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)

Ten cases of multiple myeloma seen in PUMC hospital survived more than six years. 4 of them survived more than ten years. 6 patients were of IgA type. Features of those cases included: (1) symptoms mild; (2) incidence of anemia low; (3) percentage of tumor cell in bone marrow also relatively low; (4) blood urea nitrogen, creatinine and calcium normal; (5) maintenance therapy rather long. The prognostic factors and the current general situation of treatment were briefly discussed.
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PMID:[Report of 10 cases of multiple myeloma surviving more than 6 years]. 181 84

Out of 436 studied patients with plasmocytic myeloma 67 (15.0%) survived over 5 years from the beginning of antineoplastic treatment, and 18 survived over 10 years from the first symptom of the proliferative process. The patients with long survival were younger at the time of diagnosis than the whole studied group and had normal creatinine and calcium levels in the serum. Nearly half these patients had I or II stage of clinical progression and IgG monoclonal protein. Treatment with melphalan only was given to 17 patients, 33 were treated with melphalan, followed by vincristine, cyclophosphamide, BCNU, prednisone and doxorubicin. Polychemotherapy was given from the time of the diagnosis to 13 patients, and 4 received radiotherapy or 60Co irradiation besides chemotherapy. In 81% of the analysed cases a good response was obtained. Thirteen patients are alive. In 5 cases myeloid leukaemia, in 1 case bronchogenic carcinoma and in 1 case liver carcinoma were the causes of death.
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PMID:[Clinical and laboratory analysis of the cases of multiple myeloma with over 5-year survival time from the beginning of the antineoplastic treatment]. 182 66

28 patients with progressing painful bone metastases (18 breast cancer, 9 myeloma and 1 low grade lymphoma) received pamidronate 60 mg by 24 h continuous infusion for at least 2 courses (range 2-12). In patients urinary calcium and hydroxyproline excretion significantly decreased in relation to diminution of bone resorption. 9 of 18 breast cancer patients and 8 of 9 evaluable patients with myeloma had symptomatic improvement. Sclerotic areas of previously lytic lesions appeared in 8 breast cancer patients and in 1 myeloma patient. Transient fever developed in 1 patient and local phlebitis in 2. Among the 28 patients, 15 did not receive any anticancer treatment or have any change of the anticancer therapy during pamidronate administration. Of 7 with breast cancer, 4 had an improvement of symptoms and 4 sclerosis on radiographs. Impressive control of symptoms was the major feature of 8 myeloma patients, but only 1 had radiographic sclerosis.
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PMID:Treatment of bone metastases from breast cancer and myeloma with pamidronate. 182 38

Bone metastases secondary to myeloma, are characterized by severe bone pain, pathological fractures, hypercalcaemia and hypercalciuria. Histological and biochemical investigations have shown a wide spectrum of abnormalities in bone turnover in patients with multiple myeloma. The increased osteoclast activity caused by various osteoclast activating factors secreted by myeloma cells, is responsible for the diffuse localized osteolytic lesions. These lesions are responsible for the symptoms and respond poorly to standard chemotherapy, justifying the use of a bone-sparing agent. Clodronate is a potent inhibitor of osteoclast activity and does not impair bone mineralization. Several studies have shown that clodronate can normalize serum calcium in hypercalcaemic patients with metastatic bone disease, and a similar response is seen in multiple myeloma. In a long-term (18 months) placebo-controlled study we have shown that clodronate, given orally at a daily dose of 1.6g, can decrease both the incidence of pathological fractures and the activity of osteoclasts, as judged by measurements in iliac crest biopsy. These results, along with those from two other studies, are promising and suggest that clodronate may inhibit the progression of osteolytic lesions in multiple myeloma.
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PMID:The use of clodronate in multiple myeloma. 183 98

