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)

Examples are presented in which normal as well as abnormal chromosome distributions could be obtained from the same individual by means of bivariate flow karyotyping. Selective stimulation of T-lymphocytes obtained by E-rosetting from the blood of a patient with acute myelocytic leukemia resulted in a normal flow karyogram. The specific stimulation of myelocytic leukemia cells with granulocyte-macrophage colony stimulating factor (GM-CSF) and interleukin 3 (IL-3) yielded flow karyograms displaying the leukemia-associated chromosome abnormalities. The resulting flow karyograms could be used to discriminate between homolog differences, which appear normally in virtually every individual, and leukemia-associated chromosomal aberrations. In the case of a female chronic myelocytic leukemia patient who received bone marrow form an HLA-identical male donor, specific stimulation of various subsets of cells enabled to discriminate between leukemic host cells and non-leukemic donor cells. Both the leukemia-specific translocations and sex chromosomes were used as markers to analyse the flow karyograms obtained from the same sample.
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PMID:Clinical applications of flow karyotyping in myelocytic leukemia by stimulation of different subpopulations of cells in blood or bone marrow samples. 230 58

The ultrastructural, light microscopical and immunological features of twelve cases of acute childhood leukemia are described. Nine cases were unclassifiable by light microscopy, morphology and cytochemistry, and three were difficult to classify because of a low percentage of Sudan-Black B positive blasts. By means of electron microscopy (including peroxidase cytochemistry), two main groups were seen: 1. Acute myeloid leukemia, in which could be distinguished a) a more differentiated myeloid leukemia, b) a leukemia with megakaryoblastic involvement and c) a minimally differentiated acute myeloid leukemia with granules present and 2. lymphoblastic leukemia. One case could not be classified. The first group included two possible cases of a hybrid leukemia with CD19 or CD10 positivity as well as ultrastructural peroxidase activity. We conclude that electron microscopy aids to further classification of minimally differentiated and hybrid acute leukemias.
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PMID:Electron microscopy: a contribution to further classification of acute unclassifiable childhood leukemia. 235 May 92

A natural tumor suppressor of human fetal liver origin with low molecular weight (LMW-NTS) was studied. The methanol extract of human fetal liver supernatant (FLS-MeOH), a crude preparation of LMW-NTS, showed preferential suppression on the growth of leukemic cell lines HL-60, L833, WEHI-3, and L1210, but less effect on the growth of normal bone marrow granulocyte-macrophage colony-forming units (CFU-GM) in vitro. Preliminary experiments showed that FLS-MeOH also exhibited preferential suppression on the growth of leukemic colony-forming units (L-CFU) from six patients suffering from acute myeloid leukemia (AML). In combination with a long-term in vitro liquid culture system, FLS-MeOH could be adopted as an effective purging agent in the autologous bone marrow transplantation treatment of myeloid leukemia.
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PMID:Preferential suppression of low molecular weight natural tumor suppressor of human fetal liver origin on the growth of leukemic cells in vitro. 238 43

Acute febrile neutrophilic dermatosis or Sweet's syndrome is a rare disease, which occasionally is seen in patients with myeloid leukemia. We present a case of Sweet's syndrome in a patient with an abnormal chromosome pattern in bone marrow aspirate. Initially the patient had flu-like symptoms with high fever. Two weeks later raised, erythematous and painful plaques appeared on the skin. Various antibiotics were ineffective, but the symptoms vanished after administration of prednisone. Six months later a fulminant acute myeloid leukemia developed, the course of which was complicated by a fatal subdural bleeding. It is concluded that Sweet's syndrome may be a cutaneous sign of a neoplastic myeloid proliferation and that a complete hematological examination including chromosome analysis is mandatory in these patients.
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PMID:Acute febrile neutrophilic dermatosis and abnormal bone marrow chromosomes as a marker for preleukemia. 240 27

