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 metabolism of 14C-lysine by leukaemic cells in acute myeloblastic, myelomonocytic, lymphoblastic and chronic myeloid leukaemia with blast crisis was studied. The investigations included lysine metabolism to CO2, lipids, organic acids and nucleotides and its incorporation into cellular proteins. The obtained results were compared with determinations carried out in granulocytes and lymphocytes of healthy subjects. Cells in acute leukaemias metabolized 14C-lysine in a similar range. In relation to normal cells the range of lysine metabolism to lipids in the leukaemic cells was significantly higher (p less than 0.01), while that of organic acids was significantly lower (p less than 0.05). The activity of 14C-lysine metabolism depended on the number of blast cells in the sample and the type of acute leukaemia. Neoplastic cells in blast crisis and in acute myeloblastic leukaemia incorporated more actively 14C-lysine into proteins than cells in acute myelomonocytic and acute lymphoblastic leukaemia (p less than 0.05). Similar differences in lysine metabolism were observed between myelomonocytes and blast cells from acute lymphoblastic leukaemia (p less than 0.05).
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PMID:[Lysine metabolism in acute leukemia]. 29 72

Pulmonary function was measured before and at intervals after treatment in 44 patients who received a bone marrow transplant for chronic myeloid leukaemia in the chronic phase. All patients were treated with cytotoxic drugs, total body irradiation, and post-graft immunosuppression. Thirty four patients surviving for 12 months were followed at three monthly intervals and 16 patients for 24 months. Fifteen patients received unmanipulated donor marrow cells and 29 patients received donor marrow cells depleted of lymphocytes ex vivo with the monoclonal antibody Campath-1. The 21 patients treated early in this study received 10 Gy of total body irradiation whereas the 23 patients treated more recently, who were all T lymphocyte depleted, received 12 Gy. Pretransplant lung function for the group was normal and was similar in survivors (n = 34) and nonsurvivors (n = 10), and in smokers (n = 8) and non-smokers (n = 36). (Carbon monoxide transfer factor--TLCO) was under 75% of predicted normal in nine patients before transplantation. TLCO, carbon monoxide transfer coefficient (KCO), FEV1, and vital capacity (VC) values were lower 6 and 12 months after bone marrow transplant than initially. The greatest decline was in TLCO, from an initial value of 89% to 66% at 6 and 70% at 12 months. The 16 longer term survivors showed significant recovery of function between 6 and 24 months after bone marrow transplant for TLCO, KCO, and VC, the increase ranging from 6.3% to 7.3% predicted. Airflow obstruction (FEV1/VC ratio less than 70%) developed in one patient. The major factors associated with deterioration in pulmonary function at 6 and 12 months after transplantation in the 34 survivors (stepwise multiple regression analysis) were (a) transplantation with T cell depleted donor marrow (p less than 0.005) and higher total body irradiation dose (p less than 0.02) with a fall in KCO and an increase in the FEV1/VC ratio; (b) chronic graft versus host disease with a fall in VC (p less than 0.01); and less fall in KCO (p less than 0.01); and (c) acute graft versus host disease with a fall in FEV1 (p less than 0.01). It is considered that most patients who survive the short term risks of bone marrow transplant have only minor long term impairment of pulmonary function.
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PMID:Pulmonary function after bone marrow transplantation for chronic myeloid leukaemia. 304 53

In a companion paper we demonstrated that normal peripheral blood granulocytic precursor cells differentiate after 2-3 weeks in suspension culture. In the studies described here leukemic blast cells obtained from 14 patients with acute myelocytic leukemia (AML) and two patients with chronic myelocytic leukemia in blastic crisis were cultured in McCoy's 5A medium containing 15 per cent fetal bovine serum for 2-3 weeks at 37 degrees C in an atmosphere of 5 per cent CO2-95 per cent room air. 'Spontaneous' myeloid differentiation (20 x 10(4) viable mature myeloid cells ml-1) occurred in the cultures of cells obtained from 8 pts. The differentiation was granulocytic in three cases, monocytic in four cases and of mixed type in one case. Differentiation was independent of the growth of the cells in culture and occurred in four cases after the first week. Monocytic differentiation was seen only in AML of the FAB M4 type whereas granulocytic or mixed differentiation were seen only in AML of the FAB M1 or M2 types. When PHA leucocyte conditioned medium (PHA-LCM) was added to the cultures monocytic/macrophage differentiation was favoured. Inducers of the differentiation of the HL-60 cell line (N-methylacetamide, cytosine arabinoside, or retinoic acid) had no consistent effect on the differentiation and were at times inhibitory. Three patients received therapy with low dose cytosine arabinoside and no correlation was observed between the outcome of the treatment and leukemic cell differentiation in culture in the presence of the drug.
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PMID:Differentiation of myeloid cells in liquid culture: 2. Acute myelocytic leukemia cells. 347 87

