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)

When human myeloma cells are pulsed for one hour with 3H-uridine and chased for six hours in fresh medium containing unlabeled uridine, the processing of 45 S rRNA precursor into the stable 28 S and 18 S rRNA components can be followed. However, when the cells are chased in exogenous adenosine instead of uridine, the accumulation of 18 S rRNA is selectively inhibited. Cells pulsed with 3H-adenosine and chased in the absence of exogenous nucleosides exhibit normal rRNA precursor processing, while cells pulsed simultaneously with 3H-uridine and 3H-adenosine and chased with uridine and adenosine are deficient in labeled 18 S rRNA. Consequently, the inhibition of 18 S rRNA accumulation by adenosine is not an artifact of labeling nor is it relieved by an equal molar concentration of uridine. The wasting of 18 S rRNA in human myeloma cells is similar to that reported to occur in normal lymphocytes during the quiescent state.
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PMID:Wasting of 18 S ribosomal RNA by human myeloma cells cultured in adenosine. 127 May 22

A 66-year-old man with kappa-light chain multiple myeloma had adult Fanconi syndrome. Renal tubular transport abnormalities consisted of renal tubular acidosis, renal glycosuria, aminoaciduria, phosphaturia and renal hypouricemia. After therapy for multiple myeloma, urinary Bence Jones protein became undetectable, and all these renal tubular abnormalities except urate wasting were corrected. Histological examination revealed electron-dense tubular and rod-like deposits in proximal tubular epithelium. This clinical observation suggests that the renal tubular transport defects were secondary to the myeloma process, possibly due to Bence Jones proteinuria.
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PMID:Adult Fanconi syndrome secondary to kappa-light chain myeloma: improvement of tubular functions after treatment for myeloma. 211 47

A disease in mink has been discovered that has many of the features of collagen diseases in man. Affected animals suffer from wasting with leukopenia and thrombocytopenia as well as plasma cell infiltration, hypergammaglobulinemia, glomerulonephritis, arteritis and amyloidosis. Cell-free filtrates and ultracentrifugates from diseased animals induced the disease in normal mink, and aleutian genotypes were unusually susceptible to infection. This genotype was characterized by abnormal lysosomal structures in all the granule-forming cells, resembling the Chediak-Higashi syndrome of man. Anti-gamma-globulin factors similar to human rheumatoid factors were reported, although tests for antibodies such as ANF and LE factors have been negative. Arteritis and glomerulonephritis lesions stained positively for gamma-globulin, and Coombs-type sensitized red cells have been detected in the majority of affected mink. Some mink develop a monodispersion of hypergammaglobulinemia resembling the serum protein changes in human myeloma. These studies highlight genetic, immunological and microbiological causative factors in a mink disorder resembling human collagen disease.
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PMID:Viral plasmacytosis (Aleutian disease) of mink resembling human collagen disease. 533 35

We describe the development of severe hypophosphatemia and urinary phosphate wasting in two patients with multiple myeloma. In both cases, the serum phosphorus was repeatedly less than 1.0 mg/dL despite vigorous replacement, and the calculated fractional excretion of urinary phosphorus was greater than 100%. Neither patient demonstrated other tubular defects typical of Fanconi's syndrome. With treatment of the myeloma, both patients achieved normalization of the serum phosphorus and no longer required phosphorus supplementation. We believe that multiple myeloma should be considered in the differential diagnosis in patients with profound hypophosphatemia, urinary phosphate wasting, and otherwise intact tubular function.
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PMID:Profound hypophosphatemia and isolated hyperphosphaturia in two cases of multiple myeloma. 904 Dec 22

Thalidomide, initially introduced as a sedative, was withdrawn from the market in the early 1960s after it was found to be a teratogen. However, it later found use as an investigational agent in the treatment of erythema nodosum leprosum, oral ulcers, graft versus host disease, and wasting associated with the human immunodeficiency syndrome. Its antiangiogenic properties were recognized in the early 1990s during a period where the importance of angiogenesis became increasingly apparent as a critical step in the in the proliferation and spread of malignant neoplasms. This led to the evaluation of thalidomide as an antiangiogenic agent in the treatment of several cancers. Thalidomide has already become part of standard therapy for the treatment of patients with relapsed and refractory multiple myeloma. It has also been found to have varying degree of benefit in various other malignancies. Although more clinical trials are needed, Kaposi' s sarcoma and myelofibrosis represent other malignancies in which thalidomide has already demonstrated promising activity. The mechanism of action of thalidomide in cancer is still unclear, but do appear to be mediated by several other mechanisms in addition to its anti-angiogenic properties. This article reviews the current status of thalidomide for the treatment of non-plasma-cell malignancies.
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PMID:Thalidomid: current role in the treatment of non-plasma cell malignancies. 1519 11

Interleukin-6 (IL-6) is a 4-helical protein that binds to a specific IL-6 receptor on target cells and to two molecules of the promiscuous signal transducing protein, glycoprotein 130 (gp130). Structure-function analysis has led to the definition of molecular contacts between IL-6 and its receptor subunits. This knowledge has led to the design of competitive antagonistic proteins that retain their receptor binding capability, but fail to stimulate one or both gp130 proteins; the properties of such recombinant antagonistic proteins are compared with traditional neutralising monoclonal antibodies targeted at IL-6 or receptor subunits. Furthermore, several strategies have been employed to construct molecules with increased bioactivity. Possible therapeutic applications in putative IL-6 dependent haematologic disorders, e.g., Castleman's disease (CD), POEMS syndrome, multiple myeloma, and bone diseases, e.g., Paget's disease, osteoporosis, are outlined. IL-6 antagonists could also, in theory, suppress inflammatory activity in rheumatic and autoimmune diseases and could prevent secondary amyloidosis. This principle may prove advantageous in myocardial infarction (MI) and unstable angina pectoris. More generally, IL-6 antagonists could improve the wasting and microcytic anaemia of chronic diseases. IL-6 antagonists might slow down development of mesangio-proliferative glomerulonephritis (MPGN). Hyperagonistic variants of IL-6 have a potential use in the ex vivo expansion of haematopoietic progenitor cells and as thrombopoietic agents. They might well be the first drugs to aid liver regeneration in vivo.
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PMID:The therapeutic potential of interleukin-6 hyperagonists and antagonists. 1598 26

Hypophosphatemic osteomalacia is a rare but important complication of multiple myeloma. In these cases, the pathophysiology of the phosphate renal wasting notably differs from oncogenic osteomalacia and is due to light-chain nephropathy, resulting in proximal tubular dysfunction which is not restricted to phosphate handling. These patients seems to have a distinct type of plasma cell disorder characterized by a slow progression of the tumor and by an early phase dominated by the metabolic complications of the renal proximal tubular dysfunction. For this reason hypophosphatemic osteomalacia is the presenting feature that leads to the diagnosis of multiple myeloma in most of these patients. Recognition of this complication is important, since supportive treatment with phosphate supplements and calcitriol may substantially alleviate pain and weakness associated with hypophosphatemia.
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PMID:Acquired hypophosphatemic osteomalacia associated with multiple myeloma. 1611 95