Total serum calcium concentration was raised in a 63-year-old lady with multiple myeloma and markedly elevated serum IgA kappa-paraprotein concentration. Symptoms of hypercalcaemia were absent, and serum ionized calcium was normal, suggesting calcium binding by the abnormal protein. This was demonstrated directly after isolation of the paraprotein and characterization of the calcium/protein interaction. After reduction of the paraprotein with mercaptoethanol, sodium dodecyl sulphate polyacrylamide gradient gel electrophoresis revealed two bands corresponding to light and heavy chains, but under non-reducing conditions the isolated paraprotein migrated in a series of bands, possibly representing polymeric forms of the basic immunoglobulin moiety.
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PMID:Hypercalcaemia due to calcium binding by a polymeric IgA kappa-paraprotein. 187 67

Hyperphosphatemia (HP) is usually seen in patients with hypoparathyroidism, renal failure, and tumor lysis. The authors described a patient with HP due to a phosphate-binding immunoglobulin (Ig). An 86-year-old woman had serum phosphate levels as high as 4.75 mmol/l, (normal, 0.77 to 1.45 mmol/l). Serum ionized calcium, blood urea nitrogen (BUN), creatinine, and N-terminal parathyroid hormone (PTH) levels were normal, but serum 1,25-dihydroxyvitamin D level was subnormal at less than 12 pmol/l (normal, 36 to 146 pmol/l). Serum total protein was elevated at 105 g/l (normal, 60 to 80 g/l), and additional studies confirmed a diagnosis of immunoglobulin G (IgG) multiple myeloma. Results of in vitro studies using anti-human IgG antibodies showed that the IgG of the patient bound inorganic phosphate. Several isolated case reports have documented spurious HP due to interference of the paraprotein in the routine serum phosphate assay. In only one patient, however, has actual binding of phosphate to a myeloma protein been documented. The studies of the authors document phosphate binding by an IgG paraprotein and suggest that in this setting HP may be of physiologic significance as evidenced by depressed serum levels of 1,25-dihydroxyvitamin D.
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PMID:Hyperphosphatemia in multiple myeloma due to a phosphate-binding immunoglobulin. 191 79

In a group of 136 completely followed up patients with multiple myeloma, the prognostic significance of the immunological myeloma types, of 20 different single prognostic factors, of 15 clinical staging systems, and of 6 morphological classifications was retrospectively investigated by means of the calculation of mean survivals, survival curves, and responses to chemotherapy. A univariate analysis was employed in order to correlate each prognostic parameter at presentation with the survival in the whole group; a multivariate analysis according to the Cox's hazards regression model was used in order to select the most powerful prognostic variables. The patients were grouped according to the myeloma immunological types, to the mean value of each single prognostic factor, and to each stage of the clinical and morphological systems. Causes of death were also related to immunological multiple myeloma types. All single variables, except age and serum calcium, presented a significant relationship with the survival, even if at different significance levels. Cox's regression model selected among them, serum levels of beta 2-microglobulin, percentage of bone marrow plasma cells, hemoglobinemia, lytic bone lesions, and Bence-Jones proteinuria as the most significant factors related to survival. Each clinical and morphological staging system divided groups of patients with significant differences in mean survivals, or in survival curves, or in response to therapy. Multiple myeloma type IgA and micromolecular, with Bence-Jones proteinuria, and type lambda were associated with a poor prognosis, with low therapeutical response, and with the development of fatal renal failure. All these parameters, together with new prognostic factors, are useful in the prognostic evaluation, and, when applied in different steps of the diagnosis and the therapy, allow of studying the clinical course of multiple myeloma under different perspectives, in order to have a more complete picture of the disease and of the single patient.
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PMID:Classification and prognostic evaluation in multiple myeloma. A retrospective study of relationship of survivals and responses to chemotherapy to immunological types, 20 single prognostic factors, 15 clinical staging systems, and 6 morphological classifications. 192 60

