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 total of 412 cases of acute leukaemia were examined for the presence of nuclear terminal deoxynucleotidyl transferase (TdT) by indirect immunofluorescence. Of the 129 cases of acute myeloblastic leukaemia (AML FAB groups M1/M2) examined, 18% (n = 23) had significant proportions (greater than 10%) of TdT-positive blasts. Although most of these AML cases (n = 18) were of poorly differentiated (M1) type; 5 cases of AML showing features of granulocytic differentiation (M2) were also found to be TdT-positive. Even though TdT was generally more strongly expressed in the M1 group and associated with other markers of myeloid immaturity (Ia positive and lack of chloroacetate esterase), there was no inverse relationship with Sudan black or myeloperoxidase activity. In addition, although the proportion of AML-M1 cases with increased TdT-positive cells was slightly higher (18/95, 19%) than for the AML-M2 group (5/34, 15%) the results suggest that the presence of nuclear TdT in leukaemic myeloblasts may not only reflect cellular immaturity but may also be due to maturational asynchrony in otherwise well-differentiated blasts.
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PMID:TdT expression in acute myeloid leukaemia. Haemopoietic immaturity or maturational asynchrony? 342 68

Although it is well recognized that granulocytic sarcoma can cause localized lymphadenopathy, widespread nodal involvement by acute myelocytic leukemia (AML), clinically mimicking non-Hodgkin's lymphoma, has only been previously described twice. We report the clinicopathological, immunological, and cytochemical features of two patients who had widespread, prominent lymphadenopathy secondary to AML as well as concurrent marrow leukemia (M1 and M2). For one patient the lymphadenopathy was the predominant abnormality prompting him to seek medical attention, while the second patient had symptoms of infection following a 9-month history of myelodysplasia. The disease in both patients was aggressive; one patient survived only 1 week and the other survived only 5 weeks after diagnosis. In both cases the granulocytic sarcoma was confirmed by cytochemistry studies (naphthol ASD-chloroacetate esterase on tissue sections and myeloperoxidase on imprint smears), and electron microscopy, including morphology (both cases) or ultrastructural localization of myeloperoxidase (case 2). Non-specific esterase activity was not detected in either patient's blasts, although serum lysozyme was elevated in both cases. Immunological studies revealed reactivity of both patients' cells with panleukocyte, MY4, MY7, OKM-1, and Leu-M1 monoclonal antibodies and with alpha-1-antitrypsin and muramidase antibodies. The cells of one of these patients also reacted with anti-S-100 protein. Although the cytochemical studies indicated that both cases exhibited only myeloid differentiation, the immunological markers suggested that the tumor cells possessed some features of monocytes, perhaps explaining their propensity for widespread tumor formation. Morphological, immunological, cytochemical, and ultrastructural methods of diagnosing granulocytic sarcoma are presented.
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PMID:Acute myelocytic leukemia manifested by prominent generalized lymphadenopathy: report of two cases with immunological, ultrastructural, and cytochemical studies. 345 62

Bone marrow and/or peripheral blood cells from 12 patients with acute promyelocytic leukemia (APL) were cultured in soft agar or methylcellulose in the presence of 15% human placental conditioned medium as a source of colony stimulating factor. Buffy coat cells, taken from ten patients when APL was diagnosed, produced a growth pattern in soft agar that was characterized by a high incidence of small, relatively uniform clusters of promyelocytes, which, when stained in situ, reacted strongly with myeloperoxidase, Sudan black B and chloroacetate esterase. In six cases, the leukemic origin of the cluster forming cells was demonstrated by the presence of the t(15;17) in these cells. During periods of complete remission the small clusters were replaced by larger and more diverse aggregates which had a normal karyotype. At relapse the small cluster growth pattern returned. The growth pattern of small clusters is more commonly associated with APL than with other types of acute myeloid leukemia.
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PMID:A characteristic CFU-GM growth pattern in acute promyelocytic leukemia. 347 28

