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)

Hybridoma cell lines secreting monoclonal antibodies that bind to a surface antigen of human neutrophils have been prepared by fusion of mouse myeloma cells with spleen cells from mice immunized with human neutrophils. Several of the monoclonal antibodies (AHN 1-6) were specific for a neutrophil surface antigen and did not bind lymphocytes, monocytes, red blood cells, platelets, or basophils. All of the granulocyte-specific antibodies immunoprecipitated a polypeptide of 145,000 daltons and an isoelectric point of about 4.5 and other heterogeneous polypeptides of 105,000 daltons. These same components were the major lactoperoxidase-labeled proteins precipitated by hyperimmune mouse serum. The antibodies were further characterized for binding to several human myeloid leukemia cell lines and cells from patients with myeloid or lymphoid leukemia. All antibodies bound the HL-60, ML1, ML2, ML3, K562, and U937 myeloid leukemia cell lines. None of the antibodies bound the RPMI 6410 Raji, RPMI 8226, MOLT 4, or Daudi lymphoid cell lines. All of the hybridoma cell lines (AHN 1-6) produced IgM antibodies that were cytotoxic.
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PMID:A human granulocyte-specific antigen characterized by use of monoclonal antibodies. 684 44

Information from the NCTR control pathology data base was examined to morphologically classify and correlate the incidence off hyperplastic and neoplastic hematopoietic lesions with age in over 15,000 male and female mice of a variety of strains. Hyperplasia affected lymphoid and reticular cells, erythropoietic and granulopoietic cells, mast cells, plasma cells and megakaryocytes. Neoplastic lesions included lymphocytic lymphoma, mixed cell lymphoma, histiocytic lymphoma, granulocytic leukemia, plasma cell neoplasms and mast cell neoplasms. Most hyperplastic and neoplastic hematopoietic lesions increased wtih age and most were slightly more common in the female than in the male mice.
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PMID:Morphologic classification and correlation of incidence of hyperplastic and neoplastic hematopoietic lesions in mice with age. 726 36

It is well known that radiation can cause myeloid leukemia. However, no excess of chronic lymphocytic leukemia has been observed. Myelomatosis, like chronic lymphocytic leukemia, is a tumor of B lymphocytes. To determine whether this disease has a radiogenic origin, we surveyed all cohorts of persons exposed to radiation for which data on cancer-related mortality are available. An excess of myeloma was found in most cohorts. However, a striking deficit was found in two groups irradiated intensely for uterine neoplasms (three cases observed, 10.71 expected; P = 0.012). All other groups combined had a highly significant excess (50 observed, 22.21 expected; P = 2 X 10(-7)). The largest relative risk appeared among persons receiving internal doses of alpha-particles (14 observed, 3.24 expected; P = 2 X 10(-5)), but a significant excess (13 observed, 6.33 expected; P = 0.026) was also found in patients receiving only therapeutic or diagnostic gamma-rays or x-rays. Most cases occurred 15 to 25 years after exposure.
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PMID:Radiation-induced myelomatosis. 744 44

In 1976, an accident in a plant near Seveso, Italy, exposed the local population to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Persons residing in three zones of decreasing TCDD contamination (A, B, and R) and a reference population were followed up for cancer occurrence in 1977-1986. The most exposed subgroup (A) was small, and only 14 cancer cases were observed. In zone B, hepatobiliary cancer was elevated, especially for those living in the area for > 5 years [relative risk (RR) = 2.8; 95% confidence interval (CI) = 1.2-6.3]. Men exhibited an increase in hematologic neoplasms, most notably lymphoreticulosarcoma (RR = 5.7; 95% CI = 1.7-19.0). Women experienced an increased incidence of multiple myeloma (RR = 5.3; 95% CI = 1.2-22.6) and myeloid leukemia (RR = 3.7; 95% CI = 0.9-15.7). In zone R, the incidence of soft tissue tumors and non-Hodgkin's lymphomas was elevated, particularly among persons living in the area for > 5 years (RR = 3.5; 95% CI = 1.2-10.4 for sarcomas, and RR = 2.0; 95% CI = 1.2-3.6 for non-Hodgkin's lymphomas). Breast cancer among females was below expectations in the most contaminated zones, and a clear deficit for endometrial cancer was observed in zones B and R.
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PMID:Cancer incidence in a population accidentally exposed to 2,3,7,8-tetrachlorodibenzo-para-dioxin. 839 84