A patient with chronic myelogenous leukemia, treated for two years with busulfan, presented with increasing dyspnea of several months' duration. Despite a normal chest radiograph, there was a markedly reduced carbon monoxide (CO) diffusing capacity (41% of predicted normal) and a restrictive ventilatory pattern on pulmonary function testing. Gallium-67 scanning revealed diffuse uptake in both lungs. The busulfan was discontinued and therapy was changed to hydroxyurea. Three months later the patient was without symptoms, the CO diffusing capacity had risen to 64% (of predicted), and the Ga-67 scan had returned to normal. The chest radiograph remained normal. Despite the lack of biopsy proof, we believe Ga-67 scanning was an aid in the early detection of cytotoxic-induced lung disease in a reversible stage. Gallium-67 scanning may be useful in the early deagnosis of pulmonary injury from cytotoxic agents.
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PMID:Early detection of busulfan lung: report of a case. 693 68

Fas antigen, also termed APO-1 or CD95, is a transmembrane protein and a member of the tumor necrosis factor receptor/nerve growth factor receptor superfamily which mediates apoptosis upon oligomerization. The Fas/Fas ligand system is considered to be a key regulator of apoptosis. Recently, we have demonstrated that Fas antigen expression is induced by low-dose irradiation of some types of lymphomas, and we also demonstrated that irradiation-induced Fas antigen expression increased with the passage of time until peaking at 48 h after irradiation in CML-C1, CML-C2, DL-40, and DL-95 cell lines. In this study, we also examined the potential cytotoxicity of Fas ligand peptide against several types of lymphoma/leukemia cell lines that showed induction of Fas antigen expression under irradiation. Flow cytometry analysis was performed at 6, 24 and 48 h after irradiation. Samples (1 x10(6) cells/ml) from irradiated and non-irradiated cells of each cell line were incubated with or without 5 microg/ml of Fas ligand peptide for 2 h at 37 degrees C in a humidified atmosphere of 5% carbon dioxide (CO2) in air. The killing effect of Fas ligand against cell lines of CML-C1, DL-40, and DL-95 were clearly identified as the percentage of cells with Fas antigen expression induced by irradiation. Concerning HD-70 cell line, for which soluble Fas antigen has been identified, the killing effects were clearly observed in samples pre-treated with PBS washings. To our knowledge, this is the first report describing a possible application of the Fas/Fas ligand system in treatment of certain types of malignancies in which Fas antigen is inducible by irradiation.
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PMID:Cytotoxicity of Fas ligand against lymphoma cells with radiation-induced Fas antigen. 985 30

The correlation between pCO2 values in blood and in exhaust gas from the oxygenators was examined during cardiopulmonary bypass (CPB) using one bubble oxygenator and three membrane oxygenators. Forty-seven CPBs were performed, 17 with Compactflow (Dideco, Italy), 10 with Maxima (Medtronic Inc., USA), 10 with Cobe CML (Cobe Laboratories, USA) membrane oxygenators and 10 with Hi-Flex (Dideco, Italy) bubble oxygenators. Blood samples were taken both from arterial and venous lines of the oxygenator. A capnometer was connected to the oxygenator gas exhaust port and CO2 fraction was measured at the time of drawing blood samples. CO2 pressure in the gas phase was calculated from the product of the CO2 fraction and water vapour-corrected barometric pressure. Blood gases were measured at 37 degrees C and the pCO2 value was corrected to the temperature of the arterial line. The correlation between blood and exhaust gas pCO2 was good in all the oxygenators examined, ranging from 0.921 to 0.976. The standard error of estimate (SEE) was in the range of about +/- 2 mmHg for all the oxygenators. The systematic error (slope and intercept of the correlation line) varied depending on the construction of the oxygenator, with countercurrent design having the best overall correspondence. Based on the results of this study it can be concluded that arterial or venous CO2 pressure can be monitored with a capnometry device coupled to the oxygenator gas outlet port.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Monitoring of CO2 exchange during cardiopulmonary bypass: the effect of oxygenator design on the applicability of capnometry. 1017 88

In the conventionally treated group of patients with chronic myelogenous leukemia (CML) the prognosis has been significantly improved by interferon-alpha (IFN-alpha). Several side effects in association with IFN-alpha treatment have been reported. Here we present the first case of a CML patient with reversible pulmonary artery hypertension (PAH) during IFN-alpha therapy. The patient received IFN-alpha-2b (up to 10 million U/day) for 6 months until he started to complain of dyspnea on exertion and an afebrile non-productive cough. An echocardiography and right heart catheterization showed signs of right heart failure with PAH (80 mmHg). A reduced carbon monoxide diffusion capacity and partial respiratory insufficiency were noted. Inflammatory markers were not elevated and pulmonary infiltrates could not be detected. Respiratory infections, thromboembolic causes or autoimmune diseases were carefully ruled out. IFN-alpha was suspected as causative agent, because experimental investigations in sheep showed that IFN-alpha can stimulate the thromboxane cascade which resulted in transient PAH. A reduced pulmonary diffusion capacity had been observed secondary to PAH. After discontinuation of IFN-alpha, our patient's clinical status improved rapidly. After 6 months the pulmonary artery pressure had returned to near normal values (35 mmHg) and the pulmonary diffusion capacity was normal. It took one year until the electrocardiogram reverted to the pre-IFN-alpha pattern. PAH should be included in the differential diagnosis of patients treated with IFN-alpha who complain of exertional dyspnea in the absence of inflammatory signs.
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PMID:Pulmonary artery hypertension during interferon-alpha therapy for chronic myelogenous leukemia. 1144 36

