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)

A chimeric mouse-human antibody (C beta 1) was constructed that recognized the principal neutralizing domain (PND) of human immunodeficiency virus type 1 (HIV-1) gp120. The constant (C) immunoglobulin regions (C gamma 1 and C kappa) of a mouse monoclonal antibody, 0.5 beta, were substituted for the human C gamma 1 and C kappa by recombining the DNA modules encoding variable or C regions. The DNA constructs were then transfected into X63 Ag8.653 myeloma cells. A clone with a high production of the chimeric antibody (C beta 1) was selected. This antibody was tested for its biological activity against HIV-1. It bound to the surface of HTLV-IIIB-infected cells and reacted with gp120/160 with equal affinity and specificity to that of the parental 0.5 beta murine monoclonal antibody in a Western blot assay. Neutralization and/or enhancement of HIV infection were evaluated with C beta 1 and 0.5 beta. Both C beta 1 and 0.5 beta neutralized cell-to-cell infection and cell-free virus infection by HTLV-IIIB. Antibody-dependence enhancement of HIV infection was not observed with either C beta 1 or 0.5 beta in the presence or absence of human complement. Antibody-dependent cell-mediated cytolysis (ADCC) and antibody-dependent complement-mediated cytolysis (ACC) were observed with C beta 1 but not with the parental 0.5 beta. These findings suggest that the neutralizing antibodies to PND may neutralize but not enhance HIV infection. Furthermore, the high levels of ACC and ADCC shown against HIV-infected cells by C beta 1 indicate that the clinical application of such monoclonal antibodies may be possible.
AIDS Res Hum Retroviruses 1992 Jun
PMID:Characterization of a mouse/human chimeric monoclonal antibody (C beta 1) to a principal neutralizing domain of the human immunodeficiency virus type 1 envelope protein. 138 Feb 58

58 death certifications (40 males and 18 females) of residents of the Canton of Vaud (Switzerland) which reported AIDS as the cause of death in 1986-1989 were matched with the list of incident cancers available since 1974 from the Vaud Cancer Registry. Such linkage was successful for 20 individuals (age range 25-63, median 37), mostly males (18/20), homosexual or bisexual (11/18) and affected by Kaposi's sarcoma (14 males and 1 female). Other identified neoplasms included one Burkitt's lymphoma, one prostate adenocarcinoma and one multiple myeloma (whose histological picture included, however, lymphocytosis in addition to plasmocytosis). Three additional malignancies (one undifferentiated skin cancer, one carcinoma of the salivary glands and one in situ cervical carcinoma), and one myelodysplastic syndrome had also been diagnosed from 1 to 2 years before AIDS death. Cancer was mentioned on the death certificate, in addition to AIDS, in only 2 cases. Albeit of limited size, the present report confirms that a systematic integration of AIDS and cancer registration statistics provides additional information, of particular interest for histological classification, on the AIDS-cancer relationship.
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PMID:Linkage of death certification of AIDS and cancer registration in Vaud, Switzerland. 151 73

This prospective study was designed to determine the efficacy of iodized talc pleurodesis in patients with pleural effusions. Thirty-four patients underwent this treatment (three bilaterally) between October 1, 1989, and March 31, 1991. All patients had to have complete or nearly complete lung reexpansion after tube thoracostomy with fluid drainage less than 100 ml in 24 hours. A slurry containing 5 gm of talc and 3 gm of thymol iodide was instilled into the pleural space through the chest tube. Chest tubes were removed after complete reexpansion and clearing of the effusions, usually in 3 to 5 days. The patients' ages ranged from 26 to 88 years (average 50 years). Eighteen patients had lung carcinoma, two had mesothelioma, and one each had carcinoma of the ovary, breast, or anorectum, multiple myeloma, schwannoma, or Hodgkin's lymphoma. Two patients had an unknown adenocarcinoma primary and five other patients had acquired immunodeficiency syndrome. One patient had congestive heart failure. Nineteen patients had left, 12 had right, and three had bilateral pleural effusions. The effusion was serosanguineous in 26 and serofibrinous in eight patients. Serial chest radiography showed complete response in all patients. The period of follow-up ranged from 1 to 21 (average 4.9) months, with no recurrences. Twenty-three patients have died during the follow-up period, and there was no sign that reaccumulated pleural effusion existed in any, despite clinical evidence of systemic tumor progression. These observations indicate that intrapleural instillation of a slurry of iodized talc is a safe, adequate, and effective treatment for control of neoplastic or benign pleural effusions.
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PMID:Iodized talc pleurodesis for the treatment of pleural effusions. 156 70