A reliable and reproducible modified method was developed for the cytochemical demonstration of the so-called 'platelet' peroxidase at the light microscopy (LM) level. Interestingly, not only normal platelets and megakaryocytes showed the peroxidase activity, but also normal lymphocytes. As with the ultrastructural platelet peroxidase (PPO) method, myeloperoxidase (MPO) was also demonstrated in granulocytes. Peroxidase activity was exhibited by blast cells of acute myeloid leukaemia, including megakaryoblasts of megakaryoblastic leukaemia, by hairy cells of hairy cell leukaemia, by centroblasts of centroblastic lymphoma and by plasma cells of plasma cell leukaemia. The enzyme activity was also demonstrated in the mast cells of systemic mastocytosis. It seems that different forms of peroxidase are present in most haemic cells. Fixation and conditions of incubation are probably the determining factors for their demonstration. The method may allow further cytochemical discrimination at the LM level between blast cell populations which are negative for MPO by standard methods.
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PMID:Cytochemical demonstration of 'platelet' peroxidase at the light microscope level. 366 2

A MCA raised against the human acute myelogenous leukaemia cell line KG1 reacted with only KG1 among 26 haematopoietic cell lines covering the major lineages. It reacted with early myeloid (M1/2), 1 of 2 acute myelomonocytic (M4) and most non-B non-T leukaemias, including blast crises of CGL. Among M1-AML cells, both MPO+ and MPO- blasts were BI-3C5+. Blasts in 3 Tdt+ M1-AMLs were simultaneously BI-3C5+. BI-3C5 reacted with 4% cells in normal BM, many of which were histologically recognisable as myeloid precursors. 8-15% of BI-3C5+ cells in BM were simultaneously Tdt+, and all were weakly Ia antigen+. BI-3C5 was unreactive with all peripheral leucocytes, with M3 and M5 AMLs, with lymphoid and myeloid leukaemias of "mature" phenotype (T-ALL, B-ALL, CLL, CGL) and with non-haematopoietic cell lines. BI-3C5 precipitated a 120K moiety from 125I-labelled KG1 membranes. It was not blocked by J5 anti-cALLA. The potential use of BI-3C5 in the classification of acute leukaemias is discussed.
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PMID:A novel monoclonal antibody BI-3C5 recognises myeloblasts and non-B non-T lymphoblasts in acute leukaemias and CGL blast crises, and reacts with immature cells in normal bone marrow. 385 2

Chloroacetate esterase (CAE) reactivity is associated with acute nonlymphocytic leukemia (ANLL) and, to the author's knowledge, has not been reported in acute lymphoblastic leukemia (ALL). The authors have identified a single patient whose blasts displayed CAE reactivity from a review of 400 newly diagnosed patients with ALL. The diagnosis of ALL in this case was based upon morphologic evaluation (FAB:L1), presence of terminal deoxynucleotidyl transferase (TdT), the absence of reactivity with myeloperoxidase, and the failure of leukemic blasts to mark with a panel of anti-myeloid monoclonal antibodies. Remission was induced promptly with standard ALL therapy. This case demonstrates that punctate CAE positivity rarely can occur in ALL, and, therefore, CAE is not entirely specific for ANLL. The authors conclude that CAE positivity should not be used as a sole criterion to diagnose ANLL in the absence of supporting morphologic, cytochemical, immunocytologic, or clinical information.
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PMID:Chloroacetate esterase positivity in acute lymphoblastic leukemia. 385 55

