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)

Twenty-one (100%) Haitians and 42 (21.5%) of 192 native black Americans autopsied in a 33-month period at Jackson Memorial Hospital, Miami, were included in this review. All autopsied materials were examined. Among the Haitians autopsied, infectious diseases accounted for 11 (52%) of 21 deaths. Toxoplasma encephalitis was the leading cause of death (five cases). Other infectious causes of death included disseminated cryptococcosis (one), disseminated cytomegalovirus diseases (one), Pneumocystis carinii pneumonia (one), chronic active hepatitis B (two), and bacterial pneumonia (one). Malignant neoplasms were also found to be causes of death and these included a single cases of each of the following: adenocarcinoma of the lung, multiple myeloma, diffuse histiocytic lymphoma, hepatoma, and Kaposi's sarcoma. Deaths of the remaining cases were due to hypertensive cardiovascular diseases (two), rheumatic heart disease (one), glomerulonephritis (one), and intimal fibroplasia of coronary arteries (one). Seven Haitian cases fulfilled the Centers for Disease Control case definition for the acquired immune deficiency syndrome (AIDS). For comparison, autopsies of black Americans were chosen from conditions that would most likely predispose them to opportunistic infections. Among the autopsies on black Americans there were no cases of opportunistic infections or Kaposi's sarcoma that were considered to be consistent with the AIDS.
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PMID:Unusual causes of death in Haitians residing in Miami. High prevalence of opportunistic infections. 634 27

The augmenting effect of vaccinia virus infection of tumor cells on induction of tumor-specific resistance was examined in mice. C3H/HeN mice were primed intraperitoneally (ip) with live vaccinia virus after whole-body irradiation with 250 rad of X-rays. Three weeks later the mice were immunized ip 3 times at weekly intervals with syngeneic murine hepatoma MH134 or spontaneous myeloma X5563 which had been infected in vitro with vaccinia virus and subsequently irradiated with 7000 rad of X-rays. One week after the third immunization, the mice were challenged with 1 X 10(5) viable cells of MH134 or X5563 ip or 1 X 10(6) tumor cells intradermally (id). On ip challenge with viable MH134 cells all mice that had not been pretreated died within 3 weeks due to ascites tumor out-growth, whereas all mice that had been vaccinia virus-primed and immunized with vaccinia virus-infected MH134 cells survived. On ip challenge with X5563 cells, the percentage survival of vaccinia virus-primed and vaccinia virus-modified tumor-immunized mice was 80%. On id challenge with MH134 and X5563 tumor cells, in un-treated mice tumors grew to more than 5 mm in diameter within 3 weeks, whereas 90% and 60%, respectively, of the mice that had been vaccinia virus-primed and immunized with vaccinia virus-infected tumor cells showed no tumor out-growth. Pretreatment by only immunization with vaccinia virus-infected cells or vaccinia virus-priming and immunization with virus non-infected tumor cells were not effective for preventing induction of tumor-resistance to either ip or id challenge with MH134 or X5563 tumor cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Additional evidence for the augmented induction of tumor-specific resistance in vaccinia virus-primed mice by immunization with vaccinia virus-modulated syngeneic tumor cells. 638 60

Mouse myeloma cells were fused with splenocytes from a mouse that had been immunized with RNA polymerase I purified from a rat hepatoma. Hybridoma cells were selected and colonies secreting antibodies directed against the enzyme were detected by analysis of cell culture supernatants in a solid phase radioimmunoassay. Two of these cell lines were grown on a larger scale and the interaction between the immunoglobulins obtained from them and RNA polymerase I was studied in detail. Antibodies from both of the hybridoma cell lines were able to inhibit DNA-dependent RNA synthesis catalyzed by RNA polymerases I and III, but not that catalyzed by polymerase II. The antibodies were also capable of reducing the RNA chain elongation reaction catalyzed either by RNA polymerase I associated with isolated nucleoli or by enzyme preinitiated in vitro on calf thymus DNA. Inhibition of RNA polymerase I activity by the monoclonal antibodies was inversely related to the nucleotide concentration. In contrast, the DNA concentration had relatively little effect on inhibition by the antibodies. Analysis of immune complex formation between the antibodies and isolated individual enzyme subunits demonstrated that the monoclonal antibodies were directed against the largest (Mr = 190,000) polypeptide of the polymerase I. These data indicate that the largest subunit of RNA polymerase I contains an immunological determinant in common with RNA polymerase III and suggest that the polymerase I polypeptide of Mr = 190,000 contains a catalytic center involved in RNA chain elongation.
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PMID:Monoclonal antibodies directed against mammalian RNA polymerase I. Identification of the catalytic center. 663 Feb 16

