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)

Erythroid colonies were grown in vitro in plasma clot cultures. Normal adult rat bone marrow responded to exogenous erythropoietin with the formation of an average of 2 colonies/10(3) cells plated. No erythroid colonies were observed in cultured normal spleen preparations. Shay chloro-leukemia cells administered iv induced an acute myelogenous leukemia. During the progressive stages of the disease, the numbers of erythrocyte colony forming units (CFU-E) in the marrow decreased; concomitantly, these progenitors appeared in leukemic spleen cultures. Paralleling changes in CFU-E, the numbers of nucleated red blood cells in the marrow declined but increased in the leukemic spleen. However, compensatory spleen erythropoiesis was transient, due to continued leukemia cell colonization. The loss of erythroid progenitor cells from the bone marrow played a significant role in the anemia associated with this leukemia.
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PMID:In vitro erythroid colony formation in acute myelogenous leukemia in the rat. 106 27

Premature chromosome condensation (PCC) has previously been observed in tissue culture and is believed to arise from asynchronous mitotic activity in multinucleated cells in which the affected nucleus is in interphase and at least one nucleus is in metaphase. Such cells have been noted following fusion induced by virus infection, spontaneously, and after treatment with cytochalasin B. The phenomenon has also been observed in malignant pleural effusions, but has not previously been described as a feature of hematologic disease. In this study, we report the observations of PCC in seven patients. Six of these patients had either acute myeloblastic leukemia or acute myelomonoblastic leukemia in association with the features of erythroleukemia, i.e., leukoerythroblastic reaction in the blood, and erythroid multinuclearity, "megaloblastoid" changes, and PAS-positive staining of erythroid precursor cells in the bone marrow. In all patients, erythroid multinuclearity has been noted. However, not all patients with erythroleukemia exhibit PCC. In this series, three additional patients have had similar bone marrow morphologic changes without PCC. The finding of PCC in erythroleukemia may have important implications as to etiology of this disorder.
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PMID:Premature chromosome condensation in human leukemia. 106 46

Hemopoietic cell proliferation was studied in a patient suffering from preleukemia characterized by peripheral pancytopenia and hypercellular bone marrow with ineffective erythropoiesis. Two years later when overt acute myelogenous leukemia had developed the study was repeated. The kinetics of proliferation were investigated by a new method which allows evaluation of the rate and time of DNA synthesis in individual morphologically defined cells. Erythropoiesis was found ineffective to the same degree in both stages of disease. The rate of erythroid cell proliferation, however, was reduced in overt leukemia only. The myeloid system showed a grossly reduced production rate of myeloblasts in preleukemia whilst the same parameter was strongly increased in leukemia. This high production rate of myeloblasts in overt leukemia was interpreted as indication of a far-reaching self-maintenance of the myeloblast pool in this stage of disease. The proliferative activity of the individual myeloblasts was reduced already in preleukemia, and even more so in leukemia. In order to explain the amplification of the myeloblast pool with the onset of overt leukemia a change in the mode of myeloblast divisions is assumed. For this a transition from steady state to some degree of exponential growth gives the most plausible explanation.
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PMID:Proliferative behavior of hemopoietic cells in preleukemia and overt leukemia observed in one patient. 107 Apr 63

Six cases of congenital leukemia were encountered in pediatric autopsies carried out over a period of 7 years. The postmortem findings of these cases were analysed and presented along with antemortem peripheral and bone marrow smear. All the cases were diagnosed as acute myeloid leukemia. Gross changes were observed in lungs, liver, spleen and kidneys. Histological abnormalities were detected in these organs as well as the heart, pancreas and intestine. Lymph node follicles were well preserved in all. The thymus showed a normal lobular pattern with interstitial infiltrate. Bone marrow showed myeloid blast cells with depletion of the erythroid and megakaryocytic cells.
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PMID:Congenital leukemia--organ involvement in six autopsy cases. 130 13

Myeloperoxidase (MPO)- and Sudan Black B-not more than 3%-positive, esterase staining-negative, lymphoid, megakaryocyte lineage and erythroid surface marker-negative and electron microscopic platelet peroxidase-negative acute leukemia (AL) was diagnosed as acute undifferentiated leukemia (AUL), and myeloid marker (CD13, CD33), electron microscopic MPO (EMMPO), and DNA analysis of immunoglobulin heavy chain and T cell receptor as well as chemotherapy and its reactivity were examined. Of 239 cases of AL, 10 (4.2%) were AUL, and of these 10 cases, 9 were CD13 or CD33-positive AML-MO (MO) cases. Of 9 cases examined for EMMPO, 4 (44%) were positive, and of 3 cases of MO subjected to DNA analysis, 1 and 1 showed rearrangements of immunoglobulin heavy chain and T cell receptor beta chain, respectively. Of 6 cases of MO on myeloid induction therapy, 1 and 1 showed complete remission (CR) and partial remission (PR), respectively, each having lymphoid genotype, and 4 showed no remission (NR), being 3 of them EMMPO-positive. Of 2 cases on lymphoid induction therapy, 1 and 1 showed CR and NR, respectively, the former being EMMPO-positive MO. BHAC-EM therapy with behenoyl cytosine arabinoside, VP-16 and mitoxantrone performed on 2 cases refractory to any one of both these myeloid and lymphoid induction therapies led to CR in all these 2 cases.
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PMID:[Acute undifferentiated leukemia from the viewpoints of diagnosis and therapy]. 133 62

