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)

Four monoclonal antibodies against human erythrocyte membrane antigens were established. The antigenic determinants of KOR-E1, E3, E6 were Pr1h antigen, Wrb antigen, and the trypsin sensitive portion of glycophorin A (EnaTS) respectively. The antigen recognized by KOR-E4 could not be determined. The reactivities of these antibodies with normal hematopoietic cells, malignant hematopoietic cell lines (N = 31), and fresh leukemic cells obtained from 128 patients with various types of leukemias were studied. All antibodies reacted only with erythrocytes among peripheral blood cells, and also KOR-E6 reacted only with erythroid cells among bone marrow cells. KOR-E3 had no reactivity with any cell lines examined, and KOR-E1 and KOR-E4 were reactive with some lymphoid cell lines. However, KOR-E6 had specific reactivities with erythroid (HEL, K562), megakaryocytic (CMK-1), multiphenotypic (KOPM-28), and basophilic (KU-812) cell lines. The antigen (glycophorin A) recognized by KOR-E6 was expressed on a small population of mononuclear cells separated from acute lymphoblastic leukemia (3/70), acute myelogenous leukemia (2/12), monosomy 7-myeloproliferative disorder (1/1), juvenile CML (1/1), and transient myeloproliferative disorder with Down's syndrome (4/12), although it could not be determined whether these cells were leukemic cells or not. KOR-E6 was reactive with a large population of leukemic blasts in erythroleukemia (2/2) and acute megakaryoblastic leukemia (3/6). Thus, KOR-E6 appears to be an erythroid marker of leukemic cells.
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PMID:[Monoclonal antibodies against human erythrocyte membrane antigens and their reactivities with hematopoietic cells]. 261 36

We report a lethal case of congenital erythroleukemia presenting on the first day of life with peripheral blast cells and a leukemic infiltrate in the placenta. Although initial bone marrow examination did not fulfill the French-American-British (FAB) cooperative group criteria for acute myelogenous leukemia (AML), including M6, a malignant clone was confirmed by cytogenetic analysis: 49,XX, +8, +19, +21. Evolution to erythroleukemia (M6) occurred over a two-month period. The diagnosis of erythroleukemia was supported by immunophenotyping employing an antibody to glycophorin A. The clinical course was complicated by liver failure of unknown etiology. Comparison to previously reported cases of early childhood erythroleukemia is made.
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PMID:Congenital erythroleukemia: a case report with morphological, immunophenotypic, and cytogenetic findings. 266 May 43

Previously we showed that starvation of HL-60 promyelocytic leukemia cells for a single essential amino acid induced irreversible differentiation into more mature monocyte-like cells. Although not an essential amino acid, glutamine is important in the growth of normal and neoplastic cells. The glutamine analogue, alpha S,5S-alpha-amino-3-chloro-4,5-dihydro-5-isoxazoleacetic acid (acivicin) inhibits several glutamine-utilizing enzymes and therefore depletes cells of certain metabolic end products. The current study was designed to examine in vitro the effects of acivicin on growth and differentiation of several established human myeloid leukemia cell lines, including the HL-60 cell line, and of freshly isolated cells from patients with acute nonlymphocytic leukemia (ANLL). Four-day culture of HL-60 cells with acivicin at concentrations of 0.1 to 10.0 micrograms/mL (0.56 to 56 nmol/L) decreased cell growth by 33% to 88% as compared with untreated control cells. Viability of cells was greater than 92% for untreated cells and 93% to 41% for acivicin-treated cells. Cells treated with acivicin differentiated along a monocytic pathway as shown by increased H2O2 production and alpha-naphthyl butyrate esterase (NSE) content. Differentiation was time and dose dependent, and was irreversible. Changes in H2O2 production and NSE content were partially abrogated by co-culture with 10 mmol/L exogenous cytidine and guanosine but not by co-culture with other nucleosides or glutamine. At these concentrations of acivicin, differentiation was associated with expression of the N-formyl-methyl-leucyl-phenylalanine-receptor (FMLP-R) on 8% to 29% of cells as compared with 8% for control cells. Acivicin potentiated the differentiating effects of interferon-gamma, tumor necrosis factor, dihydroxyvitamin D3, dimethylsulfoxide, and retinoic acid. Culture of cells from the U937 (monoblastic), K562 (erythroleukemia), and KG-1 (myeloblastic) cell lines resulted in decreased growth and viability, but not consistently in differentiation. Acivicin decreased survival of freshly isolated ANLL cells and increased their H2O2 production and NSE content. These results suggest that the glutamine analogue acivicin may be useful as a differentiating agent with antileukemia activity in patients with ANLL.
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PMID:Monocytoid differentiation of freshly isolated human myeloid leukemia cells and HL-60 cells induced by the glutamine antagonist acivicin. 279 Jan 98

