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)

Monoclonal antibodies against lymphocytic choriomeningitis virus (LCMV), a natural, high-replicating, noncytolytic pathogen in mice, were obtained from fusions between myeloma cells and lymphoid cells of mice of different H-2 haplotypes at various times (4-24 d) after infection. Supernatants from growing hybridomas were tested in a RIA, and approximately 15% of all supernatants were positive when tested for specificity on infected vs. uninfected cells of different haplotypes. Upon retesting for specific fluorescence, only some RIA+ supernatants exhibited specific surface staining of acetone-fixed infected cells or unfixed infected cells. In all these experiments and using various detection methods we could not find antibodies with any preference of recognition of viral antigen in conjunction with the H-2 haplotype of the responder mouse. The absence of H-2 restricted antibodies after a primary virus infection in vivo, whether assayed by RIA or surface immunofluorescence, suggests that antibodies obtained in other experiments using infected tumor cells for induction and in the RIA may not represent the general case.
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PMID:Monoclonal antibodies against viral determinants are not restricted to the K/D end of the major histocompatibility complex. 243 38

In 21 patients with haemophilia, 10 with acute leukaemia, 12 with malignant lymphomas, and 12 with multiple myeloma in whom the risk of viral infection is increased the following antibodies were determined: anti- CMV, anti-HIV, anti-HBs, and HBs antigen by ELISA test. Anti-CMV were found mainly in acute leukaemia (90%), in haemophilia (71.4%), in malignant lymphoma (41.7%) and multiple myeloma (33.3%). In 19% of cases of haemophilia anti-HIV antibodies were present. In other groups these antibodies were not found. In acute leukaemias mostly anti-HBs antibodies were present. The group of haemophiliacs is particularly exposed to infection by these viruses which is connected unquestionably to blood transfusions.
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PMID:[Anti-HBS, anti-CMV, and anti-HIV antibodies and HBS antigen in patients with hemophilia, malignant lymphomas, leukemias and multiple myeloma]. 256 46

Two hybridomas which secrete monoclonal antibody (McAb) against polymerized human serum albumin (PHSA) were obtained by the fusion of SP2/0 myeloma cell with immune murine spleen cells. One of the McAb was identified as mouse IgG1, the other was IgM. The titers of these purified McAb was 1:16 364 with passive hemagglutination assay (PHA). After labelling with 125I by chloramine-T method, a solid phase radioimmune assay for detecting the PHSA has yielded in 21 positive results, out of 126 HBsAg positive sera, but 53 HBsAg negative sera were all negative. At present we have not seen any report of PHSA present in circulation. PHSA may be as a bridge bind receptor between HBV and hepatocytes and then initiate infection. The appearance of PHSA in HBsAg positive sera could be the result of the damage of the liver during virus infection. More work should be done for this explanation.
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PMID:[Development and application of hybridoma secreting monoclonal antibody against poly-human serum albumin]. 259 20

Four patients with multiple myeloma refractory to conventional chemotherapy received high-dose melphalan. All experienced multiple oral complications. Extensive neutropenic ulceration and orofacial herpes simplex virus infection caused considerable morbidity in three patients during prolonged periods of neutropenia.
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PMID:Oral complications of high-dose melphalan in multiple myeloma. 347 6

A patient with disseminated herpes simplex virus infection, documented by direct immunofluorescence, and untreated multiple myeloma with abnormal immunoglobulins is presented. Reports of infections with intracellular pathogens in myeloma patients are rare, whereas pyogenic infections have been amply documented. Partly in consequence of this, the untreated disease has been thought of as a relatively pure defect in humoral immunity. Review of present knowledge suggests that cell-mediated immunity is of paramount importance in combatting and containing infection with this virus. Thus, immune defects in multiple myeloma, and its infectious complications, may be more complex than appreciated by current concepts of this disease based on previously reported cases.
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PMID:Disseminated herpes simplex in untreated multiple myeloma. Paradox of present concepts of immune defects. 421 37

A stable hybridoma cell line, IIG8-203-2, that secretes a monoclonal antibody of the immunoglobulin subclass M was obtained by fusion of mouse myeloma cells with spleen cells of mice that had been immunized with the viral polypeptide VP2 of simian virus 40. The monoclonal antibody recognizes viral polypeptides that migrate with VP2 polypeptides in a sodium dodecyl sulfate-polyacrylamide gel. It also recognizes two intracellular polypeptides (29,000 and 37,000 daltons) in a detergent-insoluble fraction extracted 30 h after virus infection of TC7 cells.
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PMID:Isolation of a monoclonal antibody viral polypeptide VP2 of simian virus 40. 618 47

