglobulin (beta2m) have been realized in 111 patients with a monoclonal gammapathy. The level of beta2m is significantly higher (p = 0,0001) in the group with monoclonal gammapathy (M = 4,75 mg/l +/- 5,62) than in normal subjects (M 1,38 mg/l +/- 0,38). In a group with monoclonal gammapathy with renal failure, the level of beta2m is higher (M = 7,07 mg/l +/- 7,76) than in a group with renal failure alone (M = 3,45 mg/l +/- 1,91). The difference is significant (p = 0,005). The level of beta2m is higher in IgA monoclonal gammapathies (M = 5,61 mg/l) than in IgG (M = 4,18 mg/l) or IgM (M = 4,37 mg/l) gammapathies, but the differences of the means between the three groups are not significant. The assay of beta-2m does not allow to distinguish myeloma (M = 3,18 mg/l +/- 1,83) from benign monoclonal gammapathy (M = 3,22 mg/l +/- 1,32) and is not useful when the diagnosis is difficult.
Pathol Biol (Paris) 1978 Sep
PMID:[beta2-Microglobulin and monoclonal gammapathies (author's transl)]. 8 81


1 2 3 4 5 6 7 8 9 10 Next >>