The Southeastern Cancer Study Group conducted a phase I-II trial of sequentially administered 5-azacitidine and amsacrine in patients with refractory adult acute leukemia from September 1980 to March 1983. The 5-azacitidine was administered by continuous iv infusion on Days 1-4 at doses ranging from 112 to 200 mg/m2/day, while amsacrine was given at doses ranging from 75 to 150 mg/m2/day on Days 5-8. The doses of 5-azacitidine and amsacrine were alternately escalated through six dose levels during the phase I portion of the trial. Of 128 patients entered, 102 (80%) were evaluable for response. Remission was achieved in 13 of 80 evaluable patients with acute myeloid leukemia, in one of 12 evaluable patients with acute lymphoid leukemia, and in none of 11 patients with blastic transformation of chronic granulocytic leukemia. Three remissions occurred in patients with acute myeloid leukemia who were refractory to initial induction chemotherapy with cytarabine and anthracycline combination chemotherapy. Remissions were relatively durable, lasting a median of 28 weeks in the 13 patients with refractory acute myeloid leukemia (range, 14-54 weeks). Toxic effects included universal severe myelosuppression, hyperbilirubinemia at a frequency and severity similar to those seen with amsacrine used as a single agent, moderately severe stomatitis and diarrhea, three incidents of amsacrine-related cardiac dysrhythmia, and a single case of probable drug-related cardiomyopathy. This combination has activity in the treatment of myeloid leukemia, which is primarily resistant to cytarabine and anthracyclines, and could have a role in primary management.
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PMID:Sequentially administered 5-azacitidine and amsacrine in refractory adult acute leukemia: a phase I-II trial of the Southeastern Cancer Study Group. 241 Jan 19

The active metabolite of vitamin D known as 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] is a major physiologic regulator of mineral metabolism in man. The compound is also a potent inducer of differentiation of a human promyelocytic leukemia cell line known as HL-60. The induction of differentiation of myeloid leukemia cells to functional end cells offers an appealing therapeutic prospect. We investigated the ability of 1,25(OH)2D3 both to induce in vitro the differentiation of blast cells taken from patients with acute myelogenous leukemia and to improve hematopoiesis in vivo in patients with the myelodysplastic syndromes (preleukemia). We found that high concentrations (10-6 M) of 1,25(OH)2D3 significantly induced the in vitro differentiation of blast cells as measured by morphology, phagocytosis, and superoxide production. A concentration of 10-9 M 1,25(OH)2D3 had no effect on blast cell differentiation. We gave 2 microgram/day of 1,25(OH)2D3 to 18 patients with myelodysplastic syndrome (preleukemia) in an attempt to improve their hematopoiesis. During therapy, their peak peripheral blood granulocyte, platelet, and macrophage concentrations were slightly elevated as compared to their baseline, starting levels. Eight patients had a partial or minor peripheral blood response to the compound during the administration of 1,25(OH)2D3. However, no patient showed significant improvement of peripheral blood cell or marrow blast cell counts by the end of the study (greater than or equal to 12 weeks) as compared to their starting levels. Seven of the patients developed leukemia before or by 12 weeks of treatment. Nine of the 18 patients developed hypercalcemia. Taken together, the study shows that high concentrations (10-6M) of 1,25(OH)2D3 can induce differentiation of leukemia blast cells in vitro, but the administration of 1,25(OH)2D3 to patients with the myelodysplastic syndromes (preleukemia) does not have an enduring therapeutic effect. Hypercalcemia prevented administering greater amounts of 1,25(OH)2D3. In the future, the use of new vitamin D analogs that induce hematopoietic cell differentiation without inducing hypercalcemia might allow the achievement of higher blood levels of the inducing compound and might be medically useful for selected preleukemic and leukemic patients.
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PMID:1,25-Dihydroxyvitamin D3: in vivo and in vitro effects on human preleukemic and leukemic cells. 241 38

Granulocytic sarcoma (GS) is an extramedullary tumor composed of granulocytic precursor cells. The tumor usually develops during the course of myelogenous leukemia or myeloproliferative disorders and may represent the initial manifestation of leukemia. Rarely, GS is recognized as an isolated tumor without any evidence of leukemia. However, in such cases, leukemia generally develops within 1 to 2 years of the diagnosis of GS. We are reporting a case of a 45-year-old woman who was diagnosed as having an isolated GS of the right breast in August 1980. She was treated with a partial mastectomy followed by 1 year of combination chemotherapy as used in the cases of acute myeloblastic leukemia and has remained free of disease to the present time. That is, she has not developed leukemia or recurrence of GS for 64 months. Based on this experience and on the review of the literature, we recommend that all cases of GS be treated with combination chemotherapy as in cases of acute myeloblastic leukemias.
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PMID:Isolated granulocytic sarcoma: report of a case and review of the literature. 242 54

