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)

gamma-Glutamyl transpeptidase, an enzyme that catalyzes gamma-glutamyl transfer from gamma-glutamyl compounds to amino acid and peptide acceptors, and which is known to be localized in the membranes of many epithelial cells, was found in a variety of lymphoid cells. The lymphoid cell enzyme is located on the cell surface, and exhibits substantially the same substrate specificity as the enzyme found in epithelial cells. Human and rat (but not mouse) lymphocyte gamma-glutamyl transpeptidase was stimulated by treatment of the cells with mitogens. Normal human peripheral B-cells were more active than T-cells, but the reverse relationship of activities was found in chronic lymphocytic leukemia lymphocytes. Human lymphoblastic lines vary markedly in activity. In general, cell lines with B- and T-characteristics from patients with lymphoproliferative diseases had much lower activities than those of B-cell lines derived from normal subjects. The highest activity found was in a human myeloma line active in synthesis of an immunoglobulin light chain. The data indicate that gamma-glutamyl transpeptidase is a surface marker reflecting differentiation in normal and neoplastic cells.
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PMID:gamma-Glutamyl transpeptidase, a lymphoid cell-surface marker: relationship to blastogenesis, differentiation, and neoplasia. 0 85

An increase in the serum copper (Cu++) level has been described as a sensitive index of disease activity in several hematologic and nonhematologic malignancies. In order to explore the diagnostic value of Cu++ compared to other hematochemical parameters frequently abnormal in malignancies, Cu++, serum alpha2 globulin (alpha2), plasmatic fibrinogen (Fibr), the erythrocyte sedimentation rate (ESR), and serum iron (Fe++) have been detected and evaluated in 267 patients affected with the following diseases: Hodgkin's lymphoma (HL), non-Hodgkin's Lymphomas (NHL), Acute Leukemias (AL), Chronic Myeloid Leukemia (CML), Chronic Lymphocytic Leukemia (CLL), Myeloma (MM), and Breast Cancer (BC). The best correlation between Cu++ increase and disease activity has been found in HL, NHL, AL, and BC. In these diseases, when the considered parameters were compared, Cu++ and ESR showed a similar pattern, i.e., a high frequency of abnormalities in active disease. It is concluded that Cu++ represents a good complement to some other aspecific parameters in evaluating the activity and diffusion of neoplasias and the therapeutic results, particularly in HL, NHL, AL and BC.
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PMID:The diagnostic value of serum copper levels and other hematochemical parameters in malignancies. 7 79

Mouse NS-1 myeloma cells were fused with spleen cells from mice that had been immunized with cells from a human melanoma, M1804. Hybrid cells were grown in selective medium and tested for production of antibody to surface antigens of M1804 cells. Three hybrids that produced antibodies that bound to the melanoma cells but not to autologous skin fibroblasts were cloned. Antibodies produced by two of the clones were cytotoxic to M1804 cells in the presence of rabbit complement. Extensive specificity tests showed that the antibodies produced by the clones bound strongly only to M1804 cells; significant, although weaker, binding occurred with 2 of 11 allogeneic melanomas. Apart from weak binding of the antibody produced by one of the clones to a breast carcinoma, binding assays of five carcinomas, one sarcoma, and fibroblasts from 17 individuals were negative, as were cytotoxic tests of 10 lymphoblastoid cell lines and peripheral blood lymphocytes from 68 normal donors and 12 chronic lymphocytic leukemia patients. This suggests that we have identified one or more determinants of a melanoma-associated antigen(s), whose expression is limited to a small proportion of melanomas.
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PMID:Cell surface antigens of human melanoma identified by monoclonal antibody. 28 77

Despite the incomparability in the reporting of leukemia and lymphoma incidence among populations and the relative rarity of these diseases, real differences in rates are discernible from available data. In general, the incidence of each of the leukemias and lymphomas is lower in Japan than in other Pacific rim populations whose rates are known. Particularly striking is the low incidence of CLL in Japan. Among Japanese in Hawaii, rates of some of these cancers (lymphosarcoma, CML) approach those of whites, whereas rates of other cancers (Hodgkin's disease, multiple myeloma, ALL, CLL, and AML) more closely resemble those of native Japanese. The number of Chinese living in countries served by population-based cancer reporting systems is too small for any firm conclusions to be made about leukemia and lymphoma incidence in this group. The incidence of these diseases in certain other nonwhite Pacific rim residents (i.e., Mexican Americans, blacks, and Maoris) is, by and large, similar to that of whites.
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PMID:Geographical variation in the incidence of the leukemias and lymphomas. 29 90

One important factor in the production of the immunologic deficiency in myeloma appears to be the alteration of the surface immunoglobulin by a macromolecular, RNA containing factor released by the tumor. In contrast, the cells of chronic lymphocytic leukemia are not influenced by factors outside the cell and their lack of immunologic reactivity is due to an intrinsic defect. These characteristics may be occasionally important in differential-diagnostic considerations.
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PMID:Significance of surface immunoglobulin in murine and human myeloma and chronic lymphocytic leukemia. 30 97

