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)

It was previously observed that MOPC-315EL, a subline of the BALB/c myeloma tumor MOPC-315, varies in its ability to interact with primary anti-H-2d cytotoxic thymus-derived lymphocytes (CTL) while remaining invariant in its expression of cell surface antigens recognized by anti-H-2d sera. This paper demonstrates (a) that secondary anti-H-2d CTL also fail to recognize the late tumor cells, and (b) that two other CTL systems (anti-minor histocompatibility antigens and anti-2,4,6-trinitrophenyl), which require recognition of both H-2 products and other surface antigens, also fail to react with the late tumor cells. The defect in the late tumor cells was evident when they were used as targets, inhibitors, and stimulators of CTL activity.
Eur J Immunol 1978 Sep
PMID:Loss of reactivity of a BALB/c myeoloma tumor with allogeneic and syngeneic cytotoxic T lymphocytes. 30

In a patient with chronic lymphocytic leukaemia, two M components of the IgGkappa and IgGlambda classes were demonstrated in the serum at the time of diagnosis. The patient was first followed without treatment; after 18 months multiple myeloma developed. At that time, immunofluorescence study of lymphocytes of the peripheral blood showed mainly membrane-bound immunoglobulins (S-Ig) of the IgGkappa class. The bone marrow disclosed a definite predominance of plasma cells with cytoplasmic IgGlambda, suggesting that the two B cell-derived diseases had arisen from two different cell clones. During the development of multiple myeloma, the serum concentration of the M component IgGlambda increased. Concurrently, the M component of IgGkappa gradually disappeared from the serum, and the concentrations of the normal immunoglobulins IgA and IgM declined. Following cytostatic treatment, the concentration of the myeloma-derived M component IgGlambda was halved and simultaneously the M component IgGkappa reappeared in the serum. To our knowledge, this case is the second reported of chronic lymphocytic leukaemia and multiple myeloma indicating development of the two diseases from different cell clones, and the first reported cases with myeloma-induced suppression of M-component secretion from malignant cells.
Scand J Haematol 1978 Sep
PMID:Chronic lymphocytic leukaemia with subsequent development of multiple myeloma. Evidence of two B-lymphocyte clones and of myeloma-induced suppression of secretion of an M-component and of normal immunoglobulins. 30 24

A competitive radioimmunoassay for a saline-soluble human thymus-leukemia-associated antigen (HThy-L) was applied for quantitation of this antigen in leukemia and normal hematopoietic cell lines. Highly increased quantities of HThy-L were detected in all T-cell leukemia lines tested, regardless of the presence or absence of receptors for sheep erythrocytes. This elevated level of HThy-L in combination with high terminal deoxynucleotidyl transferase and adenosine deaminase activities and the presence of a T-lymphocyte-specific surface antigen appear to represent stable phenotypic characteristics of T-cell lines. Most normal B-cell lines had low quantities of HTy-L. The level of HThy-L was slightly elevated in a considerable number of lymphoma B-cell lines and in all non-T, non-B leukemia cell lines tested. No relationship existed between quantities of HThy-L and an expression of different surface immunoglobulin isotypes in B-cell lines. Low quantities of HThy-L were detected in leukemia myeloid and myeloma cell lines as well as in B-cell leukemia lines originating from patients with B-cells acute lymphoblastic leukemia. Apparently, the increased quantities of HThy-L in T-cell leukemia lines may be related to certain stages of T-cell differentiation at which leukemia cell transformation occurs.
J Natl Cancer Inst 1979 Sep
PMID:Quantitation of human thymus-leukemia-associated antigen in established hematopoietic cell lines by radioimmunoassay. 31 16

Spleen cells from a LEW.AVN rat immunized with cells from an MNR rat were fused with mouse myeloma cells to produce hybrid cell lines. One of these hybridomas produced a monoclonal antibody that was cytotoxic for bone marrow-derived (B) but not thymus-derived (T) cells. The antigen defined by this antibody is determined by a gene linked to the major histocompatibility complex (MHC). The antigen is also present on B cells of most mouse strains and is determined by an MHC-linked gene in this species as well. In both rats and mice, the gene determining the antigen maps within the immune response region of the MHC. All human B-cell lines, but not T-cell lines, and B but not T cells of all human donors tested so far are also positive for this antigen. Among human-mouse somatic cell lines that have lost various human chromosomes, this B-cell antigen is present on all lines that are positive for HLA antigen but is absent from all lines that have lost HLA.
Proc Natl Acad Sci U S A 1979 Sep
PMID:Monoclonal antibody directed to a B-cell antigen present in rats, mice, and humans. 31 63