Pulmonary function in 42 patients with chronic myelogenous leukemia (CML) was tested before and after HLA-matched (39 related, 3 unrelated) allogeneic bone marrow transplantation (BMT) between 1985 and 1999. Pulmonary function tests (PFTs) including ventilatory capacity, lung volumes, and diffusion capacity for carbon monoxide (DLCO) were performed before and 3, 6, 12, and 24 months after BMT, and every 12 months thereafter. Possible pre- and post-BMT risk factors were evaluated for their influence on pulmonary function. Patients were divided into two groups according to their survival duration for more than 12 months or not. Pretransplant PFTs were essentially normal except for mild reduction in DLCO values in the short-term survival group. Overall pulmonary function changes revealed persistent and significant decrease of forced vital capacity (FVC) and DLCO values after BMT. The DLCO values reached abnormal levels (< 80%) and showed a trend of incomplete recovery. Decrease of forced expiratory volume in the first second (FEV1) and vital capacity were also noted but the FEV1/FVC ratio remained within normal limits after BMT. Transient fall of total lung capacity after BMT was noted. However, its values did not reach abnormal levels such as to cause restrictive ventilatory impairment. Possible risk factors including gender, smoking, bronchiolitis obliterans, acute and chronic graft-versus-host disease (GVHD) were found to have significant influences on posttransplant pulmonary function changes by multiple regression analysis. Most patients except those who developed bronchiolitis obliterans were clinically asymptomatic. Development of bronchiolitis obliterans was the most important factor to cause both clinical symptoms and impaired pulmonary function. In summary, pulmonary function changes before and after HLA-matched allogeneic BMT in long-term survivors of CML only showed modest dysfunction. The primary negative presentation with the development of oxygenation defect had no clinical significance in most patients. The influences on the impairment of pulmonary function were multifactorial.
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PMID:Pulmonary function changes in long-term survivors of chronic myelogenous leukemia after allogeneic bone marrow transplantation: a Taiwan experience. 1244 18

Pulmonary function tests were performed in 20 patients with chronic myeloid leukemia before and after human leukocyte antigen-matched allogeneic sibling hematopoietic stem cell transplantation (HSCT) to identify any conditioning treatment effects on post-transplant function from January 1995 to December 2002. Of 20 patients, eight received non-myeloablative conditioning treatment and 12 received conventional myeloablative conditioning treatment. Pulmonary function tests including forced vital capacity (FVC), forced expiratory volume in the first second (FEV1), and diffusion capacity for carbon monoxide (DLCO) were performed pretransplant, 6 and 12 months post-transplant. Possible pre-HSCT and post-HSCT risk factors were evaluated for association with pulmonary function. The results showed that myeloablative conditioning treatment had greater negative impact on FEV1, FVC, and DLCO than non-myeloablative conditioning therapy. We conclude that non-myeloablative allogeneic HSCT may apply a better transplant choice in patients who need special concern with post-transplant pulmonary function changes.
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PMID:Relatively favorable outcomes of post-transplant pulmonary function in patients with chronic myeloid leukemia receiving non-myeloablative allogeneic hematopoietic stem cell transplantation. 1565 7

The aim of this study was to investigate the inhibitive effect of artesunate (ART) on CML cell line K562 and its influence on VEGF expression in vitro. Human CML cell line K562 cells were cultured in RPMI 1640 medium supplemented with 10% heat-inactivated fetal calf serum. All cells were cultured in a humidified atmosphere of 5% CO2 at 37.0 degrees C. K562 cells in logarithmic growth phase were collected and seeded in RPMI-1640 medium, and were treated with ART. At the indicated time points, viable cells were counted by trypan blue exclusion method. Each assay was triplicated. K562 cells were treated with ART at different concentrations. Morphological changes were observed with invert microscope. VEGF expression in K562 cells treated with ART at different concentrations and in the control group were detected by enzyme-linked immunosorbent assay (ELISA). The results indicated that ART obviously induced growth inhibition in K562 cells. The relationship between cell inhibition rates and the concentrations of ART showed a dose-dependent manner (p < 0.01). VEGF expression of K562 cells treated with ART at different concentrations decreased significantly (p < 0.01). No significant change of VEGF expression in control group was observed (p > 0.05), while VEGF expression was down-regulated significantly in experiment groups (p < 0.01). The inhibition rate of K562 cells increased in time and concentration-dependent manners. In K562 cell lines treated with ART, VEGF expression was up-regulated at first and then down-regulated to a lower level. It is concluded that ART inhibits k562 cell proliferation in a dose and time dependent manner. The mechanism underlying the inhibitive effect of ART on K562 cells may be realized through down-regulation of VEGF expression.
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PMID:[Suppressive effect of artesunate on K562 cell growth and its influence on VEGF expression]. 1871 59


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