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)

Adenosine deaminase (ADA) activity was measured in plasma, erythrocytes, and mononuclear cells from 18 patients with acute and chronic leukemia. High levels of ADA activities were found in plasma, erythrocytes, and mononuclear cells from patients with acute leukemia, especially acute lymphoblastic leukemia, and blastic crisis of chronic myeloid leukemia. Serial determination of plasma ADA activities was done in 9 patients with acute leukemia. All patients untreated or in relapse had an elevation of plasma ADA activity, which decreased to normal or subnormal levels during complete remission. On starch gel electrophoresis, plasma ADA in leukemic patients separated into two bands. The major band showed a mobility identical to that of normal red cells and mononuclear cells, and the minor band corresponded to that of normal plasma ADA. Enzymatic and immunological studies were performed on ADA from leukemic cells of acute myeloid and lymphoblastic leukemia. There were no differences in Michaelis constant for adenosine, thermostability, electrophoretic mobility, immunological reactivity, and specific activity between ADA of leukemic cells and normal mononuclear cells. These results strongly suggest that the increased ADA activity in leukemic cells is caused by an increased synthesis of a structurally normal enzyme and that increased plasma ADA activity in leukemic patients reflects an increment of leukemic cells in bone marrow. Therefore, serial determination of plasma ADA activities seems to provide a good indicator of the total mass of leukemic cells in bone marrow.
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PMID:Adenosine deaminase (ADA) in leukemia: clinical value of plasma ADA activity and characterization of leukemic cell ADA. 398 5

Eleven academic institutions were selected to study mitoxantrone administered on a schedule of 10 mg/m2/d for five days initially and later at 12 mg/m2/d for five days, each given as a 30 minute intravenous (IV) infusion each day. Patients with acute or chronic leukemia were stratified by leukemic type and clinical status and included one group of patients considered to be in relapse after complete remission from previous chemotherapy and another group of patients considered refractory to standard induction and/or salvage chemotherapy. During the initial treatment schedule, complete remissions were obtained in two of seven patients with acute nonlymphoblastic leukemia, in one of three patients with acute lymphoblastic leukemia, but in none of the patients with chronic granulocytic leukemia in blast crisis. The durations of remission for these three patients were 22, 57, and 78 days, respectively. An increase in mitoxantrone dose to 12 mg/m2/d produced complete remissions in 8 of 19 evaluable patients with acute nonlymphoblastic leukemia, in one of ten patients with refractory acute nonlymphoblastic leukemia, and in one of four patients with chronic granulocytic leukemia in blast crisis. Each of these patients required only a single course of mitoxantrone to achieve remission; the median time to remission was 37 days (range 18 to 64 days). Remission duration ranged from 35 days (chronic granulocytic leukemia) to 186 days, with the median duration for those patients with acute nonlymphoblastic leukemia achieving remission being 135 days. Of the six patients with acute lymphoblastic leukemia, none achieved remission at the higher dose level. Drug-related gastrointestinal toxicity included mucositis (25%), diarrhea (21%), and nausea and vomiting (61%). Systemic infection (nonfatal) was experienced by 21% of patients and alopecia by 17%. Other side effects that occurred occasionally were hepatic dysfunction, decreased renal function, confusion, lethargy, anxiety, and fever. Possible drug-related phlebitis developed in one patient, and a single episode of minor epistaxis was reported in another. Cardiovascular toxicity was low. At a mitoxantrone dose of 10 mg/m2/d for five days, one patient developed hypotension, and one episode of congestive heart failure was reported in another. At the higher dose of 12 mg/m2/d, no drug-related hypotension, congestive heart failure, tachycardia, or chest pain were reported. These data indicate that mitoxantrone is a promising single drug for the treatment of acute nonlymphoblastic leukemia and possibly for acute lymphoblastic leukemia.
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PMID:Mitoxantrone in the treatment of relapsed and refractory acute leukemia. 638 65

Gangliosides from normal leukocytes and the cells of 25 patients with acute and chronic leukemia were tested for the presence of the disialoganglioside II3-alpha-N-acetylneuraminosyl-alpha 2----8-N-acetylneuraminosyllactosylceramide (GD3). GD3 was detected by immunostaining thin-layer chromatographs with an anti-GD3 monoclonal antibody (AbR24). Among the myeloid cells tested, acute leukemia cells were positive for GD3, whereas chronic leukemia cells and normal neutrophils did not have detectable GD3. A range of GD3 reactivity was apparent within the acute myeloid leukemia cells; gangliosides from pure myeloid leukemia cells stained more intensely than those from leukemia cells with monocytic characteristics. All lymphocytic leukemia cells (chronic and acute) contained GD3, but this ganglioside could not be detected in extracts from normal lymphocytes. A ganglioside extract from the cells of a patient with hairy cell leukemia was also positive for GD3 immunostaining. These results demonstrate that normal leukocytes and chronic myelogenous leukemia cells are distinguished from other lymphoid and nonlymphoid leukemia cells on the basis of GD3 ganglioside expression.
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PMID:Differential expression of ganglioside GD3 by human leukocytes and leukemia cells. 648 84

