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)

Human granulocyte catalase (hydrogen peroxide:hydrogen peroxide oxidoreductase, EC 1.11.1.6) was purified from chronic myeloid leukemia cells. The purification procedure included heat precipitation, ammonium sulphate fractionation, DEAE-Sephadex chromatography, gel chromatography on Sephadex G-200 and isoelectric focusing with an approximate yield of 30% and a 1000-fold purification. The molecular weight of the subunit obtained by sodium dodecyl sulphate electrophoresis was 65 800. So20,w was 11.6 +/- 0.24. The pH-optimum was 6.6-6.7 and the spectrum showed a major peak at 405 nm and shoulders at 500, 540 and 625 nm typical for catalase. The electrophoretic mobility was towards the anode at pH 8.6 and identical to normal granulocyte and erythrocyte catalase. These three species of catalase gave the reaction of identity on immunodiffusion and crossed immunoelectrophoresis. The content of catalase and its activity of isolated granulocytes were approximately identical in normal and chronic myeloid leukemia granulocytes while the specific activity of leukemic catalase was higher than normal. No difference in catalase content was found between mature and immature leukemic granulocytes.
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PMID:Purification of human granulocyte catalase in chronic myeloid leukemia. 40 30

Thirteen leukemic patients with disease refractory to conventional chemotherapy were treated with 1.0 to 7.5 g/m2 of Cytosine Arabinoside (Ara-C) over 29 drug cycles. Drug infusions were spaced at 12-hour intervals; a maximum of four doses was administered over 36 hours. After single dose tolerance had been established, three or four dose cycles were given at 2- to 30-day intervals. There were three partial remissions (PR) and one complete remission (CR) in a treatment group of four patients with AML, five with ALL, two with lymphoma converted to leukemic phase, one CML in blast crisis, and one promyelocytic leukemia. Five of the patients were septic and considered terminally ill at the time of treatment. All other patients had evidence of drug responsiveness. The nadir of the white count occurred from 3 to 12 days after treatment, with subsequent recovery of the peripheral granulocyte count between days 12 and 28. Toxicity included nausea and vomiting (GI symptoms) in twelve patients, central nervous system (CNS) disturbances in eight patients, one episode of inappropriate antidiuretic hormone syndromes (SIADH), one of hyperuricemia, and fever in eleven patients. There was no evidence of hepatic or renal dysfunction. These high doses of Ara-C appear useful for treatment of patients with refractory leukemia. Hospitalization is brief and toxicity acceptable.
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PMID:High dose cytosine arabinoside (HDARAC) in refractory acute leukemia. 49 9

Of 400 female and 58 normal nonommunized male sera approximately 10% were cytotoxic for a panel of allogeneic granulocytes. Sera with strong alloreactivity were also autoreactive, which emphasized the large autoimmune component of most alloantisera against granulocytes. The cytotoxic granulocyte autoantibodies were complement dependent, of the IgM class, and exhibited optimum cytotoxic activity in vitro at 5 degrees C precomplement incubation temperatures with papain-treated cells. The sera were unreactive with autologous or allogeneic B and T lymphocytes, monocytes, and red blood cells but were cytotoxic for adult and cord granulocytes, eosinophils, and chronic myeloid leukemia cells. Granulocyte autoantibodies were present in 53% of sera from 57 patients with systemic lupus erythematosus (p less than 0.00002) but were not found in increased frequency in the sera of patients with 28 other diseases. We conclude that a single tissue-specific antigenic determinant(s) called "G" may be present on granulocytes and is the target of naturally occurring autoantibodies.
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PMID:Autoimmune cytotoxic granulocyte antibodies in normal persons and various diseases. 69 99

