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

A novel human myeloid leukemia cell line, NKM-1, was established from a patient with acute myeloid leukemia (FAB classification M2). The cells were positive for myeloperoxidase staining and cluster of differentiation 15 cell surface antigen. Radiolabeled recombinant human granulocyte (G) colony-stimulating factor (CSF) was used, and 60 specific binding sites/cell with a Kd 100 pmol/liter were demonstrated on the cell surface. 125I-G-CSF binding was not inhibited by interleukin-3, granulocyte-macrophage CSF, or macrophage (M) CSF. NKM-1 cells also expressed M-CSF receptors detected by c-fms mRNA expression. In concordance with the receptor expression, NKM-1 cells proliferated in response to exogenous G-CSF or M-CSF in a dose-dependent manner (0.1-100 ng/ml), while interleukin-3 or granulocyte-macrophage CSF had no effect. Colony-forming capacity of NKM-1 cells in semisolid agar was also enhanced with the addition of 10 ng/ml of G-CSF or M-CSF but decreased at higher concentrations. During CSF stimulation, no remarkable changes were observed morphologically and phenotypically. The stimulatory effect of G-CSF and M-CSF on the cell growth was additive. Neither G-CSF-binding capacity nor c-fms mRNA expression was altered by pretreatment with M-CSF or G-CSF, respectively. This cell line may provide a useful in vitro model for the study of CSF roles in myeloid leukemia cell proliferation.
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PMID:A novel human myeloid leukemia cell line, NKM-1, coexpressing granulocyte colony-stimulating factor receptors and macrophage colony-stimulating factor receptors. 170 53

Human granulocyte colony-stimulating factor (G-CSF) receptors on human acute leukemia cells were investigated using human G-CSF iodolabeled by the lactoperoxidase method. Among various human leukemic cell lines, only cells of myelogenous lineage including HL-60, THP-1 and U937 had one type of high-affinity receptor for G-CSF, as shown by Scatchard analysis. Fresh leukemia cells from 19 patients with acute myelogenous leukemia (AML) were then studied. Specific receptors for G-CSF were demonstrated on blast cells in all 19 cases, the mean number of G-CSF receptors per AML cell ranging from 95 to 1436. G-CSF receptors on AML cells appeared to be a single affinity type, although some variations were observed. The mean number of G-CSF receptors on leukemic cells from patients with either FAB M3 or FAB M2 was greater than that of cells from patients with M1 (p less than 0.01, p less than 0.10, respectively). Moreover, the mean number of receptors for G-CSF on CD13- and CD34-positive AML cells was higher than that on CD13-negative and CD34-positive AML cells (p less than 0.01), and the mean number of G-CSF receptors on CD7-positive AML cells was lower than that for CD7-negative AML cells (p less than 0.10). Since the FAB classification and surface phenotypes reflect maturation stages, our findings indicate that the distribution of G-CSF receptors, even on AML cells, may be related to the maturation process.
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PMID:Human granulocyte colony-stimulating factor receptors in acute myelogenous leukemia. 170 27

Cytogenetic examination of bone marrow cells was performed in 43 patients with myelodysplastic syndrome (MDS). MDS was diagnosed from bone marrow biopsies and smears according to the FAB classification. Of all 43 patients 24 (56%) had clonal karyotype changes including frequently monosomies of chromosomes #5 and #7 as well as interstitial deletions of the long arm of #5, 5 q-. Chromosome aberrations were observed in patients belonging to all FAB-subgroups, e.g. 11/15 patients with RA, 6/10 with RAEB, 5/9 with RAEB/T, and 1/9 with CMMoL. Complex chromosome aberrations involving more than 2 chromosomes occurred predominantly in patients with RAEB/T (4/9) but also in patients with RA (2/15) and RAEB (2/10), and correlated significantly (p less than 0.002) with a shorter survival. No correlation was found between chromosome aberrations and the development of ANLL in 9/43 patients (21%).
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PMID:[Cytogenetic examination of bone marrow cells in stem cell diseases of myelodysplastic syndromes]. 170 72