Human and mouse lymphocytes were surface-labeled by lactoperoxidase-catalyzed iodination, or by galactose oxidase oxidation followed by reduction with tritiated sodium borohydride. The labeled cells were lysed with Nonidet P-40. Proteins binding to Helix pomatia A hemagglutinin (HP) were isolated by affinity chromatography on HP-Sepharose and analyzed by sodium dodecyl sulfate polyacrylamide gel electrophoresis and autoradiography. A major cell surface glycoprotein (apparent mol. wt. 150 000, using reducing conditions) on human lymphocytes was responsible for almost all binding of HP. This protein was present on normal and malignant thymus-derived lymphocytes, e.g. thymocytes, blood T cells and T leukemia cell lines. It was also found on chronic lymphocytic leukemia cells, one null cell leukemia line, one unidentified leukemia line, one lymphoblastoid cell line of B origin and on one stem cell lymphoma line. In contrast, this protein was not found on various B cells at different steps of differentiation, e.g. four B lymphoma lines or one myeloma line. It was also absent from a histiocytic leukemia line. However, two of the four B lymphoma lines and the myeloma line had another HP-binding surface glycoprotein (mol. wt. 200 000) instead of the 150 000 protein. Studies of mouse lymphocytes similarly showed that thymus-derived lymphocytes (normal and malignant) but not normal adult B cells expressed a major HP-binding surface glycoprotein of apparent mol. wt. 130 000 (reducing conditions).
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PMID:Helix pomatia A hemagglutinin: selectivity of binding to lymphocyte surface glycoproteins on T cells and certain B cells. 30 19

Three different neoplasms of B cell lineage, chronic lymphocytic leukemia, immunoglobulin A (IgA) myeloma and immunoglobulin G (IgG) myeloma were detected in three patients who had heavy occupational exposure to asbestos dust. Two of the patients had coexistent pulmonary asbestosis, whereas the third patient had a pleural mesothelioma subsequent to his initial presentation with myeloma. Defective cell-mediated immunity and hyperactivity of B cell function have previously been noted in patients with asbestosis. We suggest the possibility that these asbestos-related immunologic derangements may predispose to the development of immunoproliferative and lymphoproliferative neoplasms, since such tumors have been observed in a variety of other settings, characterized by protracted hyperactivity of the immune system.
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PMID:Asbestos-associated neoplasms of B cell lineage. 31 9

Specific anti-human T-cell serum was prepared in rabbits by multiple subcutaneous injections of human brain homogenates in incomplete Freund's adjuvant. The serum was exhaustively absorbed with human RBCs, lyophilized human liver, lyophilized normal human serum, and peripheral blood lymphocytes from patients with chronic lymphocytic leukemia (CLL). Specificity of the antiserum for human T lymphocytes was tested by indirect immunofluorescence. It stained 70 to 80% of lymphocytes in circulation, 95% of thymus, 27 to 35% of spleen, 5 to 10% of tonsil lymphocytes, and over 90% of phytohemagglutinin-stimulated lymphocytes in vitro. Only T-dependent areas of cryostat-sectioned human lymph nodes stained with the antiserum. It did not stain circulating lymphocytes which formed HEAC rosettes, plasma cells in marrows of multiple myeloma patients or macrophages. After removal of HEAC rosettes by centrifugation in Ficoll-Hypaque, 75% of interface cells formed E rosettes and 65 to 75% stained with the antiserum. The antiserum was used in studies of lymphocytes in chronic and acute lymphocytic leukemias, lymphomas, and other lymphoproliferative diseases. Numbers and distribution in the circulation, spleen and nodes of lymphocytes bearing the T marker were significantly altered in patients with these disorders.
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PMID:Reactivity of anti-human brain serum with human lymphocytes. 31 6

Mitogen induced cellular cytotoxicity (MICC) was noted to be markedly increased in patients with multiple myeloma as compared to normal controls and to patients with chronic lymphocytic leukemia (CLL). Enhanced MICC was present at various effector-to-target cell ratios and at several mitogen concentrations. Removal of adherent, phagocytic cells by carbonyl iron, glass wool, or rayon columns abolished the MICC response from the peripheral blood of both multiple myeloma patients and normal controls. Thus, the effector cell mediating MICC may be monocytic in origin and closely resembles the suppressor cell for immunoglobulin synthesis described in patients with multiple myeloma. Our data suggest that the MICC assay with chicken red blood cells as targets may provide a convenient method for identifying pathologic conditions where this cytotoxic effector cell population plays an active role.
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PMID:Mitogen induced cellular cytotoxicity (MICC) in multiple myeloma. 32 83

PBL of 14 patients with FL were examined by membrane fluorescence using anti-Ig antibodies (mu, gamma, delta; kappa, lambda), spontaneous rosette formation with SRBC and rosette formation with SRBC coated by antibody-complement complexes (EAC). Eight of the patients were untreated. In 3 patients monoclonal Ig were detected in the serum or urine. 7 patients exhibited clonal proliferation as judged by analysis of surface Ig. In addition, normal or elevated figures for EAC rosettes were found. The strong expression of S. Ig in PBL of FL patients is in contrast to the findings in CLL and multiple meloma, the increase of EAC-rosettes is shared by myeloma patients. It follows that membrane properties of PBL as studied in this work is of value in the diagnosis of malignancies of the B-cell system.
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PMID:Surface markers on peripheral blood lymphocytes of patients with follicular lymphoma suggesting a clonal origin. 34 63


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