Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Relations between clinical course and change in aldolase (ALD) isoenzyme pattern were investigated on the peripheral and bone marrow blood of normal subjects and patients suffering from leukemia, multiple myeloma, hypoplastic anemia and other hematological disorders. Similar examination was performed on human leukemia cells and on sera and leukocytes from Donryu rats inoculated with rat leukemia cells (DBLA-6), induced by NBU. In addition to the enzyme activity, isoenzyme pattern was analyzed electrophoretically. The results obtained were as follows: 1) FDP/F1P ratios of the peripheral and marrow blood were high in untreated leukemia. After the induction therapy, the ratio in the marrow blood was high, but decreased in peripheral blood. 2) In complete remission, both ratios were decreased to normal level. 3) In the early relapse of leukemia, the marrow blood showed a high ratio in spite of normal value in the peripheral blood. During full relapse or reinduction therapy, FDP/F1P ratio remained high in both the peripheral and marrow blood. 4) Atypical hypoplastic leukemia showed a significantly high ratio in the marrow, but a low ratio in the periphery. No difference in either ratio was detected between hypoplastic anemia and normal subjects. 5) Zymogram of leukemia cells from leukemia patients showed that ALD-A was predominant more clearly than in normal leukocytes. ALD in normal leukocytes was composed mainly of ALD-A and its hybrids with ALD-B and ALD-C. 6) The ratio in sera and leukocytes from rats inoculated with DBLA-6 cells was increased with exacerbation of leukemia. ALD-A was predominant in rat leukemia cells on the zymogram. It is concluded that aldolase isoenzymes, especially the FDP/F1P ratio, are useful in estimating clinical course of leukemia, particularly in deciding early relapse of leukemia in bone marrow. These laboratory findings are also useful in differentiating atypical leukemia from hypoplastic anemia.
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PMID:[Clinical and experimental studies on aldolase and its isoenzymes in leukemia and allied hematological disorders (author's transl)]. 29 6

Serum aldolase concentrations were determined in 78 patients with acute myelogenous leukaemia (AML). Mean serum aldolase concentration (+/- SD) at the time of diagnosis was 28.3 U/L (+19.4). 71.8% of AML patients had increased serum aldolase concentrations. The highest hyperaldolasaemia were observed in patients with acute myelomonocytic leukaemia and acute monoblastic leukaemia. The monocytic involvement in AML patients was significantly related to serum aldolasaemia. Human aldolase gene has been located on chromosome 16, whose structural aberrations are frequent in AML patients with monocytic involvement, explaining the link between serum hyperaldolasaemia and the monocytic involvement in AML patients.
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PMID:The effect of monocytic involvement of hyperaldolasaemia in patients with acute myelogenous leukaemia. 227 37

Subunit specific radioimmunoassay for aldolase isozymes were developed for the quantification of human aldolase A and B. Aldolase B immunoreactivities were predominantly high in adult normal liver, while aldolase A was distinctly low. Aldolase A was high, while aldolase B was low in neonatal liver compared with the adult liver. Aldolase A immunoreactivities were almost the same as those of aldolase B in fetal liver (28 weeks). Aldolase A was predominantly found in human hepatoma tissues, whereas aldolase B was distinctly low in the same hepatoma tissues. With regard to human hepatoma cell lines, aldolase A was also predominantly found in HepG2 and PLC/PRF/5 cell lines, whereas aldolase B levels were extremely low. Almost the same results were obtained from mRNA expression of aldolase A and B in human hepatoma cell lines by the method of northern hybridization. Effects of various reagents on differentiation of hepatoma cell lines were investigated. Neither Dimethyl Sulfoxide (DMSO) and 12-O-Tetradecanoylphorbol-13-acetate (TPA), which are known to be the inducers of differentiation of human leukemia cell lines such as HL-60, nor Transforming Growth Factor-beta 1 (TGF-beta 1) and Hepatocyte Growth Factor (HGF), which are known to be growth inhibitors, could cause the differentiation of hepatoma cell lines in the alteration of aldolase isozymes. The same data were shown in mRNA expression of aldolase isozymes. These results suggest that aldolase A immunoreactivities and mRNA expression are both predominantly high in hepatoma cell lines, and the reagents such as DMSO, TPA, TGF-beta 1 and HGF which tried to differentiate the hepatoma cell lines used in this study were not effective in the alteration of aldolase isozymes.
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PMID:[Immunoreactivities and messenger RNA expression of aldolase A and B in human hepatoma cell lines]. 786 61