We reviewed 4 gastrectomized cases associated with chronic leukemia. Three patients had chronic myelogenous leukemia, one had hairy cell leukemia. Subtotal gastrectomy was performed in all cases; two operations were for gastric cancer and two for bleeding gastric ulcers. The spleen was removed in three patients without any trouble. There were no difficulties in managing the patients during and after surgery and their leukemia was not aggravated during these periods.
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PMID:[Four gastrectomized cases associated with chronic leukemia]. 658 35

Monoclonal antibody T305, prepared by immunizing mice with the T-ALL derived cell line RPMI-8402, immunoprecipitates a single chain glycoprotein with m.w. 160,000 daltons (under reducing conditions) or 180,000 daltons (under nonreducing conditions). In immunofluorescence assays, antibody T305 reacted with a subpopulation of T cells in normal blood (22 +/- 6%), thymus (28 +/- 11%), and lymph node (24 +/- 6%). Increased frequency of T cells reactive with antibody T305 was found in peripheral blood of patients with infectious mononucleosis (greater than 80%), graft-vs-host disease after bone marrow transplantation (65 +/- 11%), acquired immunodeficiency syndrome (53 +/- 12%). The T cells in synovial fluid of patients with rheumatoid arthritis had increased frequency of antibody T305 reactive cells (59 +/- 8%) as compared to their peripheral blood (18 +/- 7%). Two color immunofluorescent studies demonstrated that the T305+ T cells predominantly co-stained with antibody Leu 2a (suppressor/cytotoxic subset) in both normals and disease state blood. After cell sorting to obtain T305+ and T305- subpopulations, we demonstrated that a) natural killer and antibody-dependent cellular cytotoxicity activity in normal blood was in the T305+ but not T305- T cells; b) cytotoxic T cells induced by mixed lymphocyte reaction were predominantly T305+; c) T305- T cells could be induced in vitro to express T305 antigen by mitogens or allogeneic B cells; d) the DNA content of T305+ and T305- T cells in normal blood was similar (greater 95% of cells with G0/G1 level); e) after mitogen stimulation, T305 antigen induction on previously T305- cells occurs before S-phase; and f) significantly more [3H]-thymidine after mitogen stimulation was incorporated by originally T305- cells than by originally T305+ cells (p less than 0.001). The T305 antigen was not restricted to T cells because it was also found on myeloid precursors in bone marrow but was not present on polymorphonuclear leukocytes, red blood cells, platelets, muscle, liver, skin, kidney, lung, or brain. Antibody T305 was found on 24/25 cases of acute leukemia (6 T-ALL, 10/11 cALL, 7 AML, and 1 AMOL) but not on 18 cases of chronic leukemia (B-CLL, T-CLL, null CLL, CML). The importance of the T305 antigen is that it is present on a high number of T cells in certain autoimmune diseases and on virtually all acute leukemia cells. Its distribution on immature and in vitro activated cells suggests that it may represent a receptor for signals related to cellular replication or differentiation.
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PMID:A novel cell surface antigen (T305) found in increased frequency on acute leukemia cells and in autoimmune disease states. 660 45

The effects of bestatin was studied in 17 patients with acute and chronic leukemia, and three patients with malignant lymphoma with or without concomitant chemotherapy. Complete remission was obtained in eight patients with acute leukemia and in three patients with malignant lymphoma. Definite effects on both clinical and hematological findings have not been observed in patients with chronic myelogenous leukemia. The PPD and PHA skin reactions increased in about 60 percent of the patients examined. Effects of bestatin on hematological and immunological parameters were obtained at a daily dose of from 30 to 90 mg of bestatin everyday for more than 2 weeks. Bestatin appeared to be useful for the maintenance therapy of hematological malignancies. No side effects due to bestatin were detected.
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PMID:The effect of bestatin on patients with acute and chronic leukemia and malignant lymphoma. 693 Jan 19