Plasma membranes prepared from rat livers inhibited the in vitro growth of various mammalian cells including hepatoma cells in a concentration-dependent manner, showing almost complete arrest of cell growth at 0.1 mg protein/ml. Some of these cells tested, i.e., leukemia (L1210 and P388) and myeloma (P3-NS-1/1-Ag4-1) cells, were labile in the presence of plasma membranes (losing the viability), and CHO (Chinese hamster ovary) cells became round without detaching from the substratum. The culture medium preincubated with liver plasma membranes no longer supported the growth of hepatoma cells (AHI3 and AH66F). However, the 'conditioned' medium supplemented with L-arginine, supported the growth of the cells. Moreover, the addition of L-ornithine to the cultures containing plasma membranes markedly reduced the inhibitory effect of plasma membranes. The plasma membrane preparations were found to possess considerable arginase activity. There results seem to indicate the possible involvement of arginase in the inhibition of cell growth by liver plasma membranes.
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PMID:Arginase as an inhibitory principle in liver plasma membranes arresting the growth of various mammalian cells in vitro. 720 Aug 4

DNA polymerase beta was purified from various mammalian cells, i.e. mouse myeloma, rat liver, rat ascites hepatoma cells, rabbit liver, pig liver, and calf thymus cells. The apparent molecular weights of the polypeptides composing these enzymes were all about 40,000, as determined by sodium dodecyl sulfate polyacrylamide gel electrophoresis. Moreover, tryptic peptide maps of these enzymes after radioiodination with 125I indicated that the molecular structures of the enzymes were basically identical. No difference was detected in the peptide maps of the mouse and rabbit enzymes, and only a few of the 22 spots in the fingerprint of the mouse enzyme were not detected in that of the rat enzyme. Furthermore, the peptide maps of DNA polymerase beta's from normal and malignant rat cells differed in only one spot.
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PMID:Structural homology of DNA polymerase beta from various mammalian cells. 720 93

Mutagenesis of a region of human interleukin (IL)-6 which is important for triggering signal transduction via the IL-6 receptor beta-chain (gp130) has lead to the isolation of a variant of human IL-6 (IL-6.Q160E/T163P), which could antagonize the biological activity of wild type IL-6 on the human EBV transformed B cell line CESS and the human hepatoma cell line HepG2. Surprisingly this antagonistic IL-6 variant had an agonistic effect on the human myeloma cell line XG-1, albeit at a 1000-fold higher concentration than wild type IL-6. This residual activity of the mutant arose from triggering gp130, because it could be inhibited by a gp130 specific mAb. Extensive mutagenesis of residues between Q153 and H165 of human IL-6, a region which is partly homologous in cytokines which also signal via gp130 (oncostatin M, ciliary neurotrophic factor, leukaemia inhibitory factor, IL-11), did result in the isolation of a second antagonist for IL-6 activity on CESS and HepG2 cells. However on XG-1 cells this variant was active as well. These results suggest that (an) additional region(s) of the IL-6 molecule might be involved in gp130 triggering. Recently we indeed found that residues Lys42-Ala57 are also important for gp130 triggering. Inhibition experiments with neutralizing IL-6R alpha-chain specific mAb show that this region can be functionally separated from the Q153-H165 region. These findings have important implications for the development of receptor antagonists of IL-6 and IL-6 family members.
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PMID:Functional distinction of two regions of human interleukin 6 important for signal transduction via gp130. 757 77