Carboxylic esterase isoenzymes isolated from a panel of well-characterized continuous human leukemia-lymphoma cell lines were separated by isoelectric focusing. Typical isoenzyme patterns designated Mono 1/Mono 2 (for monocyte-associated), My 1/My 2 (for myeloid or myeloma), Lym 1/Lym 2 (for lymphoid) and Und (for undifferentiated) could be reproducibly discerned. The Mono patterns contained one unique isoenzyme encoded by the monocyte-specific esterase gene. This comparative analysis of 255 leukemia-lymphoma cell lines covered the major cell lineage that are affected by hematological neoplasias. The results showed that (except for myelomas) lymphoid-derived malignancies, both leukemias and lymphomas, expressed primarily the Und and Lym esterase isoenzyme profiles. In contrast, myeloid leukemia cells and the related erythroid and megakaryocytic cell lines displayed mainly the My patterns. The Mono patterns were detected predominantly in monocyte-derived leukemias. As the B-lymphocytic hierarchy progresses from pre B-cells via B-cells to plasma cells, number and intensity of the isoenzymes increased as well from the Und pattern to the My isoenzyme profile. Hodgkin's disease and anaplastic large cell lymphoma lines displayed heterogenous isoenzyme profiles consistent with their heterogenous cellular origin. The present study using continuous leukemia-lymphoma cell lines as model systems provides a biochemical characterization of different hematopoietic cell lineages and stages of differentiation.
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PMID:Esterase isoenzyme profiles of 255 leukemia-lymphoma cell lines from all hematopoietic cell lineages. 872 42

The survival, proliferation, differentiation and function of normal hematopoietic cells are negatively and positively controlled by various cytokines. Survival and proliferation of leukemic cells appears to be influenced, at least in vitro, by several cytokines. Among the different hematopoietic cell lineages, megakaryocytopoiesis represents a complex and unique hematopoietic system that is thought to be supported by some well-known cytokines; however, the hypothetical lineage-specific main regulator of platelet production, termed thrombopoietin (TPO) had remained elusive. Recently, characterization of the proto-oncogene c-mpl revealed structural homology with the hematopoietic cytokine receptor superfamily, specific expression on cells of the megakaryocytic lineage and functional involvement in megakaryocytopoiesis. Several groups purified and cloned the MPL ligand. Extensive in vitro and in vivo studies have shown that the MPL ligand has activity in stimulating both megakaryocytopoiesis and platelet production proving that this ligand is the long-sought growth factor TPO itself. The MPL receptor was found at the mRNA and/or protein level in 40-80% of primary acute myeloid leukemia (AML) cases in various series. MPL expression was not limited to certain morphological FAB types, although the highest percentages were seen in the M6 (erythroid) and M7 (megakaryocytic) subclasses. Among the myelodysplastic syndromes (MDS), MPL expression was detected in one third of the cases, in particular in refractory anemia with excess of blasts and chronic myelomonocytic leukemia. Lymphoid malignancies such as acute lymphoblastic leukemia (ALL), non-Hodgkin's lymphoma (NHL) and myeloma were MPL-negative. Among the large panel of human leukemia-lymphoma cell lines studied, MPL expression occurred predominantly in lines with erythro-megakaryocytic phenotypes. Nearly all primary and continuously cultured non-hematopoietic solid tumor samples were negative for MPL expression. A significant portion of AML cases and of erythroid, megakaryocytic and myeloid leukemia cell lines co-expressed TPO and MPL mRNA transcripts, although no biologically active TPO appeared to be secreted by these cells. In several studies TPO induced in vitro proliferation of 14-37% of primary AML cases, predominantly of the M2 and M7 subtypes. TPO significantly enhanced the cytokine-induced growth of AML cells in a substantial fraction of cases responsive to GM-CSF, IL-3, IL-6 or SCF. While none of 30 growth factor-independent erythro-megakaryocytic leukemia cell lines responded to TPO with increased proliferation, TPO strongly augmented the growth of several constitutively cytokine-dependent cell lines (eg HU-3, M-07e, TF-1) which can be made TPO-dependent and used as bioassays. Neither in primary cells nor in cell lines did TPO appear to induce any signs of morphological, functional or immunological differentiation. Expression of the MPL receptor is not correlated with a proliferative response to TPO. In summary, extensive studies on normal human and animal cells demonstrated the specificity and function of the MPL receptor and proved that its ligand TPO is the major physiological regulator of megakaryocytopoiesis. The data reviewed here document the wide expression of the MPL receptor on AML cells and also suggest some proliferative effects on certain leukemia cells, apparently on non-megakaryocytic AML cells as well. Thus, experimental evidence supports the notion that TPO may contribute, at least in part, to leukemogenesis, especially in combination with other hematopoietic cytokines which is of clinical significance. TPO-responsive cell lines represent powerful tools for such analyses.
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PMID:Thrombopoietin: expression of its receptor MPL and proliferative effects on leukemic cells. 875 57

