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)

There is no doubt about the leukemogenic effect of benzene in man. The evidence is as follows: (1) The incidence of leukemia in shoeworkers exposed to benzene in a period of 8 years in Istanbul was 13.6/100,000, which is significantly higher than that for leukemia in the general population. (2) Following the phase-out of benzene in Istanbul, the number of leukemic workers decreased and none were reported in the subsequent 3 years. (3) The development of leukemia in pancytopenic patients with benzene exposure was observed in 13 out of 51 patients. (4) The differences in the distribution of the types of leukemia in individuals exposed and in nonexposed groups were as follows: acute leukemia 96.1% in the former group, and 46% in the latter group. The high percentages of acute erythroleukemia and preleukemia were other interesting findings in the exposed group. (5) Two cases of leukemia were observed in a 6-year period at a tire cord manufacturing plant with 550 workers. At one location in the plant the concentration of benzene measured by gas chromatography was nearly 110 ppm. Additionally, we have studied 12 cases of malignant lymphoma, four cases of multiple myeloma, and six cases of lung cancer, all of whom were chronically exposed to benzene. The possible role of benzene in the etiology of these malignancies is discussed.
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PMID:Malignancies due to occupational exposure to benzene. 400 2

Two hundred and thirty-six cases of multiple primary cancer associated with hematological malignancies, collected from 35 medical institutions in Japan, are reported. Based on the time interval between the first cancer and the second cancer, they were divided into three groups: synchronous cancer (94 cases), metachronous cancer subsequent to hematological malignancy (61 cases) and metachronous hematological malignancy subsequent to carcinoma (76 cases). The most common initial cancers were acute leukemia (including atypical leukemia and erythroleukemia), non-Hodgkin's lymphoma, multiple myeloma and chronic myelogenous leukemia of the hematological malignancies, and gastric cancer of the carcinomas. Patients with cancer of the uterus and breast in the metachronous cancer group metachronously developed hematological malignancies more frequently than those in the synchronous cancer group. Multiple primary cancer was observed more frequently in men than in women both in the synchronous cancer group and in the group with metachronous cancer subsequent to hematological malignancies. Acute leukemia was the most frequent disease type in incidence among the metachronous hematological malignancies. This secondary acute leukemia was characterized by a mostly granulocytic nature, poor response to chemotherapy and poor prognosis.
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PMID:Multiple primary cancers associated with hematological malignancies. 400 83

The expression of the B2 antigen, defined by a monoclonal antibody, was studied on Burkitt lymphoma lines, lymphoblastoid cell lines, leukemia and myeloma lines, hybrids between different hemapoetic cell lines, and EBV-converted sublines of originally EBV-negative, B2-negative B lymphoma lines. In confirmation of earlier results, the expression of B2 was found to be restricted to a relatively narrow portion of the B cell maturation pathway. Non-B cell-derived lines were uniformly negative. Hybrids derived from the fusion of highly B2-positive and B2-negative or low B2 expressing lines of B cell origin were B2-positive. In contrast, fusion of B2-positive Burkitt lymphoma lines with the primitive human erythroleukemia line K562 resulted in the complete extinction of B2 expression. These findings are in line with the expected behavior of a B cell differentiation marker. EBV conversion of the EBV-negative, B2-negative Ramos lymphoma line by the transforming B95-8 substrain of the virus regularly induced the expression of B2, whereas conversion with the nontransforming P3HR-1 substrain had no such effect, in spite of the continued presence of EBV-DNA and EBNA in both types of EBV-converted sublines. The possibility that B2 induction may reflect the action of the transforming gene(s), present in B95-8 but deleted from the P3HR-1 virus, and the implications of this possibility for the functional mapping of the EBV genome are discussed.
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PMID:Induction of an activated b lymphocyte-associated surface moiety defined by the B2 monoclonal antibody by ebv conversion of an EBV-negative lymphoma line (Ramos): differential effect of transforming (B95-8) and nontransforming (P3HR-1) EBV substrains. 630 Feb 35