From October 1987 to November 1993 we evaluated the serum levels of ammonia and amino acids in 85 patients with multiple myeloma. Six of the 85 cases of multiple myeloma demonstrated hyperammonemia and none of the known causes of hyperammonemia, such as liver failure, could be identified in these patients. All six patients also showed serum amino acid disturbances and conscious disorders in various degrees. In this study we compared these abnormalities in multiple myeloma with those in chronic liver failure (n = 14), the basic diseases of which were liver cirrhosis in six cases and liver cirrhosis complicated hepatocellular carcinoma in eight cases. There was a marked difference in the levels of individual serum amino acids between these two groups. The level of glycine was significantly higher in the multiple myeloma group (P < 0.001); on the other hand, that of tyrosine was significantly higher in the liver failure group (P < 0.005). The histidine (P < 0.005) and arginine (P < 0.005) levels were lower in the myeloma group. The ratio of glycine to tyrosine (Gly/Tyr) was 16.7 +/- 4.85 in the myeloma group and 1.7 +/- 0.12 in the liver failure group. The ratio of glycine to tyrosine was an important criterion for differential diagnosis.
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PMID:Serum amino acid disturbance in multiple myeloma with hyperammonemia. 759 24

Six hybridoma cell lines (AP1-AP6) secreting monoclonal antibodies (McAb) against PAI-1 were obtained by fusing the murine myeloma cell line SP2/0 with the spleen cells from Balb/c mouse immunized with recombinant PAI-1 expressed in E. coli. These antibodies were purified by SPA affinity chromatography. All McAbs recognized rPAI-1 and PAI-1 from the human hepatoma cell line HepG2. The titers of ascites were more than 10(6). The antibody-antigen affinity constants (Kaff) for anti-PAI-1 McAb measured by EIA were between 3.45 x 10(7)-1.05 x 10(10) M. AP2 and AP3 McAbs were effective in quenching the activity of PAI-1. Partial quenching of PAI-1 activity was achieved with AP4, AP5 and AP6 McAbs respectively. AP1 McAb had no effect upon PAI-1 activity. Three of the six McAbs (AP1, AP4 and AP5) bound to the PAI-1/t-PA complex, while the others did not. The PAI-1 was purified 51 folds to homogeneity from serum free medium of HepG2 with the recovery rate of 92% by one-step procedure using Sepharose 4B conjugated with anti-PAI-1 McAb (AP1, AP3 and AP4). A sandwich ELISA for the measurement of PAI-1 antigen in human plasma was developed, based on anti-PAI-1 McAb against non-overlapping epitopes. The mean value of plasma PAI-1 for the healthy donors was 24.7 +/- 7.75 ng/ml measured by ELISA.
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PMID:Preparation, characterization and application of monoclonal antibodies against PAI-1. 780 88

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

In a consecutive series of 317 patients with hepatocellular carcinoma (HCC), 32 (10.1%) had 35 extrahepatic primary malignant neoplasms (PMNs) (3 patients had triple cancers). Twenty-five PMNs occurred before the diagnosis of HCC, 7 were synchronous and 3 metachronous. These 35 PMNs were: 6 cancers of the colon, 3 of the stomach, 1 of the rectum, 4 of the breast, 2 of the lung, 1 of the larynx, 3 of the prostate, 1 of the penis, 1 of the urinary bladder, 1 of the uterus, 2 of the skin, and the remaining 10 were immunoproliferative cancers, all of B cell origin (7 non-Hodgkin's lymphoma, 2 multiple myeloma, and 1 chronic lymphocytic leukemia). Thus, in this series, B-lymphocyte-derived neoplasms were the most frequent PMNs associated with HCC. These 10 patients showed no difference for age, male:female ratio, HCC cytotype, presence of cirrhosis, alcohol abuse, markers related to hepatitis B and C virus, and serum level of alpha-fetoprotein when compared with the 22 patients with HCC and other PMNs and the 285 with HCC alone. B cell neoplasms constitute half of the synchronous or metachronous cancers, and must, therefore, be kept in mind in the management of HCC patients.
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PMID:Extrahepatic primary malignant neoplasms associated with hepatocellular carcinoma: high occurrence of B cell tumors. 805 89


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