The multidrug resistant (MDR) phenotype has been suspected as a major cause of treatment failure in hematologic malignancies. Numerous studies have investigated the expression of the MDR1 gene product, P-glycoprotein, in leukemia, lymphoma and myeloma. Studies in myelogenous leukemia and myeloma have so far provided best evidence for a significant correlation between P-glycoprotein expression and response to chemotherapy, although large discrepancies in the proportion of positive cells limit any definite conclusion. Differences in P-glycoprotein detection techniques and methodology may account for the divergent results thus emphasizing the necessity for standardized methods of detection. Despite this, encouraging clinical results have been obtained using MDR modulators in combination with conventional chemotherapy to inhibit the activity of the P-glycoprotein pump. The paper summarizes currently available clinical data and provides guidelines for future trials aimed to reverse the MDR phenotype. The potential of idarubicin to overcome the MDR phenotype is also discussed.
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PMID:The MDR phenotype in hematologic malignancies: prognostic relevance and future perspectives. 876 51

We conducted a proportional mortality study of 1043 deaths among men who took part in an antimalarial campaign in Sardinia, Italy from 1946 to 1950. DDT comprised 94% of the insecticide used during the campaign, and was sprayed over the soil of the entire region at an average concentration of 10 mg/m2, as well as in all dwellings and animal shelters. Expected deaths were derived from the proportional mortality rates of the general Italian male population, specific by cause, 5-year age groups, and 5-year calendar periods in the period from 1956 to 1992. The proportional mortality ratio (PMR) for cardiovascular diseases was significantly decreased, while nonmalignant respiratory diseases showed a 22% increase in risk of borderline statistical significance. Significant increases in risk among workers exposed to DDT in application or inspection jobs were observed for liver and biliary tract cancer (PMR = 228; 95% C.I. = 143-345) and multiple myeloma (PMR = 341; 95% C.I. = 110-795). The PMR for myeloid leukemia was also increased (PMR = 189; 95% C.I. = 38-552), although it was not statistically significant. PMRs for liver and biliary tract cancer and myeloid leukemia were also elevated among workers who did not have direct occupational contact with DDT (liver and biliary cancer: PMR = 210; 95% C.I. = 117-346; myeloid leukemia: PMR = 170; 95% C.I. = 19-614). No trends occurred according to length of employment in exposed jobs. These preliminary results are somewhat in agreement with experimental studies in rodents and previous epidemiologic findings. Expansion of the cohort to include all applications, and collection of information to improve exposure assessment is needed to clarify these findings.
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PMID:Long-term health effects of the occupational exposure to DDT. A preliminary report. 947 44

While several epidemiologic studies have indicated a link between smoking and the risk of developing hematolymphoproliferative cancers (chiefly leukemias, lymphomas, and multiple myelomas), in particular myeloid leukemia, the role of tobacco in the etiology of these neoplasms remains unclear. To evaluate the potential impact of tobacco use on development of leukemia, lymphoma, and multiple myeloma, we conducted a cohort study of 334,957 Swedish construction workers using prospectively collected exposure-information with complete long-term follow-up. A total of 1,322 incident neoplasms occurred during the study period, 1971-91. We found no significant association between smoking status, number of cigarettes smoked, or duration of smoking and the risk of developing leukemias, lymphomas, or multiple myeloma. There was a suggestion of a positive association between smoking and the risk of developing Hodgkin's disease, although the rate ratios were not significantly elevated, except for young current smokers. No positive dose-risk trends emerged. Our study provides no evidence that smoking bears any major relationship to the occurrence of leukemias, non-Hodgkin's lymphomas, or multiple myeloma.
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PMID:Smoking and the risk of leukemia, lymphoma, and multiple myeloma (Sweden). 948 63

All-trans retinoic acid (ATRA) is a vitamin A derivative that induces the differentiation of myeloid leukemia cells in vitro and in vivo. Several investigators have recently reported that ATRA downregulates the production of interleukin-6 (IL-6) and the expression of IL-6 receptor (IL-6R) and also inhibits the proliferation of myeloma cells. It has also been reported that myeloma cells express Fas antigen, and in some of these cells apoptosis was induced by treatment with anti-Fas monoclonal antibody (mAb). In the present study, we demonstrated that ATRA increased Fas expression in the human myeloma cell line, U266B1. We observed that both apoptosis induction and growth inhibition were enhanced in cells exposed to a combination of anti-Fas mAb and ATRA compared with cells exposed to either treatment alone. We also examined whether ATRA modulated bcl-2, an anti-apoptosis protein, in U266B1 cells. Flow cytometry analysis revealed that the mean fluorescence intensity of bcl-2 protein was slightly decreased in cells treated with ATRA. These results indicate that in U266B1 cells, combined treatment with anti-Fas mAb and ATRA enhances the induction of apoptosis by modulating the expression of Fas and bcl-2 by ATRA.
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PMID:All-trans retinoic acid modulates Fas antigen expression and affects cell proliferation and apoptosis in combination with anti-Fas monoclonal antibody in the human myeloma cell line, U266B1. 962 Feb 83


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