The BLA expression of eight Burkitt lymphoma lines was high, whereas it was negative in four, including the two IgG producers tested. Most lymphoblastoid cell lines (LCL) of normal origin had only a low percentage of positive cells, not significantly above background, although a few had up to 30% positives. EBV conversion of the EBV-negative Burkitt lymphoma line Ramos destabilized the high BLA expression, leading to a decrease in the average number of positive cells in the majority of the converted sublines in parallel with considerable fluctuation in antigen expression within each subline. Our group has previously shown that EBV-conversion of Ramos cells can induce certain differentiation steps (Spira et al., 1981 a). EBV-converted sublines of another EBV-negative Burkitt lymphoma, BJAB, showed a much greater stability previously and remained unchanged with regard to BLA expression in our present experiments. Eight T-cell leukemias, three myeloid leukemia lines and two diffuse histiocytic lymphomas were negative for BLA, whereas two myeloma lines were 30-40% positive. A histiocytic tumor had marginal reactions. Hybrids derived from the fusion of high with low BLA-reactive parental lines showed all three possible patterns (high, intermediate and low), provided that B-cell lines were fused with each other. Fusion of two Burkitt lymphoma lines with the K562 erythroleukemia line led to the extinction of BLA expression, as well as to the eclipse of other B-cell markers. B-lymphoma and leukemia (CLL) cells harvested directly from the patient showed a heterogeneous reactivity pattern. Strong to intermediate BLA expression was found among CLL cells and in most histological groups of B-CLL lymphomas except the centroblastic group (3/3 negatives). IgG-expressing follicular lymphomas were less reactive than IgM +/- IgD lymphomas of the same group. Immunocytomas were also low-reactive. BLA can be thus expressed on a variety of B-cell neoplasms; the degree of its expression appears to be related to the stage of differentiation.
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PMID:Expression of the BLA antigen, defined by the monoclonal 38.13 antibody, on Burkitt lymphoma lines, lymphoblastoid cell lines, their hybrids and other B-cell lymphomas and leukemias. 630 66

14 patients developed acute nonlymphocytic leukemia and 1 patient developed Burkitt's leukemia following longterm chemotherapy and/or radiotherapy for other disorders. The main primary disorders included multiple myeloma, Hodgkin's disease, non-Hodgkin's lymphoma and breast carcinoma. Acute leukemia developed earlier in patients treated by chemotherapy with or without radiotherapy than in patients treated by radiotherapy alone (63 months, range 24-132 months; 201 months, range 48 months to 30 years, respectively). 13 patients presented without organomegaly and 8 were pancytopenic. Abnormalities of myeloid and erythroid cell lines were observed in the majority of the patients. A high rate of acute erythroleukemia (5 out of 14) was found. Increased reticulin fibers were found in 3 patients. The leukemia was invariably refractory to treatment with a median survival of 4 months. The possible role of preexisting abnormal marrow structure in the development of therapy-related leukemia is discussed.
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PMID:Acute leukemia following chemotherapy and radiation therapy--a report of 15 cases. 658 10

Using a monoclonal antibody raised by fusing spleen cells from A/J mice, immunized with B10.A splenocytes and lymph-node cells, with a BALB/c myeloma, we have described a new surface alloantigen, Ly-21.2, Ly-21.2 is present in varying amounts in all lymphoid tissues, is not detectable in the brain, kidney, lung or erythrocytes, and is found in only trace amounts in the liver. Strain distribution studies showed that Ly-21.2 is present in all strains examined, including B10, except the A strain and segregation analysis of (A/J x B10) F2 mice showed that Ly-21.2 expression (1) is encoded by one gene and (2) is linked to albinism on chromosome 7. Studies performed on mice developing T-cell leukemia showed that, regardless of the etiologic agent, Ly-21.2 expression increases dramatically in mice with overt leukemia. In addition, preliminary studies suggest that expression of Ly-21.2 is linked to increased susceptibility of mice to Friend-virus-induced erythroleukemia.
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PMID:A new murine lymphocyte alloantigen, Ly-21.2, mapping to the seventh chromosome. 680 49

NALM-6-M1 is an acute lymphoblastic leukemia cell line previously shown in our laboratory to express the pre-B lymphocyte phenotype, i.e., cytoplasmic IgM+, surface immunoglobulin-. Hybridomas were produced against this cell line by fusing spleen cells from hyperimmunized mice with NS-1 mouse myeloma cells. One monoclonal antibody derived from this fusion, designated BA-1, reacted with peripheral blood B lymphocytes, chronic lymphocytic leukemias, pre-B-ALL, most non-Hodgkin's lymphomas, and most non-T, non-B-ALL. BA-1 showed weak reactivity with B lymphoblastoid cell lines and failed to react with multiple myeloma and pokeweed mitogen-induced plasma cells. BA-1 also reacted with peripheral blood granulocytes and the erythroleukemia cell line K-562. No reactivity was seen with cells of T lymphocyte origin, platelets, red cells, monocytes, or acute myelocytic leukemias. Evidence is presented indicating that the determinant recognized by BA-1 is not surface immunoglobulin, HLA-DR, or receptors for C3 or Fc. We conclude that monoclonal antibody BA-1 may be useful in the study of early stages of human B lymphocyte development.
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PMID:A monoclonal antibody (BA-1) reactive with cells of human B lymphocyte lineage. 696 48

