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)

A murine mAb, 7D3, was produced by fusion of spleen cells obtained from mice immunized with a rat thymic epithelial cell line, Tu-D3 and NS/1 myeloma cells. 7D3 antibody reacted with approximately 95% thymocytes, 17% spleen cells, less than 9% of mesenteric lymph node cells and 32% of bone marrow cells of rat origin. 7D3 also reacted with two rat thymic epithelial cell lines but not with a rat fibroblastic cell line. Immunochemical analysis demonstrated that 7D3 antibody recognized a single polypeptide with molecular weight of 80,000 in FTE cells and 80,000 to 96,000 in thymocytes. 7D3 antibody strongly inhibited the thymocyte binding to thymic epithelial cells. In addition, 7D3 antibody inhibited TPA-induced thymocyte aggregation. 7D3 negative rat thymic lymphoma cells bound to 7D3 positive thymic epithelial cells and this binding was inhibited by 7D3 antibody, indicating that a part of thymocyte-thymic epithelial cell binding was mediated by the interaction of 7D3 Ag and undefined ligand to 7D3.
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PMID:A novel cell surface antigen involved in thymocyte and thymic epithelial cell adhesion. 167 19

Protein kinase C activity of the human myeloma cell line, RPMI 8226, was studied after prepurification on DEAE-cellulose. The total protein kinase activity, eluted at 0.12 M NaCl, was 493 nmol/min/10(10) cells, but 38% was associated with membranes. The lipid dependence of cytosolic and membrane activities was only 52% and 21%, respectively. This activity increased with time, to as much as 200% for the membrane fraction after 7 days, whereas lipid dependence and the PDBu binding properties were lost. This modified activity was not due to the extinction of a copurifying endogenous inhibitor nor to classical PKC proteolysis. TPA-treatment of these cels is accompanied by a rapid, selective and complete loss of lipid-dependent activity of the cytosol, thus benefiting co-migrating lipid independent activity, with no membrane fraction recovery or PKM formation.
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PMID:Abnormal behavior of protein kinase C in the human myeloma cell line, RPMI 8226. 240 58

B-cell neoplasias such as CLL can be viewed as models of monoclonal populations restricted within discrete ranges of B-cell maturation. It is unknown whether other B-cell leukemias such as prolymphocytic leukemia (PLL), lymphoplasmacytoid immunocytoma (IC), and hairy cell leukemia (HCL) involve different B lineages or are malignant variants of B cells in successive stages of development along the same lineage. Therefore in vitro maturation was induced with the phorbol ester TPA in leukemic cell samples from 10 CLL, 4 PLL, and 4 IC patients. Morphologically, both plasmacytic and hairy cell-like phenomena were induced. The latter unexpected finding was confirmed by reaction with HD6 (CD22) antibody which stains HCL but is unreactive with plasma cells, multiple myeloma, and CLL cells. Tartrate-resistant acid phosphatase was demonstrated in TPA-cultured CLL, PLL, and IC cells, and the same isoenzyme band as in HCL was revealed by isoelectrofocusing. On the other hand, an increase of IgM messenger RNA was detected in up to 20% of the cells in CLL cultures by single-cell in situ hybridization with fluoro-chrome-labeled DNA probes. An abundance of IgM messenger RNA characterizes lymphoplasmacytoid cells as found in IC. Our data demonstrate that CLL, PLL, and IC can be induced to realize a common genetic program which bears characteristics of HCL indicating that these four entities are more closely related than previously thought.
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PMID:Phenotypic modulation of chronic lymphocytic, prolymphocytic, and lymphoplasmacytic leukemia cells by TPA: induction of TRAP isoenzyme 5 and HD6 (CD22) antigen and enhancement of IgM messenger RNA. 347 68