In a retrospective study, 45 (19.4%) out of 232 patients with MDS revealed myelosclerosis (MS) in bone marrow biopsy (BMB). Histological classification according to FAB criteria showed the following distribution: RA 21 (47%), RARS 1 (2%), RAEB 9 (20%), RAEB-T 3 (7%), and CMMol 11 (24%). Sclerosis occurred in all subtypes of MDS, but with a higher incidence in CMMol. Clinical data showed lower values of hemoglobin and lower platelet counts in MDS.MS. Life expectancy was reduced to 7.8 months, compared with 15.0 months in MDS without MS (p = 0.0026). In RA, the survival times were 9.7 months in MDS.MS, compared to 27.9 months in MDS without MS (p = 0.0035). 21 (47%) of the patients with MDS.MS experienced a transformation into ANLL. Myelosclerosis therefore seems to herald a bad prognosis.
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PMID:[Myelosclerosis in myelodysplastic syndromes (MDS). Retrospective analysis of 232 patients with MDS]. 170 73

The expression of adhesion molecules on blasts from 14 patients with acute myeloid leukemia (AML) was investigated by immunofluorescence and flow cytofluorometry. All tested blast populations expressed CD18/CD11a complex [leukocyte function antigen-1 (LFA-1)] and CD29 (very-late antigen (VLA)) and the majority were positive for CD54 [intercellular adhesion molecule-1 (ICAM-1), 78.6%] and CD56 [neural cell adhesion molecule (NCAM), 64.3%]. The expression of two other alpha chains of CD18/CD11b and CD11c varied considerably (64.3% and 42.8% of positive cases, respectively). Only one case (AML-M4) showed a weak expression of the activated platelet antigen CD41b. None of the tested blasts expressed the vitronectin receptor (CD61/CD51). No significant correlation between the expression of adhesion molecules and the FAB type of leukemia could be found. All tested blast populations were completely resistant to NK-mediated cytotoxicity and relatively resistant to LAK-mediated cytotoxicity in the standard 51Cr release assay. While no statistically significant correlation of the results in cytotoxicity assays with the expression of adhesion molecules or the expression of HLA-DR antigen could be observed, 2 out of 3 completely resistant cases lacked ICAM-1. These results show that even leukemic blasts which express all of the tested adhesion molecules can still be resistant to LAK-mediated cytotoxicity.
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PMID:Resistance of leukemic blasts to lymphokine activated killer (LAK)-mediated cytotoxicity is not related to their adhesion properties. 171 15

An allogenic bone marrow transplantation (BMT) in an acute nonlymphocytic leukemia (ANLL) patient with post-transfusion hepatitis C is presented. A 13-year-old girl was admitted to our hospital on May 1988, and diagnosed as having ANLL M2 according to the FAB classification. During the induction and post-induction chemotherapy, 116 units of blood products were transfused to her as the supportive therapy until October 1988, when non-A non-B hepatitis developed. As the persistent liver dysfunction interfered with anti-leukemic chemotherapy on the protocol, allogeneic BMT from her HLA identical MLR nonreactive brother was done on July 1989. Preconditioning regimen consisted of busulfan and cyclophosphamide. GVHD prophylaxis consisted of cyclosporine A and short term methotrexate. After the BMT, her liver dysfunction once improved; her serum amino-transferase levels were normal for about 3 months. Soon after discontinuation of cyclosporine A, however, her liver function deteriorated again. The examination of hepatitis C virus antibody in her sera, which had been harvested sequentially and stored at -40 degrees C, on November 1989 revealed that she had been already seropositive at the time of BMT. The BMT-induced immunologic changes may have influenced the natural course of hepatitis C virus infection in the patient.
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PMID:[Bone marrow transplantation in a pediatric case of acute nonlymphocytic leukemia with hepatitis C]. 171 55

A translocation involving the short arm of chromosome 2 and the long arm of chromosome 4 is described in three patients, all of whom had acute nonlymphocytic leukemia (M2). One patient had M2 de novo, one progressed from refractory anemia with excess blasts in transformation to M2 over a 4-month period, and one had had sideroblastic anemia 30 years prior to development of M2. In all three patients, the translocation involved the breakpoint p23 on chromosome 2, but the breakpoints on chromosome 4 varied between q25, q31, and q35. Translocations specifically involving 2p23 have not previously been described in leukemia, but more cases are required to identify a specific association with either the FAB type or prognosis.
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PMID:Novel translocation (2;4) with consistent involvement of 2p23 in acute nonlymphocytic leukemia (M2). 172 49