We have established optimal conditions for the measurement of glucocorticoid receptors (GR) in human white cells using a whole-cell binding assay with [3H]dexamethasone as the ligand, and the subsequent determination of the GR content in normal human lymphocytes and in leukemic cells of patients with various forms of acute and chronic leukemia. A number of leukemia cell lines in continuous culture were also subjected to the GR assay, and the results were correlated with the sensitivity of these cell lines to glucocorticoid steroids in vitro. The GR content of normal human lymphocytes amounted to 4,850 +/- 1,340 (mean +/- SD) receptors/cell. The mean equilibrium dissociation constant (KD) of the interaction of [3H]dexamethasone with the GR was 1.2 x 10(-8) M. Steroidal compounds with a known glucocorticoid potency effectively competed for the binding, whereas steroids devoid of glucocorticoid activity (e.g. estradiol-17 beta and testosterone) were ineffective. The GR content of the blast cells obtained from eight patients suffering from acute leukemia and four patients with a blast crisis of chronic myelocytic leukemia was found to be highly variable (3,230-29,900 receptors/cell), while the lymphocytes of six patients with chronic lymphatic leukemia contained a rather stable GR content (2,930-5,120 receptors/cell), which was comparable with that of normal lymphocytes. GR was identified in all the 12 malignant continuous white cell lines studied. Large cells contained more GR than the smaller ones. There was no apparent correlation between the GR concentration and the sensitivity of the cells in vitro to glucocorticoids as judged by [3H]thymidine incorporation studies. Distribution of the surface markers in the leukemic cell lines did not relate to the GR concentration. We conclude that the presence of GR is probably a universal feature of the leukemic cells, and, from a clinical standpoint, probably does not alone imply steroid responsiveness.
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PMID:Glucocorticoid receptors and glucocorticoid sensitivity of human leukemic cells. 693 48

Contrarily to what happens in acute leukemia, the incidence of osteolytic lesions in chronic leukemia is exceedingly low. Three patients with chronic myeloid leukemia (CML) who developed such lesions during the chronic phase of their disease form the basis of this report. Osteolytic lesions appearing during the chronic phase of CML are different from those appearing during acute leukemia or during the acute terminal phase of CML, and the differences between both types of osteolysis are briefly reviewed. In the present cases the appearance of osteolytic lesions during the chronic phase of CML preceded for a variable period the terminal acute blastic phase. Therefore this complication must be considered as a sign of poor prognosis as it relates to the subsequent course of the leukemia. Even though other authors advise local radiotherapy as the treatment of choice of osteolytic lesions, only cytostatic therapy was given to the present patients, with good results as it regards the lesions per se.
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PMID:[Osteolytic lesions in chronic myeloid leukemia. Report of three cases (author's transl)]. 694 4

Chromosome identification techniques have shown the non-random nature of cytogenetic changes in leukemia. In addition, they have identified structural chromosome abnormalities occurring in specific types of acute leukemia as classified by the FAB criteria. Such cytogenetic sub groups are associated with differing prognoses. In acute lymphocytic leukemia, even the ploidy of the leukemic cells appears important in predicting prognosis. Identification of the Philadelphia (Ph1) chromosome has diagnostic significance in chronic granulocytic leukemia. This makes possible the classification of patients into Ph1 + and Ph1 - varieties which have different responses to therapy. Similar variations are found between the 2 groups of patients who do or do not develop additional abnormalities with blastic transformation. The implication of these findings in both acute and chronic leukemia may influence choice of therapy in the future.
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PMID:3. The value of chromosome studies in the classification and management of the leukemias. 695 40

Over the past ten years several centers have studied bone marrow transplantation following high-dose chemotherapy and radiation in patients with resistant acute leukemia. These data indicate a 10-20% two-year disease-free survival; results superior to alternative approaches. Leukemic relapse and graft-versus-host disease have been major problems. Recently, marrow transplantation has been evaluated in patients with leukemia in remission. This has resulted in improved survival in patients with acute lymphoblastic leukemia but leukemic relapse remains a major problem. Acute myelogenous leukemia patients transplanted in remission have a low rate of leukemic relapse and two-year disease-free survival rates exceeding 50%. Recently, autologous bone marrow transplantation has also been considered in patients with acute leukemia. Results to date have been disappointing with a high relapse rate. Limited studies in patients with chronic myelogenous leukemia have also been reported. Transplantation during the acute phase is usually unsuccessful and is complicated by incomplete engraftment and resistant leukemia. Transplants performed during the chronic phase have produced more encouraging results. In summary: there is an evolving role for bone marrow transplantation in the treatment of patients with acute and chronic leukemia. A final evaluation of the utility approach awaits results of controlled clinical trials.
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PMID:Bone marrow transplantation in leukemia. 703 88


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