Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023467 (acute myeloid leukemia)
 35,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Daunorubicin uptake and metabolism were studied in vitro with human myeloid leukemia cell lines (KG1, ML1); erythroleukemia cell line (K562); and myeloblasts from two untreated patients with acute myelogenous leukemia (AML). Uptake of daunorubicin by all the above was very similar, but metabolism of daunorubicin to daunorubicinol and the levels of reductase activity were extremely variable. We believe that this heterogeneity accurately reflects the in vivo situation in humans with acute leukemia. In vivo anthracyclines are subject to extensive metabolism, and the majority of patients do metabolize the drug to some extent; it is important, therefore, to use cell lines that reflect the in vivo metabolism. Conversely, rodent cell lines, which apparently lack one of the two major classes of daunorubicin reductase and do not appreciably metabolize daunorubicin, appear to be inadequate as models for studies designed to evaluate the enzymatic mechanisms of daunorubicin metabolism.
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PMID:Uptake and metabolism of daunorubicin by human myelocytic cells. 389 Nov 21

Micronomicin (MCR) at a daily dose of 120 to 360 mg was administered to patients with severe infections who had hematopoietic disorders as underlying diseases. Efficacy and safety of the drug were evaluated. The underlying diseases in the 56 patients included in the evaluation of efficacy were acute myelocytic leukemia (24 cases), acute lymphocytic leukemia (8), acute promyelocytic leukemia (6), acute monomyelocytic leukemia (4), acute monocytic leukemia (1), erythroleukemia (1), chronic myelocytic leukemia-blastic crisis (4), malignant lymphoma (3), aplastic anemia (2), and others (3). The infections were septicemia in 9 patients, suspected septicemia in 48, respiratory tract infection in 7, and perianal abscess in 2. The clinical efficacy of MCR was 'excellent' in 12 patients, 'good' in 17, 'fair' in 7, 'poor' in 30 for an efficacy rate of 43.9%. The efficacy rate classified according to infections was 22.2% in septicemia, 56.3% in suspected septicemia. The organisms isolated from the patients with septicemia were Escherichia coli in 2, Klebsiella pneumoniae in 2, Pseudomonas aeruginosa in 1, alpha-Streptococcus in 1, Serratia marcescens in 1, and Acinetobacter sp. in 1. The efficacy rate was 15.4% in the 13 patients whose causative organisms were identified. The efficacy rate for patients who had failed to respond to prior antibiotic therapy was 43.9%. The efficacy rate in patients (34 cases) with an initial neutrophil count less than 100/microliter was 44.1%. Side effect which might have been caused by MCR was skin eruption in only one episode among 83 episodes those were evaluated for safety.
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PMID:[Therapeutic effects of micronomicin against severe infections in patients with hematopoietic disorders. Hanshin Infection Study Group]. 390 33

It is a generally accepted principle of radiation biology that hematopoietic progenitor cells demonstrate dose rate independent killing by x-irradiation over the clinically relevant range for total body irradiation (TBI) (5-25 rad/min). To determine whether low dose rate (5 rad/min, or 20 rad/min) compared to conventional dose rate (200 rad/min) x-irradiation altered the clonagenic survival of leukemia and lymphoma cell lines, several permanent cell lines were studied. These included: bg/bg cl 1, mouse basophillic leukemia; LW12, [W/fu rat acute myelogenous leukemia (AML)]; and human cell lines: JY and Daudi (B-cell lymphomas); K45, (T-cell leukemia); K562, (erythroleukemia); HL60 and KG1 (monomyeloid leukemias), and U937 (human histiocytic/monocytic lymphoma). Dose rate independent killing was demonstrated at several plating densities with mouse and rat leukemia lines and all human leukemia lines tested except lines HL60 and U937. With HL60, increased plating density increased the D0 at each dose rate. This effect was not attributable to an increased plating efficiency. With line U937 there was a clear dose-rate effect with increase in D0 from 88 rad, n 4.6 at 200 rad/min, to D0 = 166, n 2.3 at 5 rad/min. The data demonstrate that some human hematopoietic tumor derived cell lines of myeloid/monocyte/macrophage lineage can exhibit atypical repair of irradiation damage in vitro. This repair may be enhanced by conditions relevant to clinical TBI including low irradiation dose-rate and cell to cell interactions by tumor cells in close proximity.
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PMID:Effect of X-irradiation dose rate on the clonagenic survival of human and experimental animal hematopoietic tumor cell lines: evidence for heterogeneity. 394 94