The immunological phenotypes of leukemia cell samples from 60 patients, of whom 54 had acute myeloid leukemia (AML), were assessed with a panel of monoclonal antibodies (Mabs) with specificity for the following epitopes: Epitopes associated with myeloid leukemia cells, Epitopes expressed only on immature myeloid cells (or subsets) and on monocytes, Epitopes only expressed on granulocytes or on granulocytes and mature myeloid cells (promyelocytes, myelocytes and monocytes), Epitopes on HLA-class II (DR) and HLA-class I molecules and on insulin receptors. This panel of Mabs proved useful to identify leukemia cells in blood and to assess their myeloid origin. The panel of Mabs was found also to be useful for immunophenotyping of leukemia cells. Furthermore, the analysis revealed considerable variations in the immunological phenotype of AML cells, reflecting antigenic heterogeneity within the individual leukemia cell population as well as abnormal or no expression of histocompatibility antigens and insulin receptors in some samples. Some of the Mabs bound preferentially to subgroups in the French-American-British (FAB) classification.
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PMID:Specificity and diagnostic implications of the reactivity pattern of a panel of monoclonal antibodies against myeloid leukemia cells. 243 58

In vitro clonal culture of leukemic cells from patients with acute myeloid leukemia (AML) showed that cells from all subtypes tested could be stimulated to proliferate clonally either by purified recombinant human granulocyte-macrophage colony stimulating factor (GM-CSF) or by human cross-reactive, purified murine granulocyte CSF (G-CSF). The responsiveness of AML populations to CSF stimulation was quantitatively variable but was within the heterogeneous range exhibited by normal granulocyte-monocyte progenitor cells. A general concordance was noted between the proliferative effects of GM-CSF and G-CSF on the individual leukemic populations. All AML populations tested specifically bound 125I-labeled murine G-CSF; the level of labeling varied widely and correlated with AML subtype. Labeling levels on individual labeled leukemic cells were within the heterogeneous range exhibited by normal cells, but significant numbers of blast cells in M2, M4, and M5 AMLs appeared to lack membrane receptors for G-CSF. The level of labeling with G-CSF did not correlate with the frequency of clonogenic cells able to be stimulated by G-CSF. The data emphasized that GM-CSF and G-CSF are equivalent proliferative stimuli for human myeloid leukemia cells. Further, despite the potential ability of G-CSF to suppress murine leukemic cells, many AML blast cells lack significant numbers of G-CSF receptors. These considerations warrant caution in future attempts to use G-CSF in the therapy of acute myeloid leukemia.
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PMID:Primary human myeloid leukemia cells: comparative responsiveness to proliferative stimulation by GM-CSF or G-CSF and membrane expression of CSF receptors. 244 28

The first monoclonal antibodies (MoAbs) to epitopes in the extracellular domain of the human c-fms proto-oncogene product (receptor for the macrophage colony stimulating factor, CSF-1) were used with flow cytometric techniques to study receptor expression on normal human peripheral blood monocytes, bone marrow cells, and leukemic blasts. On normal cells CSF-1 receptors were restricted in their expression to cells of the mononuclear phagocyte lineage. CSF-1 receptors were detected on leukemic blasts from 15 (30%) of 50 children with acute myeloid leukemia, compared with four (15%) of 26 adults. By contrast, detectable CSF-1 receptors were uniformly absent on blasts from 19 children with acute lymphoblastic leukemia. CSF-1 receptors on normal monocytes and myeloid leukemia cells could be induced to downmodulate by incubation with either human recombinant CSF-1 or phorbol esters, confirming that the receptors had functional ligand-binding sites and responded to transmodulation by inducers of protein kinase C. The numbers of receptors per cell and the percentage of positive cases were highest for leukemic blasts with cytochemical and morphological features of monocytes. However, CSF-1 receptors were also detected on a subset of leukemic blast cells with features of granulocytic differentiation (FAB subtypes M1 through M3). Southern blotting analyses of DNA from 47 cases of acute myeloid leukemia demonstrated no rearrangements within the 32 kb of genomic sequences that contain CSF-1 receptor coding exons or in the 50 kb upstream of the first coding exon. Analysis of the upstream region of the c-fms locus revealed that sequences representing the terminal 112 untranslated nucleotides of c-fms mRNA map 26 kb 5' to the first coding exon, suggesting that at least one c-fms promoter is separated from the receptor coding sequences by a very long intron. Whereas expression of the CSF-1 receptor in myeloid leukemic blasts is not restricted to cells with monocytic characteristics, the apparently aberrant pattern of receptor synthesis in a subset of cases with granulocytic features appears not to be due to chromosomal rearrangements within 50 kb upstream of sequences encoding the receptor.
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PMID:Monoclonal antibodies to the human CSF-1 receptor (c-fms proto-oncogene product) detect epitopes on normal mononuclear phagocytes and on human myeloid leukemic blast cells. 246 43


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