The isoenzyme profiles of hexosaminidase (N-acetyl-beta-D-glucosaminidase) were analyzed by isoelectric focusing on horizontal polyacrylamide thin-layer gel with special emphasis on the intermediate isoenzyme (Hex I). The expression of Hex I was examined in 87 leukemia-lymphoma cell lines, in 14 B-lymphoblastoid cell lines, in 441 cases of leukemia-lymphoma (specimens containing 80% or more tumor cells), in 22 leukemia cell lines and in 14 cases of leukemia that had been treated with phorbolesters (TPA) for induction of differentiation, and in the mononuclear cell preparations separated from peripheral blood, lymph node, thymus, bone marrow, tonsil, liver, and spleen specimens from normal donors. Hex I was detected in the leukemia cell lines arrested at early, immature or at late, mature stages of B- and T-cell differentiation, but not in cell lines blocked at intermediate stages of maturation. Most myelomonocytic leukemia cell lines and the erythroleukemia cell lines showed Hex I, whereas the B-lymphoblastoid cell lines were negative for this marker. During induction of differentiation, the expression of Hex I was lost in 13 of 15 leukemia cell lines that were originally Hex I-positive. Among the panel of the "fresh" leukemia-lymphoma cells, Hex I was found predominantly in cases of acute lymphoblastic leukemia and acute myeloblastic/monoblastic leukemia, but rarely or not at all in the mature T-, B- or myeloid malignancies. However, two out of two cases of multiple myeloma were Hex I-positive, and the Hex I expression could be induced by TPA in three of six B-cell chronic lymphocytic leukemia cases. Chronic myelocytic leukemia cells remained Hex I-negative during induction of differentiation. Hex I-positivity was not detected in the cell preparations from normal tissues, and peripheral blood indicating that the normal cellular counterpart of the Hex I-positive tumor cells are present at only low percentages within the respective cell populations. It is suggested that Hex I is a marker of early lymphoid and myeloid hematopoiesis that is no longer expressed in intermediate stages of lymphoid differentiation and in later or terminal stages of myeloid differentiation, but that is again detectable in terminally differentiated B-cells. Further studies will focus on identification and isolation of normal Hex I-positive cells.
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PMID:Occurrence of particular isoenzymes in fresh and cultured leukemia-lymphoma cells. II. Hexosaminidase I isoenzyme. 348 78

RAB-1, a new monoclonal antibody (McAb) to human leukemic hairy cell (HC) was produced. Using indirect immunofluorescence methods and microscopic or flow cytometric analysis, it was found that the RAB-1 antigen was expressed on few resting B cells and not on resting T lymphocytes, platelets, monocytes, erythroid and myeloid cells. RAB-1 expression on malignant cells was as follows: strongly positive in 15/15 hairy cell leukemia (HCL), negative with non-T and T-acute lymphoblastic leukemia and T-chronic lymphocytic leukemia (CLL); weakly expressed on myeloma and Waldenstrom cells; moderately on 10-25% of the cells in 4/10 B-CLL and 6/10 B lymphomas and in 7/7 B-prolymphocytic leukemia (PLL). Amongst human cell lines that were tested, RAB-1 reacted strongly with one HC line, moderately with the EBV-lymphoblastoid Daudi and Raji Burkitt's lines and was not expressed on Ramos, ALL, myeloid and erythroid cell lines. Normal B cells activated with PWM or anti-mu beads, and malignant B cells activated with anti-mu and TPA did not show an increase of expression of RAB-1 antigen. Interestingly, 30-40% of T4-Class II antigen positive cloned cells and T cells activated with PHA and Con.A expressed RAB-1, suggesting that this McAb recognizes surface molecule, newly induced during T-cell activation and constitutively expressed on HC and some B-cell malignancies.
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PMID:RAB-1: a new monoclonal antibody to leukemic hairy cells. 353 32

Annexin VIII is a calcium- and phospholipid-binding protein with anticoagulant activity. Annexin VIII mRNA was found to be specifically expressed in acute promyelocytic leukemia (APL) cells; it was not found in other types of acute myeloid leukemia (AML) nor in lymphoid malignancies. Using Northern blot analysis we investigated annexin VIII expression in 142 continuous human leukemia and lymphoma cell lines at the mRNA level. While the only APL cell line, NB-4, was indeed positive, other cell lines also displayed annexin VIII mRNA: 4/22 myeloid cell lines, 8/23 monocytic cell lines, 2/8 megakaryoblastic cell lines, 5/26 lymphoma-derived cell lines, 2/10 myeloma cell lines and 1/44 lymphoid leukemia cell lines. The strongest expression was seen in NB-4 and in the Hodgkin's disease derived cell line HDLM-2. Treatment of NB-4 cells with all-trans retinoic acid (ATRA) or the phorbol ester TPA induced terminal differentiation and down-regulated annexin VIII mRNA expression rapidly within a few hours; vitamin D3 was ineffective in this regard; the protein kinase C activator Bryostatin 1 up-regulated the expression. A panel of initially negative cell lines could not be induced by any of these biomodulators to transcribe annexin VIII. The half-life (T1/2) of annexin VIII mRNA was about 3-4 h using actinomycin D as transcription inhibitor. Treatment with ATRA or TPA prior to exposure to actinomycin shortened the T1/2 to 2 h while Bryostatin 1 extended it to 6h. As 21/141 non-APL cell lines were positive, annexin VIII cannot be used as a marker gene for APL cells; however, it might be associated with myelomonocytic or erythro-megakaryoblastic precursor cells. Annexin VIII gene expression might play a unique role in the proliferation and/or differentiation of leukemic cells and could be associated with the particular abnormal hemostasis of some leukemias.
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PMID:Expression and modulation of annexin VIII in human leukemia-lymphoma cell lines. 823 Dec 35

