Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Multiple myeloma was diagnosed in a horse on the basis of clinical signs, protein electrophoresis pattern, Bence-Jones proteinuria, and radiographic changes in bone. The horse had mild depression, weight loss, edema of the distal portion of the left hind limb, anemia, hyperproteinemia, and monoclonal gammopathy in the beta 2 region. Radiographically, punctate cortical lysis of bone was seen. Specific treatment for the multiple myeloma was not attempted and the horse was euthanatized.
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PMID:Multiple myeloma in a horse. 365

Sixty-four persons with M-components in serum were detected in a health survey of 6995 subjects in 1964. After 20 years, data could be obtained on all 64. The 45 who had died included two cases of myeloma and one of malignant lymphoma. One of the myeloma cases had started as chronic lymphatic leukemia. Three of the 19 persons alive had an increase in the size of the M-component and depression of the background immunoglobulin, but they could not be diagnosed as myeloma cases. One had a rather large but not increasing M-component and an excess of light chains. She could be a third case of myeloma in this series.
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PMID:A 20-year follow-up study of 64 subjects with M-components. 373 56

The effects of 14AC1 monoclonal antibody (McAb) on 79FR-G-41 rat glioma cells in vitro, on the formation of metastases in lung by antibody coated glioma cells, and on the growth of glioma grafts in BALB/c-nu/nu mice were investigated. The 14AC1 antibodies - isotyped as IgG2a - were obtained from a hybridoma clone established after fusion of X63-Ag8.653 myeloma cells and spleen cells of BALB/c mice hyperimmunized with 79FR-G-41 glioma cells. Antibody treatment of glioma cells in vitro caused evident cell surface alterations and pronounced growth depression of most cells. However, a few tumor cells remained unchanged in morphology and continued to proliferate. Moreover, 14AC1 antibodies drastically reduced lung metastasis by pretreated and i.v. delivered glioma cells. Additionally, 14AC1 antibodies suppressed the growth of transplanted rat gliomas in nude mice as evidenced by a longer latency period and a smaller volume of glioma grafts in treated than in control tumor bearers. Nevertheless, glioma grafts showed accelerated growth after termination of antibody treatment. Further experimental investigation is required in order to identify the precise mechanisms of the effects of McAbs on tumor cells in vitro and in vivo.
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PMID:Growth inhibition of experimental glioma grafts by monoclonal antibody treatment. 377 19

Demethoxydaunorubicin (DMDR), a new anthracycline available both for intravenous and oral administration, was given in 14 cases of leukaemia, non-Hodgkin's lymphoma (NHL) and multiple myeloma (MM) replacing either daunorubicin (DNR) or doxorubicin (DOX) in conventional chemotherapy regimes. In acute leukaemia (6 myeloblastic and 1 common lymphoblastic) there were 5 complete (CR) and 2 partial (PR) remissions; one patient, previously brought into remission with a regime including i.v. DMDR was thereafter maintained in CR with oral DMDR. Among the patients treated with the oral DMDR, 2 NHL cases were treated; 1 patient had a sustained remission of 12 months so far, with DMDR alone; another patient had a CR with a combined regime. In MM, one patient with very advanced disease treated with i.v. DMDR/CHOP did not respond, but three cases treated with oral DMDR plus other drugs showed a partial remission. Toxic effects were limited to brief episodes of nausea and vomiting in a few i.v. treated patients; a prolonged bone marrow depression was observed in one case only. No cardiotoxic effect was recorded.
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PMID:Intravenous and oral demethoxydaunorubicin (NSC 256-439) in the treatment of acute leukemia and lymphoma: a pilot study. 385 41

The present report gives information both on the clinical features at presentation and the clinical course of 7 consecutive patients with nonsecretory multiple myeloma. It provides evidence that the nonsecretory variant was closely associated with high tumor cell mass, as determined by severe anemia and/or multiple areas of bone destruction. The marked depression of normal immunoglobulins and the absence of both renal failure and hypercalcemia differentiated nonsecretory from typical myelomatosis. Finally, the survival length of patients with nonsecretory myeloma appeared to be similar to that of comparably staged patients with secretory myeloma.
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PMID:Nonsecretory multiple myeloma. Presenting findings, clinical course and prognosis. 393 4

Today there seems to be sufficient data to incriminate benzene as a potent carcinogenic agent causing leukemia, malignant lymphoma, multiple myeloma and lung cancer, as well as numerous disorders of the bone marrow depression. Other factors (such as genetic and individual susceptibility) may have a role in the development of these different types of malignancies and hematologic disorders. In this paper, data concerning all these problems are presented and discussed.
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PMID:Benzene as a leukemogenic and carcinogenic agent. 402 42

