Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The fate of beta-2-microglobulin was investigated in 17 patients with chronic myeloid leukemia by correlation analysis of the plasma concentration and various clinical measurements. The plasma concentration of beta-2-microglobulin correlated individually with white blood cell count, differential counts of band and segmented neutrophils, metamyelocytes and myelocytes, and haptocorrin concentration during the clinical course (p less than 0.002). The neutrophil granulocytes from the differential stage of myelocytes appears to be a major source of beta-2-microglobulin in chronic myeloid leukemia, and our results suggest that beta-microglobulin is is contained within the specific granules or is liberated from the plasma membranes synchronously with degranulation of neutrophils.
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PMID:Serial measurements of beta-2-microglobulin in plasma correlates with white blood cell counts and haptocorrin in chronic myeloid leukemia. 331 27

Plasma and buffy coat specimens of CML patients with untreated disease, in chronic and accelerated phase, and in overt blastic crises were analysed for the cobalamin patterns using non-polar extraction, thin-layer chromatography and bioautography. Splenic tissue specimens from four splenectomized patients in accelerated phase were analysed similarly. Cellular extracts were separated into two compartments by adsorption to haptocorrin antibodies. Plasma concentrations of all cobalamin forms were increased in CML. The proportion of methylcobalamin was significantly lower than in a reference population, and a low plasma proportion of methylcobalamin was associated with a poor prognosis. Buffy coat cells and splenic tissue had a higher proportion of 5'-deoxyadenosylcobalamin and a lower proportion of methylcobalamin than plasma; still, there was relatively more methylcobalamin than in normal tissue. The haptocorrin-bound compartment differed from the non-haptocorrin compartment in untreated or chronic phase patients by binding less methylcobalamin. An estimate of cobalamin analogues in plasma was achieved by comparing two different isotope dilution assays employing a cobalamin-specific binder, intrinsic factor, and a nonspecific binder, hog non-intrinsic factor. Values for total cobalamin and analogues were increased to the same degree in CML plasma.
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PMID:Cobalamin forms and analogues in plasma and myeloid cells during chronic myelogenous leukaemia related to clinical condition. 777 17

Individual plasma specimens from six patients with chronic myelogenous leukemia (CML) in chronic phase were incubated with [57Co]cyanocobalamin and injected into patients to study the turnover of cobalamin bound to haptocorrin and transcobalamin. The [57Co] radioactivity bound to haptocorrin and transcobalamin was determined after separating the proteins by adsorption to insolubilized antibodies to haptocorrin. The distribution of the radioactivity on the different forms of cobalamin and on haptocorrin isoproteins were determined. The fractional catabolic rate of hapatocorrin (0.102 to 0.158 d-1) and transcobalamin (3 to 29 d-1) was of the same magnitude as previously reported for a reference population. During the first 24 hours of the turnover, no change of the cyanocobalamin form was registered, indicating that conversion of cyanocobalamin to the coenzyme forms of cobalamin does not take place in the circulation. The haptocorrin isoprotein pattern changes in alkaline direction during the first 5 hours indicated that the glycoprotein was desialinated during circulation. From the calculated turnover parameter, the possible competition between transcobalamin and haptocorrin for the transport of cobalamins in CML is estimated to be of minor clinical significance. In conclusion, the increased plasma concentration of haptocorrin in CML is due to an increased liberation of haptocorrin and is not due to a decreased turnover of the protein.
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PMID:The turnover of 57Co-labeled cyanocobalamin bound to cobalamin binding proteins in patients with chronic myelogenous leukemia. 830 Dec 3

Elevated levels of serum cobalamin may be a sign of a serious, even life-threatening, disease. Diseases such as chronic myeloid leukaemia, promyelocytic leukaemia, polycythaemia vera and hypereosinophilic syndrome are often accompanied by markedly elevated levels of cobalamin in the blood. A rise in the serum cobalamin concentration is one of the diagnostic criteria for polycythaemia vera and hypereosinophilic syndrome. In haematological disorders, the increase in circulating cobalamin levels is predominantly caused by enhanced production of haptocorrin. Several liver diseases such as acute hepatitis, cirrhosis of the liver, hepatocellular carcinoma and metastatic liver disease can also be accompanied by an increase in circulating cobalamin. In liver diseases, the increase in cobalamin is predominantly caused by cobalamin release during hepatic cytolysis and/or through decreased clearance of circulating cobalamin by the affected liver. Liver disorders are not an indication for determining the serum cobalamin concentration. However, a coincidentally observed elevated serum cobalamin concentration is reason for further investigation.
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PMID:[The significance of an elevated cobalamin concentration in the blood]. 1191 9