Anemia, thrombocytopenia, and neutropenia have been observed in patients with acquired immune deficiency syndrome (AIDS) and AIDS-related complex. To investigate whether red cells (RBCs) of patients with human immunodeficiency virus infection were coated with IgG and/or complement (C3), blood samples of 239 patients were tested. The prevalence of a positive direct antiglobulin test on RBCs was 16.7 percent. By use of an enzyme-linked antiglobulin test (ELAT) to measure more accurately the number of IgG molecules per RBC in a group of 67 patients, 30 of the 67 individuals were observed to have increased numbers (mean, 155) compared to normal controls and to patients with hypergammaglobulinemia due to multiple myeloma or chronic liver disease. Hemoglobin level was correlated with the number of IgG molecules per RBC (p = 0.008), but no correlation could be demonstrated between those numbers and serum immunoglobulin (p = 0.10) or circulating immune complexes (p = 0.38). Our results with ELAT suggest that some AIDS patients may have specific binding of IgG on the surface of their RBCs, rather than nonspecific uptake; further clinical correlations are necessary to confirm these findings.
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PMID:Quantitation of red cell-bound IgG by an enzyme-linked antiglobulin test in human immunodeficiency virus-infected persons. 162 45

Epstein-Barr viral DNA (EBV DNA) has been detected in 20 to 58% of Hodgkin's disease tumors analyzed by Southern blotting or polymerase chain reaction (PCR). Because patients with Hodgkin's disease are generally immunodepressed, it is possible that the EBV is not directly involved in the pathogenesis of Hodgkin's disease but is merely detectable by molecular techniques because of reactivation of a latent infection. The purpose of this study was to determine if EBV DNA could be detected in an even higher percentage of cases of Hodgkin's disease, including acquired immunodeficiency syndrome (AIDS)-related Hodgkin's disease, by using newly designed, PCR amplification primers, and to compare the incidence of EBV DNA with the incidence of another common, latent virus (cytomegalovirus) in Hodgkin's disease tissue. The PCR was performed on DNA extracted from cells from 15 benign hyperplastic lymph nodes and from 15 cryopreserved cases of Hodgkin's disease, including 2 cases of AIDS-related Hodgkin's disease. For negative controls, PCR was also performed without template DNA and on genomic DNA from E. coli, calf thymus, a murine myeloma, and from a human cell line. After 32 cycles of amplification, a 225 base-pair amplification product comigrating with an EBV-positive control was detected in none of the negative controls but was present in 14 out of 15 cases (93%) of Hodgkin's disease, including both cases of AIDS-related Hodgkin's disease, and in 2 out of 15 cases of benign lymphoid hyperplasia. By contrast, cytomegalovirus DNA was undetectable by PCR in any of our specimens. We conclude that in our study set, the PCR procedure detected EBV-DNA but not cytomegalovirus DNA in a high percentage of cases of Hodgkin's disease, including two cases of AIDS-related Hodgkin's disease. These findings strengthen the hypothesis that EBV may be involved in the pathogenesis of Hodgkin's disease and AIDS-related Hodgkin's disease.
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PMID:Frequent detection of Epstein-Barr viral deoxyribonucleic acid and absence of cytomegalovirus deoxyribonucleic acid in Hodgkin's disease and acquired immunodeficiency syndrome-related Hodgkin's disease. 166 51

Interferons are currently the most widely used biological response modifiers. They are of high clinical value in haematological malignancies (chronic myelogenous leukaemia, multiple myeloma, non-Hodgkin lymphoma), in solid tumours (malignant melanoma, hypernephroma, pancreas neoplasms, carcinoid tumours, Kaposi's sarcoma, glioma, in ovarium, cervix and bladder carcinoma, and in basalioma) and in infectious diseases (chronic hepatitis B, chronic non-A/non-B hepatitis, chronic delta hepatitis, AIDS, Papova virus and Rhinovirus infections, leishmaniasis, leprosy) and some other conditions. Although the mechanism of action of interferons has not been explained in every detail these agents are promising therapeutic means in a number of diseases.
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PMID:Role of interferon in clinical practice. 172 32