A murine monoclonal antibody against human lysozyme (AHL MoAb) was produced and tested on normal and leukemic monocytes using flow cytometry. The antibody gave a positive reactivity on normal monocytes permeabilized by saponin (82% to 98% of positive cells) and a negative reactivity on normal permeabilized neutrophils. This monocyte-specific reactivity had not been observed using a polyclonal antibody. Nevertheless, immunoblotting detected lysozyme in both monocyte and polymorphonuclear leukocyte (PMNL) lysates. The AHL MoAb, in the presence of lysozyme substrate (Micrococcus lysodeikticus cell walls), strongly inhibited the enzymatic activity. Flow cytometric analysis of leukemic cells isolated from patients suffering from different subtypes of acute myeloid leukemia (French-American-British [FAB] classification FAB M1-5) showed a highly significant positivity of FAB M5 for lysozyme compared with the other subtypes. The present results were consistent with the detection of a lysozyme epitope by AHL MoAb located near the catalytic site in monocytes. The same epitope was probably masked in PMNL granules.
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PMID:Specific detection of monocytic lysozyme within normal and leukemic cells. 173 14

This is a review of preleukaemic states in children. In a prospective series of 109 children with AML the overt disease was preceded by MDS in 22 cases. Ten of these patients had Down's syndrome. Advanced FAB groups were represented in the series. An important subgroup is the bone marrow monosomy 7 syndrome. Cytogenetic anomalies are common in MDS, and multiple and complicated abnormalities develop in nearly all patients with progressing disease. Some children die before transformation to overt ANLL. Transformation usually occurs, few children survive. With cytostatic treatment the risk of irreversible aplasia is great. The choice of schedule should therefore be carefully considered. Bone marrow transplantation has proved beneficial in a number of cases, but these are still quite few. The dysfunction of the bone marrow preceding ALL is due to transient aplastic anaemia--spontaneous remission--overt ALL, often FAB type L1, immunophenotype CALLA. The ALL reacts to the same treatment as de novo ALL of the same type and the prognosis is the same.
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PMID:Bone marrow dysfunctions preceding acute leukemia in children: a clinical study. 173 77

In an attempt to identify prognostic factors for survival and leukemic transformation, 235 untreated patients with primary myelodysplastic syndromes (MDS) were analyzed in a single center retrospective study. To the well known FAB classification of MDS a supplementary group of patients with pure sideroblastic anemia (PSA) was added, characterized by the absence of dysplastic features of non-erythroid cells. Accordingly, the morphological subtypes were refractory anemia (RA), n = 55; PSA, n = 40; RA with ring sideroblasts (RARS), n = 33; RA with excess of blasts (RAEB), n = 53; RAEB in transformation (RAEB/T) n = 29; and chronic myelomonocytic leukemia (CMML), n = 25. Having screened 28 clinical, cytological, and laboratory parameters by univariate analysis, multiple regression analysis identified six variables with independent prognostic value: percentage of bone marrow blasts, serum LDH activity, PSA, hemoglobin concentration, age, and platelet count. If patients with PSA were excluded, the FAB classification no longer contributed independent prognostic information. Based on the results of this multivariate analysis, a simple scoring system was devised for predicting the survival of patients with MDS. A score of unity was allocated to each of the following parameters: bone marrow blasts greater than or equal to 5%, LDH greater than 200 U/I, hemoglobin less than or equal to 9 g/dl, and platelets less than or equal to 100 x 10(9)/I. As a function of their total score, patients were divided into three risk groups (group A, score 0; group B, score 1-2; group C, score 3-4), which differed significantly in both survival and rates of leukemic transformation. The cumulative survival 2 years after diagnosis was 91% in group A, 52% in group B, and 9% in group C (p less than 0.00005). The actuarial risk of transformation to acute myeloid leukemia at 2 years was 0, 19, and 54%, respectively (p less than 0.05). The inclusion of LDH enzyme levels qualified this scoring system for an accurate assessment of patients with CMML whose prognosis is viewed too favorably when rated by other scores. Furthermore, this score was able to identify those patients with RA and RARS who, without showing an excess of marrow blasts, have an unfavorable prognosis.
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PMID:Primary myelodysplastic syndromes: analysis of prognostic factors in 235 patients and proposals for an improved scoring system. 173 14


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