Splenic lymphocytes from adult C57BL/6 mice infected with purified reovirus type 1 or 3 particles were fused with NS1 myeloma cells. Approximately 300 clones were obtained from each fusion (type 1 or type 3) and the supernatants from these clones were screened by radioimmunoassay for their ability to bind virus, T lymphocytes, brain, liver, lung tissues and isolated oligodendrocytes and ependymal cells. Approximately 10% of clones (33 and 26 clones, respectively) were positive for each fusion. For reovirus type 1:21% of positive clones bound only virus, 64% bound one of the normal tissues but not virus, and 15% bound both virus and one or more of the normal tissues. For reovirus type 3: 19% of positive clones bound only virus, 73% bound normal tissue only, and 8% bound both virus and normal tissue. Only 3 positive clones were obtained from uninfected control animals. These experiments demonstrate that (a) during the course of an immune response to a virus, autoantibodies are generated which react with a large variety of normal tissues and that (b) there are shared antigenic structures between viral determinants and normal tissue that can be identified by monoclonal antibodies. Although these results suggest two mechanisms by which an autoimmune response may develop following viral infection, the biological significance of these autoreactive monoclonal antibodies remains to be elucidated.
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PMID:Autoimmunity following viral infection: demonstration of monoclonal antibodies against normal tissue following infection of mice with reovirus and demonstration of shared antigenicity between virus and lymphocytes. 632 71

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

There are two immunogenic sites on the type A influenza A/Japan/57 (H2N2) hemagglutinin (HA) that can be recognized by class I major histocompatibility complex (MHC), H-2Kd-restricted cytolytic T lymphocytes (CTLs). One of these sites encompasses two distinct partially overlapping epitopes, which span HA residues 204-212 and 210-219. During the analysis of the fine specificity of CTL clones directed to the HA 210-219 epitope, we found that one clone 40-2 also recognized the myeloma cell line P3x63-Ag8. P3x63-Ag8 is derived from the MOPC 21 myeloma and expresses an immunoglobulin (Ig) heavy chain variable region (VH) gene which is a member of the murine 7183 VH gene family. Recognition was specific for the endogenously processed MOPC 21 heavy chain in association with the Kd molecules, since the SP2/0 derivative of P3x63-Ag8, which does not make a functional Ig H chain, is not recognized. The VH epitope recognized by clone 40-2 could be mapped to a 10 amino acid peptide spanning MOPC 21 VH residues 49-58. Cross-reactivity for the VH gene product was also demonstrable in some heterogeneous populations of CTL generated in response to influenza virus infection. These results represent the first demonstration of cross-reactivity for an endogenously processed product of a self-Ig by the CTL directed to a foreign antigen and raise the possibility that the Ig VH expression may regulate the CD8+ T cell response to foreign antigens.
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PMID:Recognition of an immunoglobulin VH epitope by influenza virus-specific class I major histocompatibility complex-restricted cytolytic T lymphocytes. 750 98

Infection with human immunodeficiency virus type 1 (HIV-1) primarily involves a subgroup of T-lymphocytic cells, but other cell types are also invaded by the virus, including cell lines within the haematopoietic system. Together with infectious, inflammatory and neoplasic processes, invasion of haematopoietic tissue explains the haematological alterations which are seen during the course of infection with HIV-1. Anaemia develops in the large proportion of patients. Thrombocytopenia frequently occurs during the course of the disease, but may be seen in some patients already at the time of diagnosis, where the condition may be misdiagnosed as "idiopathic" thrombocytopenic purpura. Neutropenia is seen in all disease stages, but is most severe in patients with advanced disease. Bone marrow changes include varying degrees of dysplasia in one or more cell lines, which in some patients may mimic a myelodysplastic syndrome. The number of plasma cells is always increased. In many patients the bone marrow stroma exhibits an increased amount of reticular fibres. HIV-1 infection is associated with an increased risk of non-Hodgkin malignant lymphoma. Acute myelogenous leukaemia and myelomatosis have been described in patients with advanced disease. Treatment of the above mentioned haematological abnormalities aims primarily at reducing replication of HIV-1, thereby diminishing suppression of haematopoiesis by the virus infection, and at controlling the opportunistic infections during the course of the disease. Specific antiviral therapy (AZT) is most successful in correcting thrombocytopenia. The possibility of bone marrow suppression mediated by a toxic drug effect should always be considered in this patient group.
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PMID:[Hematological changes associated with human immunodeficiency virus (HIV-1) infection]. 831 70


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