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)

BALB/c mice were hyperimmunized with ACHN (ATCC CRL 1611, American Type Culture Collection, Rockville, Maryland), a stable in vitro cell line derived from a malignant pleural effusion in a 22-year-old man with renal cell carcinoma. The hyperimmune spleen cells were fused with NS-1 murine myeloma cells using polyethylene glycol. Hybridoma supernatants were screened for the presence of IgG reactive with detergent extracts of ACHN and nonreactive with detergent extracts of normal kidney tissue. A stable, rapidly growing clone named 5F4 was isolated. Supernatant from 5F4 was used as a primary antibody preparation for avidin-biotin complex immunoperoxidase staining of multiple cases of renal cell carcinoma, normal tissues, and other tumors. 5F4 produced IgG which reacted with a cytoplasmic structure in paraffin-embedded sections of all renal cell carcinomas tested. There was occasional, weak, granular, cytoplasmic staining of isolated tubular lining cells in adjacent normal kidney.
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PMID:A renal cell carcinoma neoplastic antigen detectable by immunohistochemistry is defined by a murine monoclonal antibody. 355

In patients with advanced multiple myeloma (MM) there is an excess of production of interleukin-6 (IL-6) in vivo, and elevated serum levels are associated with plasmablastic proliferative activity and short survival. These data prompted us to perform a clinical trial with a murine anti-IL-6 monoclonal antibody (MoAb) to neutralize the excess of this putatively deleterious factor in these patients. Ten MM patients with extramedullary involvement frequently were treated with anti-IL-6 MoAb. The MoAb was administered intravenously to 9 patients; 1 patient with malignant pleural effusion received intrapleural therapy. Of the 3 patients who succumbed to progressive MM after less than 1 week of treatment (including the only 1 treated locally), 2 with evaluable data exhibited marked inhibition of plasmablastic proliferation. Among the 7 patients remaining more homogeneous receiving the anti-IL-6 MoAb for more than 1 week, 3 had objective antiproliferative effect marked by a significant reduction of the myeloma cell labelling index within the bone marrow. One of these 3 patients achieved a 30% regression of tumor mass. However, none of the patients studied achieved remission or improved outcome as judged by standard clinical criteria. Of major interest, objective antiproliferative effects were associated with complete inhibition of C-reactive protein (CRP) synthesis and low daily IL-6 production in vivo. On the other hand, the lack of effect in 4 patients was associated with a higher IL-6 production and inability of the MoAb to neutralize it. Anti-IL-6 was also associated with resolution of low-grade fever in all the patients and with worsening thrombocytopenia and mild neutropenia. The generation of human antibodies to Fc fragment of the murine anti-IL-6 MoAb observed in 1 patient was associated with dramatic progression. These data show that anti-IL-6 MoAb can suppress the proliferation of myeloma cells and underscore the biologic role of IL-6 for myeloma growth in vivo. Furthermore, suppression of CRP and worsening of neutropenia/thrombocytopenia both indicate that IL-6 is critically involved in acute-phase responses and granulopoiesis/thrombopoiesis.
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PMID:Biologic effects of anti-interleukin-6 murine monoclonal antibody in advanced multiple myeloma. 760 99

A 77-year-old woman with hypertension was admitted to our hospital because of exertional dyspnea end peripheral edema. Chest X-ray showed cardiomegaly, pulmonary congestion and right pleural effusion. Hypertensive heart failure was diagnosed and treated, and right pleural effusion disappeared in 2 weeks. Abnormalities on laboratory data, i.e. anemia and increased ESR et al. continued after the improvement of heart failure. Serum IgG was elevated (2570 mg/dl), while IgA and IgM were decreased. Immunoelectrophoresis indicated the presence of monoclonal IgG-lambda in the serum. Bone marrow puncture revealed an increase in atypical plasma cells (38.4%). Multiple myeloma was diagnosed from these findings and treated with melphalan and prednisolone. But increases in atypical plasma cells (43.2%) and serum IgG (2573 mg/dl) continued. During treatment, right pleural effusion increased again. Thoracocentesis showed bloody effusion with numerous atypical plasma cells, and the presence of monoclonal IgG-lambda was indicated by immunoelectrophoresis. The patient died of renal and heart failure 2 months after the onset of malignant pleural effusion. Cytological examination and immunoelectrophoresis are necessary for pleural effusion in multiple myeloma.
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PMID:[A case of multiple myeloma associated with abnormal plasma cells and M-protein in pleural effusion]. 864 97

A 53-year-old woman was admitted to this institution with chest pain and dyspnea. Chest roentgenogram showed pleural effusion and multiple tumor shadows, bilaterally which represented extrapleural signs. Numerous atypical plasma cells were found in the pleural effusion. Bone marrow biopsy showed atypical plasma cells. Immunoelectrophoresis revealed monoclonal Bence-Jones protein-lambda in serum and urine. Myeloma was subsequently diagnosed and chemotherapy was started. Multiple myeloma is a plasmacytoma, and myeloma cells proliferate in the bone marrow. The incidence of myeloma associated with malignant pleural effusion is rare with only 33 cases previously reported in Japan, to the best of our knowledge.
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PMID:[A case of Bence-Jones protein-lambda positive multiple myeloma complicated by abnormal plasma cells in pleural effusion]. 961 46