The clinical, hematologic, and histological characteristics of two patients who progressed from refractory anemia to acute leukemia are described. When first studied, nuclear bridging of erythroblasts, similar to that seen in congenital dyserythropoietic anemia type I and megakaryocytic dysplasia, were the only abnormalities. Within 6 years, both patients died, the first of acute nonlymphocytic leukemia, the second of erythroleukemia. Nuclear bridging of erythroblasts in the marrow of these patients was an early and transient phenomenon and was not observed during the terminal phase of leukemia.
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PMID:Nuclear bridging of erythroblasts in acquired dyserythropoiesis: an early and transient preleukemic marker. 394 11

The bone marrow biopsy specimens of 35 patients with benign and malignant erythroid hyperplasias were examined for the presence of hemoglobin A, hemoglobin F, muramidase (lysozyme), and transferrin, using an indirect immunoperoxidase method (PAP) on Zenker's-fixed paraffin-embedded bone marrow biopsy specimens and particles. Five cases of each of the following entities were studied: erythroleukemia and erythremic myelosis, acute granulocytic leukemia with maturation (FAB M2), polycythemia rubra vera, myeloproliferative syndrome in childhood, megaloblastic anemia (B12 and folate deficiency), erythroid hyperplasia (regenerating bone marrow and hemolytic anemia), and Ph' chromosome positive chronic granulocytic leukemia. Hemoglobin A was present in both the early and late erythroid precursors in all conditions. Hemoglobin F was the predominant hemoglobin in early erythroblasts of pernicious anemia and in both early and late erythroid elements in erythroleukemia and erythremic myelosis. Small quantities of hemoglobin F were present in a few isolated clusters in other conditions. Staining for hemoglobin F may be useful in identifying immature erythroid precursors and in distinguishing some cases of dysplastic erythroid hyperplasia from neoplasia. Additionally, these findings suggest that the maturational switch in hemoglobin synthesis operates with distinct pathways under different conditions.
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PMID:An immunohistochemical study of hemoglobin A, hemoglobin F, muramidase, and transferrin in erythroid hyperplasia and neoplasia. 619 99

Freshly isolated human leukemia cells have been shown in the past to display varying in vitro responses to phorbol diesters, depending on their cell type. Specific receptors for the phorbol diesters have been demonstrated on numerous different cells. This study was designed to characterize the receptors for phorbol diesters on leukemia cells freshly isolated from patients with different kinds of leukemia and to determine if differences in binding characteristics for tritium-labeled phorbol 12,13-dibutyrate (3H-PDBu) accounted for the different cellular responses elicited in vitro by phorbol diesters. Cells from 26 patients with different kinds of leukemia were studied. PDBu or phorbol 12-myristate 13-acetate (PMA) caused cells from patients with acute myeloblastic leukemia (AML), acute promyelocytic (APML), acute myelomonocytic (AMML), acute monocytic (AMoL), acute erythroleukemia (AEL), chronic myelocytic leukemia (CML) in blast crisis (myeloid), acute undifferentiated leukemia (AUL), and hairy cell leukemia (HCL) (n = 15) to adhere to plastic and spread. However, they caused no adherence or spreading and only slight aggregation of cells from patients with acute lymphocytic leukemia (ALL), chronic lymphocytic leukemia (CLL), or CML-blast crisis (lymphoid) (n = 11). All leukemia cells studied, irrespective of cellular type, displayed specific receptors for 3H-PDBu. The time courses for binding by all leukemia types were similar, with peak binding at 5-10 min at 37 degrees C and 120 min at 4 degrees C. The binding affinities were similar for patients with ALL (96 +/- 32 nM, n = 4), CLL (126 +/- 32 nM, n = 6), and acute nonlymphoid leukemia (73 +/- 14 nM, n = 11). Likewise, the numbers of specific binding sites/cell were comparable for the patients with ALL (6.2 +/- 1.3 X 10(5) sites/cell, n = 4), CLL (5.0 +/- 2.0 X 10(5) sites/cell, n = 6), and acute nonlymphoid leukemia (4.4 +/- 1.9 X 10(5) sites/cell, n = 11). Thus, the differing responses to phorbol diesters of various types of freshly isolated leukemia cells appear to be due to differences other than initial ligand-receptor binding.
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PMID:Specific receptors for phorbol diesters on freshly isolated human myeloid and lymphoid leukemia cells: comparable binding characteristics despite different cellular responses. 631 66