In this study, we examined the effects of peripheral blood T lymphocytes from patients with acute myeloid leukemia (AML) on marrow-derived erythroid progenitors (BFU-DE and CFU-DE) growth in an in vivo culture by using the plasma clot diffusion chamber (DC) technique. The application of double-compartment chambers (each compartment separated by a membrane filter) makes the investigations of humoral effects of T lymphocytes upon marrow erythroid progenitors proliferation possible. T lymphocytes of AML-patients in the absence of a statistically significant number of monocytes suppressed the growth of BFU-DE and CFU-DE from T lymphocyte- and adherent cell-depleted marrows. The inhibition ability was restricted to the CD4-positive enriched fraction obtained from T cells by using the negative selection technique. In contrast, the CD8-positive enriched fraction had no effect on erythroid colony formation. Autologous and allogeneic BFU-DE and CFU-DE were similarly affected by the CD4-positive T cells. Treatment of T cells with monoclonal antibodies against HLA-DR before cocultures, completely abrogated the suppression of BFU-DE and CFU-DE-derived colony formation. Suppressive activity detected in the CD4-positive T cells was also totally abolished by treatment with anti-interferon-gamma antibodies; whereas the inhibition was retained after 30 Gy radiation. Under these experimental conditions, resting T lymphocytes from healthy subjects did not affect the erythroid colony formation. Our data show that in AML-patients, a circulating HLA-DR-positive, less radiosensitive subset within the CD4-positive T cells is capable of inducing an interferon-gamma-mediated suppression of erythropoiesis, at least in DC culture.
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PMID:Interferon-gamma-mediated suppression of erythroid progenitor growth by a HLA-DR- and CD4-positive subset of T lymphocytes in acute myeloid leukemia. 136 14

We investigated the expression profiles of lacto-series type 2 antigens in hematopoietic cells and their progenitors, in comparison with leukemic leukocytes. Reactivity profiles of various anti-type 2 chain monoclonal antibodies (MoAbs) with leukemic blasts from 12 patients with acute myeloblastic leukemia (AML) and those from two patients with acute unclassified leukemia (AUL) show that anti-sialosyl-Le(x) MoAb SNH3 reacted strongly with greater than 95% of leukemic blast leukocyte populations from all patients (14 of 14). Another anti-sialosyl-Le(x) MoAb, FH6, showed less reactivity than SNH3 (12 of 14 patients), while anti-Le(y) MoAb AH6 showed reactivity with only 8 of 14 patients. On the other hand, none of the anti-type 2 chain MoAbs reacted with CD34+ normal adult bone marrow (BM) mononuclear cells obtained independently from three healthy volunteers. MoAb SNH3, but not FH6 or AH6, showed complement-mediated cytotoxicity to leukemic blasts from these patients, as well as to myelogenous leukemia cell line HL60. Colony-forming unit granulocyte-macrophage (CFU-GM), but not burst-forming unit-erythroid (BFU-E), was incompletely inhibited by treatment of normal BM mononuclear cells with SNH3 and complement. The absence of type 2 chain antigen expression in hematopoietic progenitor cells and in in vitro hematopoietic colonies (CFU-GM and BFU-E) strongly suggests that application of anti-carbohydrate MoAbs, particularly anti-sialosyl-Le(x) could be useful for elimination of leukemic myeloblasts infiltrating in BM, for purging of leukemic blasts in BM, and for facilitation of autologous BM transplantation.
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PMID:Reactivity profiles of leukemic myeloblasts with monoclonal antibodies directed to sialosyl-Le(x) and other lacto-series type 2 chain antigens:absence of reactivity with normal hematopoietic progenitor cells. 137 Jun 43