The Danish Thorotrast Study was recently reestablished and improved. The cohort has been reidentified and followed up, and now comprises 1003 Thorotrast-exposed patients. For all suspected haematological cases, cytological and histological material has been revised and malignant diseases have been reclassified. The numbers of cases of leukemia and other related haematological disorders were as follows: 16 acute myeloid leukemia (AML); 8 myelodysplastic syndrome (MDS); 1 acute lymphatic leukemia (ALL); 3 chronic myeloid leukemia (CML); 4 non-Hodgkin's lymphoma (NHL); 2 multiple myeloma (MM); 2 myelofibrosis (MF); 2 chronic lymphatic leukemia (CLL). Except for CLL, all cases might be Thorotrast-induced. (Expected number of leukemias: < 2.5.) The findings in the German, Japanese, Portuguese and Danish studies are very similar. Some of the characteristic features include a high incidence of AML with several erythroleukemias, many cases of MDS, and a relatively low incidence of CML. In several studies of leukemia induced by alkylating agents, erythroleukemia is also described as a prominent feature. The possibility exists that a phase of relative predominance of erythroid elements in the bone marrow may be a common and not an unusual feature in the pathogenesis of these secondary leukemias. The findings are also compared with histopathological data from a Danish control group of de novo leukemia patients and from atomic bomb survivors with radiation-induced leukemia. The relative frequency of AML is higher among the Thorotrast-exposed patients than among the Danish control group and the A-bomb survivors. In contrast, low relative frequencies are seen for ALL and CML in Thorotrast cases in comparison with de novo leukemia cases and A-bomb survivors. It can be concluded that differences in relative and absolute frequency of leukemias and myelodysplastic syndrome exist not only between the irradiated populations and the unexposed control group, but even between groups exposed to low-LET (linear energy transfer) and high-LET radiation.
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PMID:Pathoanatomical aspects of malignant haematological disorders among Danish patients exposed to thorium dioxide. 769 89

Lap18 is a highly conserved cytosolic protein that is expressed in dividing cells. Data from a number of studies show that a range of cell lines and mitogen-stimulated normal cells cultured in PMA phosphorylate and subsequently down-regulate Lap18. This has been found to be associated with growth arrest, although it is not clear that these events are causally related. In the present study we confirm that the HL60 promyelocytic leukemia and K562 erythroleukemia cell lines, when cultured with PMA, behave in this manner. This was not the case for any of five mouse plasmacytoma cell lines and six lines derived from patients with multiple myeloma or plasma cell leukemia. All of these lines contain Lap18, although the level of this protein in the mouse but not the human plasmacytoma cell-line cells is relatively low. All the neoplastic plasma cell-line cells phosphorylate Lap18 on culture with PMA, but this does not induce growth arrest nor result in down-regulation of Lap18 expression. Further experiments are required to test whether there is a mechanistic relationship between the continued growth of plasmacytoma cell lines and their failure to down-regulate Lap18 on culture in PMA.
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PMID:Persistent growth of BALB/C mouse plasmacytoma and human myeloma cell lines in the presence of phorbol myristate acetate is associated with continued expression of Lap18 (stathmin). 775 Sep 26

The pleiotropic cytokine interleukin 6 (IL-6) plays a role in the pathogenesis of various diseases, such as multiple myeloma, autoimmune and inflammatory diseases and osteoporosis. Therefore, specific inhibitors of IL-6 may have clinical applications. We previously succeeded in developing receptor antagonists of IL-6 that antagonized wild-type IL-6 activity on the human Epstein-Barr virus (EBV)-transformed B cell line CESS and the human hepatoma cell line HepG2. However, these proteins still had agonistic activity on the human myeloma cell line XG-1. We here report the construction of a novel mutant protein of IL-6 in which two different mutations are combined that individually disrupt the association of the IL-6/IL-6 receptor (R) alpha complex with the signaltransducing "beta" chain, gp130, but leave the binding of IL-6 to IL-6R alpha intact. The resulting mutant protein (with substitutions of residues Gln160 to Glu, Thr163 to Pro, and replacement of human residues Lys42-Ala57 with the corresponding residues of mouse IL-6) was inactive on XG-1 cells and weakly antagonized wild-type IL-6 activity on these cells. By introducing two additional substitutions (Phe171Leu, Ser177Arg), the affinity of the mutant protein for IL-6R alpha was increased fivefold, rendering it capable of completely inhibiting wild-type IL-6 activity on XG-1 cells. Moreover, this mutant also antagonized the activity of IL-6, but not that of leukemia inhibitory factor, oncostatin M, or GM-CSF on the human erythroleukemia cell line TF-1, demonstrating its specificity for IL-6. These data demonstrate the feasibility of developing specific IL-6R antagonists. The availability of such antagonists may offer an approach to specifically inhibit IL-6 activity in vivo.
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PMID:Development of an interleukin (IL) 6 receptor antagonist that inhibits IL-6-dependent growth of human myeloma cells. 796 14


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