Elevation of transcobalamin I and serum vitamin B12 levels has usually been associated with increased granulocytic proliferation, such as occurs in chronic myelogenous leukemia. Two patients with metastatic cancer had extremely high serum vitamin B12 and transcobalamin I levels--greater than those seen in even the most intense granulocytic proliferation--that were not explainable by leukocytosis. The subjects' serum vitamin B12 levels were 18,750 and 21,221 pg per milliliter (normal, 471 plus or minus 174 pg per milliliter, mean plus or minus S.D.) and unsaturated vitamin B12 binding capacity 158,750 and 5,400 pg per milliliter (normal, 1153 plus or minus 313 pg per milliliter) respectively. The abnormally elevated serum binder was shown to be identical with transcobalamin balamin I in every respect. Levels of transcobalamin II and serum third binder were normal. The cause of the binder abnormality is unknown, but factors other than granulocyte proliferation may control or contribute to the production or accumulation of transcobalamin I.
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PMID:Extreme elevation of serum transcobalamin I in patients with metastatic cancer. 105 6

Remission induction was assessed by clinical and cell-culture criteria for 65 patients with acute myelogenous leukemia (AML), 11 patients with chronic myelogenous leukemia (CML) in blast crisis and 19 patients with acute lymphoblastic leukemia (ALL). Cyclophosphamide, cytosine arabinoside and vincristine (CAV) therapy resulted in complete remission in 23 of 50 previously untreated patients with AML and in 3 of the 11 patients with CML. Fourteen patients with ALL responded to vincristine-prednisone induction therapy and two to induction therapy with CAV. The median duration of survival of the responding patients was 2.2 years, compared with 4 months for the patients who did not respond to treatment. Granulopoietic colony formation, assessed by assay of colony-forming units dependent on colony-stimulating activity in culture (CFU-C), was abnormal in 37 of 42 bone marrow aspirates from patients with AML before treatement. CFU-C concentration increased when leukocyte-conditioned medium (LCM) was added to the cultures; 13 cultures had normal or elevated CFU-C concentration with LCM. Marrow cells of patients with ALL or CML in blast crisis demonstrated a similar pattern. Serial studies of marrow CFU-C concentration of 31 patients with AML demonstrated a change to a normal pattern with successful remission induction. Results of this study suggest that administration of purified LCM to leukemic patients might increase granulocyte production from potential but unstimulated granulopoietic precursors. This therapy would lessen the probability of death from infection during remission induction.
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PMID:Acute leukemia in adults: assessment of remission induction with combination chemotherapy by clinical and cell-culture criteria. 105 7

Intensive leukapheresis has been used as the initial treatment of chronic granulocytic leukemia (CGL) in six patients. The number of leukaphereses ranged from 3 in 7 days to 13 in 39 days (mean, 8 in 22 days). The procedures were well tolerated, and in all patients there was improvement in hematologic values, in most cases with considerable reduction in the peripheral leukocytosis and thrombocytosis and in the proportion of immature granulocytic cells in the circulation. Splenomegaly decreased considerably in the four patients who had more than four leukaphereses. Symptoms of sweating, malaise, and pain due to splenomegaly were rapidly relieved. Problems due to hyperuricemia did not occur, but four patients required blood transfusions for correction of anemia. This method of initial treatment of CGL appears to give more rapid relief of symptoms than does conventional chemotherapy; it incurs no risk of hyperuricemia and lessens that associated with thrombocytosis. In addition, large quantities of granulocyte-rich plasma are made available for the treatment of infections in neutropenic patients. Intensive leukapheresis deserves more widespread evaluation as the initial treatment of CGL.
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PMID:Intensive leukapheresis as initial therapy for chronic granulocytic leukemia. 106 Apr 70

Observations in six adult patients with leukaemic differential white counts, predominantly mature-celled, and with hepatosplenomegaly show that the mature-celled but fulminant (para-)neutrophil leukaemia must be differentiated from Ph1-positive chronic myeloid leukaemia. This (para-)neutrophil leukaemia is probably identical with the previously described atypical chronic myelosis of the adult, chronic myeloid leukaemia of childhood and the Pelger-like chronic myeloid leukaemia. Cardinal signs are a mature-celled differential count, short life expectancy (1 year), initial platelet deficiency, increased activity of granulocyte alkaline phosphatase, absence of Ph1-chromosome, and poor therapeutic response to busulfan. This curious and yet apparently not uncommon disease has been observed in the adult age group predominantly in men. The frequently high HbF level observed in juvenile chronic myeloid leukaemia could not be demonstrated in adults. Some of these neutrophil leukaemias are characterized by medullary fibrosis and terminal increase of immature blast cells (blast crises?) of which the diagnostic reliability is still disputed.
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PMID:[Differential diagnosis of atypical chronic myeloid leukaemia]. 106 23