A panel of eight antibodies was used by the alkaline-phosphatase/anti-alkaline phosphatase (APAAP) method to stain peripheral blood films, bone marrow smears, and cytocentrifuge preparations from 29 cases of acute myeloid leukemia. These findings were correlated with the French-American-British (FAB) classification. Leukemic cells from six cases of myeloblastic leukemia (FAB;M1) were predominantly labeled by the antimyeloperoxidase monoclonal antibody (MPO-7). Leukemic cells from the majority of eight cases of myeloblastic leukemia with maturation (FAB;M2) and progranulocytic leukemia (FAB;M3) stained with monoclonal antibodies MPO-7, NP57 (anti-elastase), and EBM11 (antimonocyte/macrophage). Leukemic cells from six cases of myelomonocytic (FAB;M4) and five cases of monocytic (FAB;M5) leukemia were most often labeled with antibodies MPO-7, NP57, and EBM11 as well as monoclonal antibodies Y1/82A (anti-monocyte) and KB90 (against the p150, 95 molecule, CD11c; a monocyte/granulocyte marker), but not with monoclonal antibody C17 (antiglycoprotein IIb/IIIa) and/or monoclonal antibody Y2/51 (antiglycoprotein IIIa). Erythroblasts from a single case of erythroleukemia (FAB;M6) were not labeled with any of the antibodies from this panel. Leukemic cells from two cases of acute megakaryocytic leukemia (FAB;M7) stained strongly with the monoclonal antiglycoprotein IIIa/IIb antibody (C17) and antiglycoprotein IIIa antibody (Y2/51). Staining by the APAAP method with this panel of antibodies was easy to perform, required no expensive instrumentation, and provided useful information in the classification of acute myeloid leukemia.
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PMID:Immunophenotyping of acute myeloid leukemia by immuno-alkaline phosphatase (APAAP) labeling with a panel of antibodies. 282 1

Cytogenetic studies were done on the leukemia cells of two patients with small cell lung cancer (SCLC) who developed erythroleukemia (acute nonlymphocytic leukemia, French-American-British M6) after combined modality chemotherapy and radiotherapy for their lung cancer. Surprisingly, both erythroleukemias exhibited the del(3)(p14p23) predominantly found in SCLC. In four other patients who had secondary erythroleukemias associated with other cancers, no deletions of 3p were found. These findings could be accounted for by one of three possible mechanisms: (a) an inherited recessive gene (anti-oncogene or tumor suppressor gene) in this region of 3p was uncovered by the combined modality therapy, (b) an inherited predisposition to damage of both chromosomes at 3p14 leads to SCLC and erythroleukemia after exposure to carcinogens and/or chemotherapy-radiotherapy, or (c) the finding of lineage specificity for the 3p deletion with the presence of the 3p deletion in SCLC and erythroleukemia suggests a common bone marrow precursor.
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PMID:Deletion of 3(p14p23) in secondary erythroleukemia arising in long-term survivors of small cell lung cancer. 284 53

An IgG human-human monoclonal hybridoma antibody, AML-19, reactive with human myeloid cells of non-malignant and malignant origin has been produced by fusion of blood mononuclear cells from a patient with acute myeloid leukemia (AML) and the human B-lymphoma cell line RH-L4. The monoclonal antibody (MAb) AML-19 was purified from hybridoma supernatant by primarily anion-exchange chromatography, in order to separate the AML-19 MAb from contaminating immunoglobulin (Ig), e.g. bovine Ig and MAb derived from the parental fusion partner, and followed by immunoaffinity chromatography. This purification method gave the highest yield and purity of the AML-19 MAb. The isoelectric point (pI) of the MAb was estimated to be 5. Inhibition assays indicate an apparent dissociation constant (Kd) corresponding to 4 x 10(-9) M and an affinity constant (Ka) to 2.5 x 10(8)M-1 to K562 erythroleukemia cells. Scatchard plot demonstrated a linear slope as a manifestation of monoclonality and a low number of AML-19 specific epitopes, estimated to 1500 per cell.
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PMID:An approach for characterization and purification of a human monoclonal hybridoma antibody. 292 9

Chromosomal banding studies were performed on 10 patients diagnosed as having the M6 subtype of acute nonlymphocytic leukemia (erythroleukemia) according to the French-American-British (FAB) Cooperative Group criteria revised in 1985. Five patients had complex karyotypic abnormalities consisting of three or more defects, four of the five had deletion 7q, and three of the four had monosomy 5 or deletion 5q; the other five patients had normal karyotype. The patients of the former group had significantly higher white blood cell and blast cell counts in the peripheral blood and a higher serum lactate dehydrogenase level than the patients of the latter group. The progress of the disease in the former group was aggressive, resulting in a very poor prognosis. In contrast, the patients in the latter group had a relatively stable clinical course, resulting in a significantly longer survival. Furthermore, erythroblasts of all the patients with normal karyotype were negative or at most weakly positive to periodic acid-Schiff reaction, whereas the cells were strongly positive in three of five patients with complex defects. Accordingly, we suggest that M6 subtype is cytogenetically heterogeneous, and that chromosomal findings are a useful prognostic indicator of this disorder.
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PMID:Cytogenetic heterogeneity in erythroleukemia defined as M6 by the French-American-British (FAB) Cooperative Group criteria. 292 79