Anti delta IK17 monoclonal antibody was produced by fusing SP2/0/Ag 14 myeloma with spleen cells of BALB/c mice immunized with normal human thymocytes. a delta IK17 antibody recognizes a 44kD cell surface protein detected on human lymphocytes. delta IK17 is expressed on human thymocytes, CD4+ and CD8+ T cell subsets, B, NK cells, as well as on activated cells. The antigen is detected on cells during the early, intermediate and late stages of lymphocyte maturation. In addition, the expression of the antigen is correlated with ontogenesis. A T+ delta IK17+ subpopulation responded poorly to TPA stimulation and provided a better helper signal for PWM-induced IgM synthesis than T+ delta IK17- cells. In addition, different levels of delta IK17 expression were detected in several hematological diseases tested.
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PMID:delta IK17: an antigen expressed on human lymphocytes. 901 40

The function of CD28 molecules that are present on malignant plasma cells of human myeloma cell lines (HMCL) was studied. First, myeloma cells expressed a similar density of CD28 antigen to that of normal T cells. The myeloma CD28 molecules were able to bind B7-Ig molecules as well as L cells transfected with a B7-1 cDNA, and anti-CD28 mAb inhibited the binding. Myeloma cells did not express B7-1 antigens but a low density of B7-2 antigens. The myeloma B7-2 molecules of two HMCL were able to bind CTLA-4 protein. No autocrine CD28:B7-2 activation could be evidenced as we found no spontaneous binding of the p85 subunit of PI-3 kinase to CD28 molecules. In addition, a blocking anti-CD28 mAb did not affect the IL-6-dependent or autonomous proliferation of the HMCL. The activation of myeloma CD28 molecules with or without TPA stimulation did not affect the proliferation, survival, differentiation, expression of activation antigens and cytokine receptors or cytokine production of myeloma cells. However, the triggering of myeloma CD28 molecules by B7-1 transfectant cells resulted in binding of the p85 subunit of PI-3 kinase to CD28 molecules as previously shown for T cell CD28 molecules. This expression of a large density of CD28 molecules able to bind B7 molecules might contribute to a downregulation of the immune control of myeloma cells.
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PMID:Malignant plasma cell lines express a functional CD28 molecule. 955 21