Serum angiotensin-converting enzyme (SACE) was analysed in 27 patients with Hodgkin's disease, 25 with non-Hodgkin lymphoma, 14 with acute leukaemia, 15 with chronic leukaemia, and 15 with multiple myeloma. SACE was depressed in these patients as a whole, with a mean level of 19.9 mu/ml, compared with 116 healthy controls (mean 24.4 mu/ml, P < 0.001). This depression was greatest in chronic leukaemia and multiple myeloma. In Hodgkin's disease no relationship was found between enzyme activity and stage, activity, histopathology, treatment, mediastinal involvement or prognosis. In non-Hodgkin patients a poor prognosis was generally associated with low SACE activity. The low SACE activity was not related to recent corticosteroid treatment, and the cause and pathophysiological significance is unexplained. Since SACE is high in the granulomatous disorder sarcoidosis (which can mimic malignant lymphnode and blood diseases) SACE analysis can be valuable in evaluating patients with mediastinal lymphadenopathy and those in whom non-caseating epitheliod granulomas are found.
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PMID:Serum angiotensin-converting enzyme in malignant lymphomas, leukaemia and multiple myeloma. 625 27

A total of 117 cases with hematological malignancies were treated with MCNU at doses of 70-100 mg/m2. Following are the results obtained. 1. MCNU showed a marked depression of cells in the cases with CML, polycythemia vera and thrombocythemia. The low level of cells was maintained for 2 to 7 months. 2. A good response was observed in several cases with blastic crises of CML. 3. No response was observed in two cases with acute leukemia. 4. Although a fair response was observed in several cases with malignant lymphoma or multiple myeloma, moderate bone marrow suppression was observed in a majority of the cases.
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PMID:[Phase II study with methyl-6[[[2-chloroethyl) nitrosoamino] carbonyl] amino]-6-deoxy-alpha-D-glucopyranoside (MCNU) in hematological malignancies]. 634 81

The 2-cyanaziridin derivative, azimexon (E), has previously been shown to have certain immunomodulatory properties. In particular, the induction of leukocytosis, the stimulation of delayed-type hypersensitivity reactions and the synergistic effect of azimexon and antibiotics in the control of lethal bacterial and fungal infections in mice prompted us to test azimexon as an adjuvant to chemotherapy in 14 myeloma patients. In a randomized double-blind cross-over study 3 X 600 mg of azimexon were added to one of two consecutive, identical chemotherapy courses consisting of melphalan/prednisone (MP) or vincristine/cyclophosphamide/melphalan/prednisone (VCMP). Chemotherapy was given during days 1-4 and azimexon or placebo were added on days 6, 10 and 14. Blood counts and natural killer (NK) cell testing were performed on days 0 and 21 of each course. With the exception of a transient taste irritation in two patients, azimexon caused no subjective side-effects. White blood cell counts were not altered by the drug; red blood cells and hemoglobin showed a borderline depression after azimexon. NK activities measured against three target cell lines (K562, IGR3, L1210) tended to increase after azimexon treatment. When added in vitro to NK assays azimexon caused a slight increase of NK activity at concentrations of 0.01-0.25 mu/ml, whereas concentrations above 1 microgram/ml were inhibitory. The increase of NK activity by azimexon was not due to the induction of interferon in the effector lymphocyte population.
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PMID:The effect of BM 12.531 (azimexon) on natural killer cell activity in myeloma patients. 636 46

In vitro and in vivo studies utilizing a combination of leukocyte interferon-alpha (IFN) and chlorambucil (CLB) were done to investigate possible synergism between a biological response modifier and a chemotherapy drug. In vitro studies utilized a human myeloid leukemia cell line (K-562) pretreated with IFN and then exposed to CLB. The combination resulted in significant depression of cell growth compared with use of IFN or CLB alone. In vivo studies involved eight heavily pretreated patients given 6 million units IFN for 5 days followed by oral CLB (16 mg/m2) for 5 days repeated every 4 weeks. Three myeloma patients had reduction in immunoglobulins and experienced clinical responses. Three of four patients with Hodgkin's disease responded after relatively short periods of treatment. One patient with a diffuse lymphocytic lymphoma had a complete unmaintained remission lasting 6 months. Toxicity was minimal, with mild fever, nausea, and vomiting. These preliminary studies suggest that IFN may be a biological response modifier when used in combination with a cytotoxic agent.
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PMID:Leukocyte interferon as a possible biological response modifier in lymphoproliferative disorders resistant to standard therapy. 651 61


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