In the present work, we have investigated the composition and hemopoietic supportive capacity of eleven normal and six acute myelogenous leukemia (AML) marrow-derived stromal adherent layers, established in the absence or in the presence of recombinant human colony-stimulating factor 1 (rhCSF-1, macrophage colony-stimulating factor). Two of six AML adherent layers were deficient in composition (i.e., no confluency, reduced numbers of macrophages and fibroblastic progenitors, and no fat cell formation), resulting in reduced CSF-1 production and a poor hemopoietic supportive capacity (assessed by the ability of an irradiated stroma to sustain the growth of myeloid, erythroid, and multipotential progenitors derived from a second innoculum of normal bone marrow). Four out of six AML adherent layers showed levels of macrophages, fibroblastic progenitors, fat cells, and CSF-1 similar to those observed in adherent layers from normal bone marrow; however, their capacity to sustain normal hemopoiesis was still significantly reduced. The deficient hemopoietic supportive capacity of all AML adherent layers correlated with the presence of a soluble activity in the culture supernatant that inhibited hemopoietic colony formation. Addition of rhCSF-1 during the establishment of AML adherent layers significantly increased their hemopoietic supportive capacity. In contrast, the hemopoietic supportive capacity of normal adherent layers was reduced by rhCSF-1. The opposite effects of rhCSF-1 on the hemopoietic supportive capacity of normal and AML adherent layers correlated with the levels of the soluble inhibitory activity, that is, increased levels in cultures containing rhCSF-1-treated normal adherent layers, and slightly reduced levels in cultures of rhCSF-1-treated AML layers. These results indicate that, despite a morphologically normal composition in most cases (four out of six), the hemopoietic microenvironment developed in long-term marrow culture (LTMC) from all AML marrows analyzed has a deficient hemopoietic supportive capacity, due, at least in part, to the production of hemopoietic inhibitor(s). Such a deficiency can be partially overcome by establishing the stroma layers in the presence of rhCSF-1.
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PMID:Composition and functional integrity of the in vitro hemopoietic microenvironment in acute myelogenous leukemia: effect of macrophage colony-stimulating factor. 146 38

Expression of the normally cryptic blood group antigen Tn has occasionally been reported in hematologic disease, but the true frequency of this change is not known. A mouse monoclonal antibody (FBT3) and immunohistochemistry were used to examine expression of the Tn antigen. Expression was not detected in 35 normal bone marrow aspirates examined, but it was detected in 5 of 725 abnormal bone marrow aspirates, including 2 (3.6%) of 55 cases of de novo acute nonlymphocytic leukemia and 2 cases that terminated in acute nonlymphocytic leukemia. In two patients, one with acute myeloblastic leukemia and the other in blast transformation of chronic myeloid leukemia, the Tn antigen was expressed on 2 percent of blast cells. In one case of non-Hodgkin's lymphoma, 4 percent of normal myeloid cells expressed the antigen. In the other two cases, one of acute myelomonocytic leukemia and the other of myelodysplasia, only 2 to 8 percent of myeloid and erythroid cells initially were Tn positive. Subsequent serial immunohistochemical studies of bone marrow aspirates and peripheral blood in these two cases showed increasing numbers of Tn-positive erythroid and myeloid cells 8 to 12 months before polyagglutination was detected serologically. Tn-positive cells increased to > 90 percent in the terminal phase in both cases of both diseases. The results suggest that Tn expression in these two patients may have conferred a growth advantage to the cells and could be related to disease progression.
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PMID:Expression of the Tn antigen in myelodysplasia, lymphoma, and leukemia. 147 Dec 47

Erythroleukemia (EL) is a rare form of myelogenous leukemia the classification and definition of which has evolved over the course of its 80-year descriptive history. In 1976 the French American British (FAB) Cooperative Group included EL within the classification system of acute myelogenous leukemias as AML-M6, and agreed on a quantitative standard to be used in the diagnosis of this disorder. The standards were revised in 1985 to the form in use today. We selected a series of 15 cases from our records which specifically fit the FAB criteria for AML-M6. Extensive direct comparison between our series and the old literature is not practical because of the changes which have occurred in classification and definition of the disease. Overall we found a rough correlation between the clinical and laboratory data shown in the old literature on EL and data from our cases. These cases underscore characteristic laboratory features which correspond to what is now defined as AML-M6: these patients present with pancytopenia, frequent peripheral blood nRBCs and no, or few, peripheral blood blasts. In addition, we note the presence of a hybrid myeloid-erythroid blast in the bone marrow in this disease and suggest that this may be characteristic of this type of AML. Old literature on EL has generally shown it to be a disease of the elderly, yet we found a subset of younger patients whose clinical outcome was significantly better than that of the older patients. Finally, EL has historically been viewed as a disease in which patients progress from a prodrome through erythroleukemia to other acute myeloid leukemia (AML) subtypes. Consistent with this idea, half of our 15 patients had been previously diagnosed with myelodysplastic syndrome or received chemotherapy. On the other hand only one of the 15 patients converted to another type of AML during his course.
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PMID:Erythroleukemia: a review of 15 cases meeting 1985 FAB criteria and survey of the literature. 148 89


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