The ultrastructure of blood mononuclear cells from two IgG myeloma patients was studied, and cells reacting with anti-idiotypic serum and polyspecific anti-Ig serum were characterized by immunoperoxidase techniques. Abnormal, mononuclear cells were present in the blood of both patients, which morphologically were classified as atypical small to medium-sized lymphocytes, polymorphic immature lymphocytes (lymphoblasts), predominantly of the lymphoplasmocytic type and atypical, plasmocytic cells or myeloma cells. Immunocytochemical observations showed that most of the abnormal cells, including atypical small to medium-sized lymphocytes, reacted with anti-idiotypic and polyspecific anti-Ig serum. Periods of relapse and remission were correlated with an increase and decrease, respectively, of the number of abnormal cells and cells which reacted with anti-idiotype and anti-Ig serum. The observations indicate that circulating lymphoid cells are part of the myeloma clone.
Acta Pathol Microbiol Scand A 1977 Sep
PMID:Ultrastructural and immunocytochemical characterization of circulating mononuclear cells in patients with myelomatosis. 33 81

A case of fatal pulmonary fibrosis and atypical epithelial proliferation (AEP) in a patient with multiple myeloma treated with melphalan is presented. Review of 10 other autopsied patients with myeloma treated with melphalan but no thoracic radiation, other cytotoxic agents, or highdose oxygen therapy revealed one other patient who died with extensive pulmonary fibrosis and AEP. Four other patients with AEP not associated with pneumonitis or fibrosis were also found, while no such changes were found in 11 autopsy controls or 11 patients with myeloma who did not receive cytotoxic agents. Melphalan should be added to the growing list of agents capable of causing severe fibrotic pulmonary reactions.
Cancer 1978 Sep
PMID:Pulmonary histopathologic changes associated with melphalan therapy. 35 22

Two patients with multiple myeloma are described in whom an unusual complication developed: pleural effusion containing myeloma cells. There are 7 previously reported cases of myeloma in the English literature with this type of effusion. Pleural effusion in myeloma may be due to plasma cell infiltration of the pleura, congestive heart failure, pulmonary embolism, nephrotic syndrome, and second neoplasms. In view of these multiple etiologies, diagnostic thoracentesis should be performed in order to treat the effusion appropriately.
Cancer 1979 Sep
PMID:Pleural effusion in multiple myeloma. 38 71

The electrophoretic mobility of peripheral lymphocytes was studied in normal subjects and patients with myeloma and bronchial carcinoma. Distinct differences in anodic mobility were noted between the sub-populations in all three groups. Total lymphocyte migration was significantly slower in the two tumour groups.
Minerva Med 1979 Sep 29
PMID:[Electrophoretic mobility of lymphocytes in multiple myeloma and bronchial cancer]. 38 69

This study presents evidence on the occurrence of an inverse relationship between activation of glycogen synthetase and inactivation of phosphorylase in a platelet preparation in vitro. The activities of glycogen synthetase and phosphorylase and the pattern of changes in these activities in platelets from controls and multiple myeloma patients were compared. Platelets obtained from multiple myeloma patients were shown to have an increased glycogen content, accompanied by an elevated level of glycogen synthetase a and a decreased activity of phosphorylase a. The pattern of changes in these enzyme activities during incubation was also different in platelets of controls and multiple myeloma patients. Extracts from patients' platelets prevented glycogen synthetase activation and phosphorylase inactivation of control platelets. Preincubation of platelets from multiple myeloma patients in control plasma resulted in an increased rate of glycogen synthetase activation, and abolished activation of phosphorylase which was found after preincubation in autologous plasma.
Clin Chim Acta 1977 Sep 01
PMID:Abnormal platelet glycogen metabolism in multiple myeloma patients. 40 57

In BALB/c mice, antibodies to the alpha-(1-3) glucosidic linkage of some dextrans (Dex) carry the idiotype of the BALB/c myeloma protein J558. Both specific antibody and idiotype are inherited in a dominant fashion, linked to the immunoglobulin (Ig) (heavy chain) allotype Igla of BALB/c mice (Eur. J. Immunol. 1975. 5: 775). In F1 hybrid mice from the parent strains SJL and BALB/c, we were able to suppress the expression of anti-Dex antibodies by immunizing prospective SJL mothers to the J558 idiotype. The state of suppression in the progeny was ascertained by immunization with Dex, and tests for the following were carried out: (a) antibodies specific for Dex; (b) inhibition of such antibodies (if present) by antiidiotypic serum to protein J558; (c) presence of the J558 idiotype; and (d) concentration of lambda1 chains (which are associated with the 558 idiotype) in the serum. SJL mothers, once immunized, conferred suppression upon several successive litters, spanning a period of 4-5 months. Suppression in F1 progeny animals lasted for 16 weeks or more. Spleen cells from suppressed F1 mice which had neither been treated with Dex nor with J558 protein, were able to confer suppression to further F1 newborn mice.
Eur J Immunol 1977 Sep
PMID:Idiotype suppression by maternal influence. 41 78


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