Surprisingly few cases of Down's syndrome with acute leukemia have been documented by chromosome banding studies of the leukemia cells. We studied a Down's syndrome child with acute myelomonocytic leukemia and found that, including this case, only 24 cases of Down's syndrome and acute leukemia have been reported with chromosome banding analysis. Twenty-three of the patients had a trisomy 21 chromosome complement, whereas, one had a translocation. The types of acute leukemia included acute myeloblastic leukemia, acute myelomonocytic leukemia, acute monoblastic leukemia, acute lymphoblastic leukemia, and erythroleukemia. Only three cases had chromosomes missing from the leukemic cells. Sixteen of the 24 patients had extra chromosomes in their malignant cells. Chromosomes #8 and #21 were extra in six cases each and chromosomes #19 and #22 were extra in four cases each. Chromosome rearrangements were observed in nine cases. Three of the nine cases had partial deletion of the long arm of chromosome #6. Cases of Down's syndrome with acute leukemia need to be reported with high-resolution chromosome banding of the leukemia cells. There is as yet no clear chromosome clue as to the precise basis of the etiologic association between Down's syndrome and acute leukemia.
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PMID:Chromosome clues to acute leukemia in Down's syndrome. 293 45

Eight cases each of erythroleukemia (AML-M6) and erythroblastic crisis of chronic granulocytic leukemia (CGLBC-E) were immunophenotyped with the help of a panel of lineage-associated monoclonal antibodies (McAbs). The latter included those reactive with erythroid progenitor (BFU-E and CFU-E) and erythroid precursors at different stages of maturation. In six of eight cases of AML-M6, erythroblasts revealed an immature phenotype, as evident from reactivity of the blast cells with McAbs directed against the earlier stages of erythroid maturation. One case had the phenotype of CFU-E, and in the remaining case of AML-M6 the erythroblasts showed a "mature" surface antigenic profile. This immunophenotypic spectrum was unrelated to the morphologic maturity of the erythroblasts. In two cases of CGLBC-E, an early erythroblastic phenotype was observed, while in as many cases a "mature" phenotype was present. Four of eight cases, however, revealed a mixed, erythroid plus myeloid phenotype. In one of the four cases, two separate blast populations, which represented erythroblasts and myeloblasts, could be identified. In the remaining three cases the blasts were morphologically homogeneous and undifferentiated. High incidence of HLA-DR positivity in the latter three cases suggests the primitive nature of blasts cells and their closeness to the putative "bipotent" myeloid stem cell. Our study has shown phenotypic heterogeneity of blast cells in AML-M6 and CGLBC-E.
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PMID:Phenotypic heterogeneity of erythroblasts in erythroblastic leukemia revealed by monoclonal antibodies. 305 43

Growth inhibitory activity of quinocarmycin citrate (KW2152) against 25 human cultured cell lines derived from leukemias and lymphomas was assessed quantitatively by regrowth assay. EC90 values (drug concentration required for 90% growth inhibition of treated cells) measured at 1-h exposure to the drug in vitro were more than 16 micrograms/ml in five of six T-cell lines derived from T-lymphoma/leukemia, hence they were insensitive to KW2152. On the other hand, four of six B-cell lines derived from B-lymphoma and three of four cell lines derived from non-T, non-B acute lymphoblastic leukemia were sensitive to KW2152 with EC90 values of 0.3 to 2.2 micrograms/ml at 1-h exposure. Six myelomonocytoid cell lines derived from acute myelogenous leukemia were also sensitive with EC90 values of 1.8 to 3.0 micrograms/ml on 1-h exposure, but two myeloid cell lines derived from chronic myelogenous leukemia and one cell line derived from erythroleukemia were insensitive with EC90 values of more than 16 micrograms/ml. The EC90 values of most cell lines decreased as exposure time increased, and those measured at 24-h exposure were similarly low and mostly in the 0.02 to 0.06 micrograms/ml range. The kinetics analysis of growth inhibitory activity of KW2152 revealed that the drug showed time-dependent action. These in vitro results, as correlated with in vivo results reported elsewhere (K. Fujimoto, T. Oka, and M. Morimoto, Cancer Res., 47: 1516-1522, 1987), suggest that daily consecutive or continuous dose therapy as well as single or intermittent large-dose therapy would be worthy of testing in the clinical trial of KW2152.
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PMID:Antitumor activity of quinocarmycin (KW2152) against various cultured leukemia and lymphoma cell lines in vitro. 316 53


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