Leukocyte kinetic studies using chromium-51 were performed in four patients with acute myelocytic leukemia (AML). Intravascular leukocyte survival was prolonged in comparision with granulocyte survival in normal subjects. Significant splenic pooling occurred in three patients, none of whom had splenomegaly. In one patient studied, circulating leukemic cells were shown to return to the bone marrow. The prolongation of intravascular leukocyte survival in AML in relapse, as in chronic myelocytic leukemia, probably depends on several factors including the presence of immature leukemic cells and the recycling of these cells from the spleen and bone marrow.
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PMID:Study of leukocyte kinetics in acute myelocytic leukemia utilizing chromium-51. 106 22

The initial rate of phagocytosis, oxygen consumption rate during phagocytosis, bactericidal capacity against Escherichia coli, and the granule protein composition of isolated mature-appearing granulocytes were studied in 23 patients with chronic granulocytic leukemia (CGL) with the simultaneous use of normal controls. The initial rate of phagocytosis was decreased (p less than 0.05) in the CGL patient group, as were oxygen consumption rate (p less than 0.001) and bactericidal capacity (p less than 0.001). Kinetic analysis of the ingestion rate showed CGL granulocytes to have the same capacity to bind the particles as normal granulocytes. Both specific and primary granule protein deficiencies were shown for CGL granulocytes, and these deficiencies were more pronounced at or near blast cell transformation. Analysis of all different granulocyte function parameters showed an inverse correlation to white blood cell counts (p less than 0.01) and to the percentage of immature granulocytes in peripheral blood (p less than 0.001). The leukocytosis doubling time was progressively shortened during the chronic course of the disease. A correlation was found between granulocyte function parameters and leukocytosis doubling time (p less than 0.001), indicating that granulocyte function was progressively deteriorating during chronic phase CGL, and may be an expression of increasing disturbance of the differentiation process.
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PMID:Granulocyte function in chronic granulocytic leukemia. II. Bactericidal capacity, phagocytic rate, oxygen consumption, and granule protein composition in isolated granulocytes. 106 28

Chronic granulocytic leukaemia (CGL) cells which contained a high concentration of unsaturated folate binding protein were incubated in suspension culture for a period of 5 h. Cell samples were periodically assayed for binder and these demonstrated active synthesis which was inhibited by puromycin, cyclo heximide, N-ethylmaleimide, and by incubation at 4 degrees C, but not by actinomycin D. Folate binding activity could also be demonstrated in the culture medium and this increased with the duration of incubation. This release of binder was inhibited by culturing the cells at 4 degrees C and by the addition of N-ethylmaleimide, but not by actinomycin D, puromycin, or cycloheximide. When the pre- and post-culture cell lysates were saturated with tritiated folic acid ([3H]PteGlu) and subjected to chromatography on DEAE-agrarose, approximately half of the bound folate eluted with 0.001 M phosphate buffer at pH 6.0 and the other half eluted with 0.2 M buffer at pH 7.2. The culture medium and plasma from this patient with CGL was well as serum from two normal subjects saturated with [3H]PteGlu and similarly chromatographed contained primarily the acidic binder and much less of the binder eluting with the low molarity buffer. Since a folate binding protein immunochemically similar to the binder in CGL cells has been identified in the serum of non-leukaemic subjects, these experiments suggest that the source of circulating folate binding protein may be the immature granulocyte.
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PMID:Studies with the folate binding protein in chronic granulocytic leukaemia cells. I. Synthesis and release of binder by cells in short-term culture. 106 9


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