Five out of 110 patients with acute myeloid leukemia (AML) showed double minutes (DM) in cytogenetic preparations. DM were found to occur predominantly in elderly patients, and in erythroleukemia or acute myelomonocytic leukemia. The five patients were apparently divided into two groups according to the number of DM per cell. Patients with few sets of DM had exclusively complex karyotypes and a poor prognosis while patients with numerous DM had otherwise normal or nearly normal karyotypes and a good prognosis. Data on 11 previously reported cases of AML with DM were collected from the literature and consistent results were revealed except that several of the 11 patients were diagnosed as having acute myeloblastic leukemia (M1 and M2 in the FAB classification), which is apparently due to differences in diagnostic criteria. Therefore, numerous or few DM in a cell might relate to different entities. When the number of DM was small they might have resulted from breakdown of existing chromosomes.
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PMID:Double minutes in acute myeloid leukemia. 635 19

Polar organic compounds, such as dimethylsulfoxide and butyric acid, are known to induce differentiation in Friend erythroleukemia cells as well as in other cell types. It has been found that many of the compounds that induce cellular differentiation, inhibit 3H-thymidine incorporation and induce cell damage when incubated with leukemic cells from patients with acute or chronic myelogenous or acute lymphocytic leukemia. These effects are time and dose dependent. Among the compounds tested, butyrate was the most potent. Parenteral administration of butyrate (500 mg/kg/day) for ten days to a child with acute myelogenous leukemia in relapse, and resistant to conventional therapy, resulted in elimination of myeloblasts from the peripheral blood, an increase in mature myeloid cells and a reduction in 3H-thymidine uptake by the patient's peripheral blood cells. Bone marrow myeloblasts were reduced from 70-80% to 20% following the course of intravenous butyrate. No impairment of liver or renal function and no coagulation abnormalities were observed during butyrate treatment. Organic agents that induce cell differentiation may provide additional reagents for the clinical management of selected cases of leukemia.
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PMID:Effect of polar organic compounds on leukemic cells. Butyrate-induced partial remission of acute myelogenous leukemia in a child. 657 94

A monoclonal antibody (LICR.LON.R10) specific for the major sialoglycoprotein of the erythroid cell membrane, glycophorin A (alpha), has been used to test the possibility that "cryptic" erythroleukemia may be diagnosed as acute lymphoblastic leukemia (ALL) or acute myeloblastic leukemia (AML). In addition to 27 overt erythroleukemias, 724 leukemias, including 329 ALL (103 in relapse), 205 AML, and 109 blast crises of Ph1-positive chronic myeloid leukemia, were analyzed. Twenty cases with a significant proportion of glycophorin-A-positive (gA+) cells were found; 8 of these (5 AML and 3 blast crises of chronic myeloid leukemia, CML) had an obvious erythroid component, but 12 others were diagnosed as AML (2), AMML (1), CML in myeloid blast crisis (4) or megakaryoblastic blast crisis (1), acute megakaryoblastic leukemia (2), or acute lymphoblastic leukemia (2). The latter two patients had no immunologic evidence supporting a diagnosis of ALL and were resistant to chemotherapy. We conclude that AML and ALL only very rarely express gA, and these are probably genuine "cryptic" erythroleukemias. Other gA+ leukemias (megakaryoblastic and CML blast crises) may arise from bi- or pluripotent stem cells and contain distinct and separable blast cell populations.
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PMID:Monoclonal antiglycophorin as a probe for erythroleukemias. 657 33

The introduction of the anthracycline antibiotics and cytosine arabinoside have significantly improved the remission induction rate for patients with acute nonlymphocytic leukemia. Erythroleukemia (M6 by French-American-British classification) has long been considered to be resistant to chemotherapy. Since 1973 we have treated 14 patients with erythroleukemia with daunorubicin 45 mg/m2 or doxorubicin 30 mg/m2 for three days and cytosine arabinoside 100 mg/m2 by continuous infusion for 7 to 10 days. Six complete remissions (43%) were obtained with remission durations of 3+, 4+, 9, 13, 29+, and 35 months. While this remission rate is somewhat lower than that obtained with other types of acute nonlymphocytic leukemia, the combination of anthracycline antibiotics and cytosine arabinoside is clearly effective against erythroleukemia. Five patients treated before mid 1976 died soon after remission induction therapy was started. Four of these five patients were treated for 6 to 9 months with prednisone, halotestin, and/or splenectomy before remission induction chemotherapy was started and three of these patients died of systemic fungal infection, suggesting that these modalities of treatment may interfere with patient tolerance to remission induction therapy. It is suggested that erythroleukemia should be treated with intensive chemotherapy soon after the diagnosis is made.
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PMID:Treatment of erythroleukemia with anthracycline antibiotics and cytosine arabinoside. 657 41


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