Actinobacillus actinomycetemcomitans produces a cytolytic peptide leukotoxin which kills susceptible target cells, including human neutrophils, monocytes, lymphocytes, and HL-60 promyelocytic leukemia cells. Cell death occurs as a consequence of colloid osmotic lysis. In the present investigation early leukotoxin-induced changes in membrane permeability were studied by flow cytometry and quantitative spectrofluorimetry in leukotoxin-susceptible and resistant targets. Within 5 s toxin-susceptible cells exhibited concentration-dependent, sustained increases in systolic free Ca2+, and this was rapidly followed by a progressive fall in membrane potential. These early manifestations of membrane injury occurred approximately 10-15 min before cell death, as reflected by flow cytometric analysis of propidium iodide stained cells. The rise in cytosolic Ca2+ was almost entirely due to an influx of extracellular Ca2+. The results of Hill plots for the action of leukotoxin on Ca2+ permeability in human neutrophils or HL-60 cells suggested that two or more toxin molecules participate in the assembly of an ion conducting pore in the plasma membrane. Changes in membrane permeability or cell viability were not observed in response to heat-inactivated toxin. Under appropriate conditions toxin-induced membrane abnormalities were inhibited by leukotoxin-neutralizing mAb or relatively high concentrations (greater than or equal to 2.5 mM) of extracellular Ca2+. Leukotoxin-resistant target cells showed no evidence of membrane injury even when exposed to high concentrations of leukotoxin for prolonged periods of time. These included resistant human K562 erythroleukemia cells and murine SP2 myeloma cells which have previously been shown to adsorb the toxin, suggesting that they possess a protective mechanism(s) which impedes toxin insertion or assembly in the lipid bilayer. These data support the concept that A. actinomycetemcomitans leukotoxin acts as a cell-specific, pore-forming protein which permeabilizes the plasma membrane of susceptible target cells.
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PMID:Early changes in cytosolic calcium and membrane potential induced by Actinobacillus actinomycetemcomitans leukotoxin in susceptible and resistant target cells. 194 Mar 58

The syndrome of osteolytic lesions and hypercalcemia is commonly associated with well-differentiated B-cell neoplasms, such as multiple myeloma. The association of this syndrome with high-grade non-Hodgkin's lymphoma is rare. We have described a 20-year-old man with a non-T-cell lymphoblastic lymphoma manifested by extensive osteolytic lesions and hypercalcemia (serum calcium value of 13.5 mg/dL), without lymphadenopathy.
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PMID:Non-T-cell lymphoblastic lymphoma with extensive osteolytic lesions and hypercalcemia. 194 37

A mAb, 10D1, was obtained by fusing spleen cells from BALB/c mice immunized with a CD3/TCR- human T cell line, P12/ichikawa, to mouse myeloma cells, P3X63-Ag8-653. 10D1 mAb is specific for T cells in that it reacted with all the T cell lines tested, but not with B or myeloid cell lines. A small fraction of normal peripheral blood T cells, preferentially CD4+, was also reactive with 10D1 mAb. Biochemical studies revealed that 10D1 mAb recognizes a disulfide-linked homodimeric molecule composed of 90-kDa polypeptide. 10D1 mAb induced a substantial proliferation of peripheral blood T cells when cross-linked with goat anti-mouse Ig antibody. The elimination of CD4+ cells totally abrogated the proliferative response induced by 10D1 mAb, whereas the elimination of CD8+ cells rather enhanced it. The proliferative response of peripheral blood T cells induced by 10D1 mAb was almost completely inhibited after modulation of the CD3/TCR complex with anti-CD3 mAb. In addition, a prompt increase in intracellular [Ca2+] was observed in a CD3+ T cell line, Jurkat but not in its surface CD3- mutant when 10D1 mAb was added. These results indicate that the 10D1 molecule is involved in a novel pathway of human CD4+ T cell activation, which is associated with the CD3/TCR-mediated pathway.
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PMID:A novel homodimeric molecule involved in human T cell activation. 196 74


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