Primary effusion lymphoma (PEL) is a new lymphoma entity occurring predominantly, but not exclusively in HIV+ patients with acquired immunodeficiency syndrome (AIDS). PEL grows exclusively in body cavities as serous lymphomatous effusion without evidence of mass disease or dissemination. The cells are infected with the newly discovered human herpesvirus-8 (HHV-8), often accompanied by co-infection with Epstein-Barr virus (EBV). Several lymphoma cell lines have been established from patients with AIDS- and non-AIDS-associated PEL. Given their phenotypical relationship to plasma cells, several cytokines may be important for growth and survival of PEL cells. We investigated the spectrum of cytokines produced by nine HHV-8+ PEL cell lines, in comparison with five Burkitt lymphoma, seven other B non-Hodgkin's lymphoma (B-NHL) and seven multiple myeloma-derived cell lines. In addition, we tested the response of the PEL cells to selected cytokines and the effects of neutralizing anti-cytokine and anti-cytokine receptor antibodies. Using specific ELISAs, PEL cell lines were found to produce large amounts of interleukin-6 (IL-6; 10-5000 pg/ml), IL-6 soluble receptor (IL-6sR; 30-600 pg/ml), IL-10 (600-80,000 pg/ml) and oncostatin M (OSM; 50-80 pg/ml) which in most cases were significantly higher than the levels produced by the Burkitt, B-NHL or myeloma cell lines; on the contrary, PEL cell lines did not elaborate significant levels of macrophage inhibitory protein (MIP-1alpha) and leukemia inhibitory factor (LIF). However, the levels of MIP-1alpha were increased 10- to 100-fold by treatment with phorbol ester TPA. PEL cell lines did not respond proliferatively to IL-6, IL-10, IL-11, LIF, MIP-1alpha, or OSM. Incubation with IL-6sR and IL-6 inhibited cell growth. Anti-IL6 neutralizing antibodies had no effect on PEL cell line proliferation; conversely, whereas anti-IL6R alone inhibited only weakly, anti-gp130 and anti-gp130 plus anti-IL6R showed strong inhibitory effects (>20% inhibition in 5/9 lines and >60% inhibition in 3/9 lines). In summary, PEL cell lines produce high amounts of cytokines (IL-6, IL-10, OSM); proliferation could be inhibited by blocking the receptors of the IL-6 signaling pathway.
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PMID:Constitutive cytokine production by primary effusion (body cavity-based) lymphoma-derived cell lines. 1021 73

When the primary site is unknown in patients with spinal metastases, there can be problems in locating the site of tumor origin. Most previous reports on metastases of unknown origin have not been limited to the spine. The purpose of this study is to assess the usefulness of laboratory analysis, chest, abdominal and pelvic CT and CT-guided biopsy in patients with spinal metastases of unknown origin (SMUO). A retrospective review of the clinical histories of 27 patients with SMUO was done. A total of 43 patients with SMUO were seen at our institution between 2002 and 2007. Of the 43 patients, 27 who underwent all 3 tests (laboratory analysis including M protein and tumor markers, chest, abdominal and pelvic CT and CT-guided biopsy) were included in this study. We retrospectively assessed the diagnostic usefulness of those 3 tests in the 27 patients. In 27 patients, the final diagnosis was obtained in 26 patients. Myeloma was the most common malignancy followed by lung carcinoma. M protein was positive in all 7 patients with myeloma and negative in patients with other malignancies. The level of tumor markers was elevated in 16 of 17 patients with a solid tumor and in all 3 with lymphoma. CA15-3 was elevated in 4 of 27 patients, CA19-9 in 5 of 27 patients, CA125 in 2 of 27 patients, CEA in 6 of 27 patients, SCC in 2 of 27 patients, NSE in 7 of 27 patients, AFP in 1 of 27 patients, PIVKA-II in 1 of 27 patients, TPA in 6 of 27 patients, IAP in 3 of 12 patients, thyroglobulin in 2 of 27 patients, sIL-2R in 3 of 24 patients, and PSA in 5 of 17 male patients. Myeloma, lymphoma and prostate carcinoma had a marker with high sensitivity and specificity (M protein, sIL-2R and PSA). Eleven primary tumor sites (40.7%) were detected (6 lung, 1 prostate, 1 kidney, 1 thyroid, 1 liver, and 1 pancreas) by chest, abdominal and CT scanning. Biopsy led to determination of the final diagnosis in 12 (44.4%) of 27 patients (5 myelomas, 3 lymphomas, 2 prostate carcinomas, 1 renal-cell carcinoma, 1 thyroid carcinoma). In the remaining 15 patients, biopsy did not lead to determination of the final diagnosis, because the histological diagnosis was either an adenocarcinoma or an undifferentiated carcinoma, the tissue sample was not diagnostic. A laboratory analysis limited to specific tumor markers such as PSA and protein electrophoresis is considered to be useful in making a final diagnosis. Chest, abdominal and pelvic CT is considered to be useful for making a final diagnosis in solid tumors, but not for hematologic tumors. A CT-guided biopsy had a low determination rate in the final diagnosis in comparison to a laboratory analysis and CT scanning for solid tumors and it is not considered to be essential for the diagnosis of hematologic tumors.
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PMID:Diagnosis of a previously unidentified primary site in patients with spinal metastasis: diagnostic usefulness of laboratory analysis, CT scanning and CT-guided biopsy. 1953 81


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