Rhabdomyolysis is an unusual complication of hematopoietic stem cell transplantation (HSCT). Cyclophosphamide has been one of the key drugs in the most common preparative regimen for HSCT. We present here a rare case of acute rhabdomyolysis following administration of high-dose cyclophosphamide. A 47-year-old woman with adult T-cell leukemia in remission was treated with high-dose cyclophosphamide as a preparative regimen for allogeneic bone marrow transplantation. Nineteen hours later, general convulsions and acidosis suddenly occurred. Levels of serum creatine kinase (skeletal muscle type), myoglobin, and aldolase were markedly elevated to 32870 IU/l, 640 ng/ml, and 240.3 IU/l, respectively. Rhabdomyolysis caused by high-dose cyclophosphamide was diagnosed, and the preparative chemotherapy was discontinued. Subsequently, her muscular signs and symptoms improved, and the results of laboratory examinations returned to normal after 2 weeks. She had previously been treated with conventional doses of cyclophosphamide, doxorubicin, vincristine, and prednisolone without evidence of rhabdomyolysis. Acute rhabdomyolysis may be an adverse effect specific to high-dose cyclophosphamide therapy.
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PMID:Acute rhabdomyolysis following administration of high-dose cyclophosphamide: case report. 1180 38

A novel bispecific single-chain fusion protein, DT2219, was assembled consisting of the catalytic and translocation domains of diphtheria toxin (DT(390)) fused to two repeating sFv subunits recognizing CD19 and CD22 and expressed in Escherichia coli. Problems with yield, purity, and aggregation in the refolding step were solved by incorporating a segment of human muscle aldolase and by using a sodium N-lauroyl-sarcosine detergent-based refolding procedure. Problems with reduced efficacy were addressed by combining the anti-CD19 and anti-CD22 on the same single-chain molecule. DT2219 had greater anticancer activity than monomeric or bivalent immunotoxins made with anti-CD19 and anti-CD22 sFv alone and it showed a higher level of binding to patient leukemia cells and to CD19(+)CD22(+) Daudi or Raji cells than did anti-CD19 and anti-CD22 parental monoclonal antibodies. The resulting DT2219, mutated to enhance its avidity, was cytotoxic to Daudi cells in vitro (IC(50) = 0.3 nmol/L). In vivo, DT2219 was effective in a flank tumor therapy model in which it significantly inhibited tumor growth (P < 0.05) and in a systemic model in which it significantly prolonged survival of severe combined immunodeficient mice with established Daudi (P < 0.008) compared with controls. DT2219 has broader reactivity in recognizing B-cell malignancies, has more killing power, and requires less toxin than using individual immunotoxin, which warrants further investigation as a new drug for treating B leukemia/lymphoma.
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PMID:A bispecific recombinant immunotoxin, DT2219, targeting human CD19 and CD22 receptors in a mouse xenograft model of B-cell leukemia/lymphoma. 1589 89

A 50-year-old woman presented with leukocytosis, anemia, and thrombocytopenia in June 2013. She was diagnosed with de novo acute myeloid leukemia with the t(16;21)(q24;q22) translocation. She received an allogeneic hematopoietic stem cell transplant from an HLA-DRB1 locus-mismatched unrelated donor in June 2014. The myeloablative preparative regimen consisted of cyclophosphamide at 60 mg/kg for 2 days and total body irradiation at 12 Gy. On Day 55, she was treated with prednisolone at 20 mg/day for acute GVHD (Grade III; Skin Stage 2, Gut Stage 2, Liver Stage 0) and gradually improved. She had fever, myalgia in the upper limbs, and asymptomatic sinus tachycardia on Day 145. Laboratory tests showed elevated CK, CKMB, aldolase, and troponin I. Electromyographic examination revealed myopathic abnormalities compatible with the diagnosis of myositis. Electrocardiography showed tachycardia and anteroseptal ST elevation, and echocardiography showed hypokinesia of the left interventricular septal wall without evidence of infection or leukemia relapse. She was immediately treated with 40 mg/day prednisolone after the diagnosis of polymyositis and cardiomyopathy, associated with chronic GVHD. The polymyositis and cardiomyopathy improved promptly after the administration of prednisolone and the patient remains in remission with a current maintenance program of prednisolone at 5 mg/day.
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PMID:Chronic GVHD complicated with polymyositis and cardiomyopathy after myeloablative hematopoietic stem cell transplantation. 2606 70