This paper aims to summarize current experience with alpha interferon and provide direction for future study. There are four areas in which alpha interferon has proven or potential activity: antiviral, premalignant, adjuvant and advanced disease settings. The three main viral diseases in which interferon alfa-2b has been shown to have activity are chronic viral hepatitis, acquired immunodeficiency syndrome, and human papilloma virus infections. In vitro studies suggest that alpha interferon may inhibit transformation of some premalignant conditions into malignant disease; e.g., vaginal intraepithelial neoplasia. In the adjuvant setting, it is possible that a biological response modifier, such as alpha interferon, may have a role in helping the immune system to destroy residual tumour cells following tumour bulk reduction with radiation or chemotherapy. A higher response rate has been seen in patients with small tumour bulk compared to those with large tumour bulk (e.g., malignant melanoma, ovarian carcinoma), and in patients with early, rather than late, disease (e.g., chronic myelogenous leukaemia, hairy cell leukaemia, multiple myeloma, non-Hodgkin's lymphoma). This may be due to efficacy in a small tumour bulk setting or due to an immunoadjuvant role. In advanced disease, the question is how best to exploit the possible synergistic effects between alpha interferon and other therapeutic modalities. The optimum dose, schedule and patient populations for combined treatment have yet to be determined. The major objective of this paper is to determine how best to capitalize upon the current state of knowledge to build for future trials of alpha interferon, and to determine whether the existing data suggest an adjuvant role for interferon after initial tumour regression.
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PMID:alpha Interferon: the potential drug of adjuvant therapy: past achievements and future challenges. 179 68

A cohort of 115 asymptomatic gay men, all seropositive for HIV, was recruited in a health screening project in Stockholm, Sweden, between Nov. 1982 and Dec. 1983 and subsequently followed and clinically evaluated after a mean observation time of 63 months. AIDS in accordance with the surveillance definition (CDC group IV C-1 and D) developed in 34 (29.6%) of the men, while 1 (0.9%) additional man died of multiple myeloma classified as CDC group IV E. Constitutional symptoms (CDC group IV A) developed in 13 (11.3%) men, while symptoms from the central nervous system classified as CDC group IV B occurred in 1 (0.9%) additional man. Minor opportunistic infections included in the definition for CDC group IV C-2 developed in 12 (10.4%) men, while 48 (41.7%) men remained asymptomatic, with or without persistent generalized lymphadenopathy (PGL). One man who died of AIDS had been treated for malignant melanoma (MM) and one who did not fulfill the criteria for CDC group IV died of MM during the observation period. The 5-year actuarial progression rate to surveillance defined AIDS was 31.5% and to CDC group IV 53.6%. No statistically significant association was found between disease progression and a number of recorded epidemiological variables, most previous and present sexually transmitted diseases (STD) (except gonorrhoea) and the presence of PGL at entry. On the other hand, reduced delayed cutaneous hypersensitivity, in particular to tuberculin, as well as the presence of a high IgG titer against cytomegalovirus (CMV), were correlated to disease progression.
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PMID:A prospective study of 115 initially asymptomatic HIV infected gay men in Stockholm, Sweden. 195 28

Pneumocystis carinii pneumonia complicated the course of two patients with multiple myeloma. The diagnosis was established in both cases by bronchoalveolar lavage, which demonstrated the typical pneumocysts. Clinical and roentgenographic improvement in both patients was observed following a course of trimethoprim-sulfamethoxazole. One patient had lymphocyte subsets performed with a CD4/CD8 ratio of 0.8; both patients were HIV antibody-negative by ELISA. Both patients tolerated prophylactic TMP-SMX given concurrently with the subsequent chemotherapy for myeloma. We suggest that the immune defect seen in multiple myeloma may have placed these patients at risk for opportunistic infections such as P carinii pneumonia; however, as opposed to patients with AIDS, our patients tolerated therapy with TMP-SMZ quite well.
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PMID:Pneumocystis carinii pneumonia complicating multiple myeloma. 199 21

Humoral immunity involves molecules in solution in biological fluids including effectors of non specific immunity (e.g. complement, cytokines) and specific immunity (antibodies) as well. Acquired humoral immunodeficiences are often multifactorial in origin and associated with defects of cell-mediated immunity. The most common etiologies are those of iatrogenic immunodeficiencies: surgery (especially splenectomy), radiotherapy, chemotherapy of leukemia and cancer, immunosuppressive treatments in organ transplanted patients. Protein-caloric malnutrition also induces cellular and humoral immunodeficiencies. Among other causes, three types of diseases may induce defective antibody production: 1/B cell neoplasias (e.g. multiple myeloma, chronic lymphocytic leukemia...) 2/renal diseases (nephrotic syndrome, renal insufficiency) and 3/various infectious diseases, including AIDS. Some principles of prevention and treatment of secondary humoral immunodeficiencies are given.
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PMID:[Secondary deficiencies of humoral immunity]. 204 15


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