We describe a patient with multiple myeloma which presented as a thoracic paraspinal tumor and myelomatous pleural effusion. He had manifested a gradual onset of upper back pain with radiation to the left chest wall for 3 months. A radiographic examination showed left pleural effusion and a paraspinal tumor with rib destruction at the--left T5-6 level. Laboratory data showed anemia and a reversed serum albumin to globulin ratio. Protein electrophoresis and immunoelectrophoresis showed a monoclonal IgG-lambda chain component in the serum, urine, and pleural effusion fluid. Ultrasound-guided transthoracic mass biopsy and thoracentesis were performed for diagnosis. Biopsy of the thoracic tumor showed a solid mass composed of immature plasma cells. The pleural effusion fluid contained numerous immature plasma cells. An immunophenotype study of the pleural effusion fluid revealed monoclonal plasma cells, compatible with malignant pleural effusion. A specimen of bone marrow was interpreted as typical for plasma cell myeloma. Local radiotherapy and chemotherapy with melphalan and prednisolone resulted in good partial remission with a stable condition. Later, however, the disease flared up and hyperviscosity syndrome developed with epistaxis and retinal hemorrhage. He died of sepsis about 15 months after the initial diagnosis.
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PMID:Multiple myeloma presenting with a paraspinal tumor and malignant effusion: case report. 1049 38

Malignant pleural effusion (MPE) in multiple myeloma (MM) is rare. Approximately 80 cases have been reported. To delineate optimal treatment and prognostic variables in these patients, we reviewed 11 MM patients with MPE. MPE developed at median of 12 months from diagnosis of MM. All the patients had high-risk disease based on complex karyotypic abnormalities including deletions of chromosome-13 (n=9), elevated beta-2 microglobulin (B2M) (n=9), high C-reactive protein (CRP) (n=8), high plasma cell labeling index (n=5) or high LDH (n=5). A significant increase in B2M, LDH, and CRP was observed at the onset of MPE. The initial diagnosis of MPE was based on positive cytology (n=9), pleural fluid cIg/DNA (n=9) or pleural fluid cytogenetics (n=4). Pleural tissue infiltration was found on pleural biopsy and autopsy in one patient each. Systemic chemotherapy comprising dexamethasone, cyclophosphamide, etoposide and cisplatin (DCEP) (n=7) and pleurodesis (n=7) were effective in resolving MPE but survival was short. High dose chemotherapy with peripheral blood stem cell support for MPE in six patients conferred no clear survival advantage. These patients died at median of four months from onset of MPE. Patients with bone marrow complex karyotypic abnormalities including deletion-13 (n=9) had a shorter (median--18 months) overall survival compared to patients with normal cytogenetics (median--38 months). MPE in patients with MM is often associated with high-risk disease including deletion 13 chromosomal abnormality and heralds a poor prognosis despite aggressive local and systemic treatment.
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PMID:Malignant pleural effusion of multiple myeloma: prognostic factors and outcome. 1608 53

Malignant pleural effusion in myeloma is a rare terminal event with 91 cases reported so far. Majority of the patients survive less than 4 months. We are presenting a short series of four such cases, who had a good clinical response to combination chemotherapy.
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PMID:Malignant myelomatous pleural effusion with good response to combination chemotherapy. 1801 5

Plasma cell leucaemia (PCL) is a rare aggressive form of multiple myeloma. It occasionally involves the pleura, causing malignant pleural effusion (MPE). MPE presents a management dilemma for physicians, given the different treatment options available with varying efficacy and side effects. We report a case of a 64-year-old man with MPE due to PCL, successfully managed with intrapleural cisplatin and a tunnelled pleural catheter. We believe this to be the first report of management of PCL-associated MPE with intrapleural cisplatin.
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PMID:Intrapleural cisplatin for management of malignant pleural effusion in a patient with plasma cell leucaemia. 2612 65

Malignant pleural effusion in myeloma (MMPE) is a rare terminal event; with a median survival is four months. All the patients usually have multiple poor prognostic factors and none of them (like beta 2-microglobulin, karyotype, Stage of disease, C-reactive protein etc.) correctly predicts the survival. We are reporting a series of five cases and evaluated the factors influencing the overall survival. All of our patients had a very good response to treatment and had a better survival compared to the reported cases so far. After reviewing the literature carefully we found that timing of development of pleural effusion is probably the most important prognostic factor. Those who develop effusion after some time lag form the initial treatment, will have a poor survival (median four months) compared to those who had effusion at the start of the disease.
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PMID:Malignant myelomatous pleural effusion-Is onset of effusion a new prognostic factor? 2726 59