The expression of two membrane antigens identified by the monoclonal antibodies (McAb) My9 and 3C5 has been investigated in cells from 80 acute leukemias. My9 was positive in the blasts of 33 out of the 38 (87 per cent) cases of acute myeloid leukemia (AML) tested, regardless of FAB subtype, and in 13 of 18 (72 per cent) cases of chronic granulocytic leukemia (CGL) in myeloid blast crisis. The reactivity of 3C5 was confined to myeloblastic (M1) AML, 85 per cent of cases, and to lymphoblastic leukemia (ALL) of B-lineage, 70 per cent of cases, including CGL in lymphoid transformation. My9 was negative in ALL except for an unusual case. The phenotype My9+, 3C5+ was seen exclusively in M1 (69 per cent) and M2 (14 per cent) AML. Ultrastructural analysis with the immunogold method in combination with the myeloperoxidase (MPO) reaction showed that expression of My9 increased in parallel with MPO activity whereas 3C5 was expressed mainly in myeloblasts with little MPO content. We conclude that the use of these two McAb will contribute to the diagnosis and classification of AML and may throw some light to the pathogenesis of biphenotypic acute leukemias, including TdT + AML.
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PMID:Characterization of myeloid leukemias with monoclonal antibodies 3C5 and MY9. 386 40

Monoclonal antibody T-11, considered specific for the sheep erythrocyte rosette-associated antigen of T cells, reacted with leukemic blasts from four of 23 patients with morphologic and cytochemical criteria for acute myeloblastic leukemia (AML). Although 83%, 87%, 88%, and 96% of the blasts from these patients reacted with T-11, only one patient demonstrated a small percentage of heat-stable E rosettes (5%). Antibody 9.6, which also reacts with the E rosette-associated antigen, was tested on blasts from two of the T-11-positive patients and was also strongly reactive (96% and 98%). Dual staining of blasts from these two patients demonstrated a small number of cells that simultaneously expressed the E rosette-associated antigen and myeloid-associated cytochemistries (myeloperoxidase [MPO] and Sudan black B). Additionally, leukemic blasts were identified that simultaneously expressed the E rosette-associated antigen and contained Auer rods. Antibody OKT-11 immunoprecipitated a 48,100-dalton glycoprotein from these leukemic blasts that is similar in molecular weight to that previously determined for the T cell surface protein (Tp50), thus providing strong evidence that this molecule can be found in some cases of AML. Because cells simultaneously expressing both the E rosette-associated antigen and MPO were identified, it would appear likely that leukemic blasts with only the E rosette-associated antigen or only MPO arose from the same progenitor. Our findings further demonstrate that the epitopes identified by antibodies OKT-11, T-11, and 9.6 are not always associated with, or sufficient for, 37 degrees C E rosette formation and can be found on blasts from patients with AML.
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PMID:The E rosette-associated antigen of T cells can be identified on blasts from patients with acute myeloblastic leukemia. 391 95

The frequency and clinical significance of acute leukemia displaying both lymphoid and myeloid characteristics was determined in 123 consecutive children using a panel of lineage-associated markers. The leukemic blasts from 18 of 95 children (19%) with the diagnosis of acute lymphoblastic leukemia (ALL) by standard diagnostic criteria expressed myeloid-associated cell surface antigens. Despite immunological evidence of lymphoid differentiation (17 CALLA + and one T cell-associated antigen +) and findings of immunoglobulin gene rearrangement, blasts from these patients reacted with one to five monoclonal antibodies identifying myeloid-associated cell surface antigens (My-1, MCS.2, Mo1, SJ-D1, or 5F1). Dual staining with microsphere-conjugated antibodies and analysis by flow cytometry confirmed that some blasts were simultaneously expressing lymphoid- and myeloid-associated antigens. Conversely, blasts from seven of 28 patients (25%) with acute nonlymphocytic leukemia (ANLL), diagnosed by otherwise standard morphological and cytochemical criteria, expressed lymphoid-associated surface antigens. Dual staining of individual blasts demonstrated simultaneous expression of myeloperoxidase (MPO) (including Auer rods) in association with either T-11, CALLA, or terminal deoxynucleotidyl transferase. Blasts from one patient with ANLL demonstrated T cell receptor gene rearrangement, while blasts from another patient demonstrated characteristics associated with T (T-11), B (CALLA and heavy-chain immunoglobulin gene rearrangement), and myeloid (MPO) lineage. There were no consistent cytogenetic abnormalities, and no patient demonstrated independent leukemic clones. Each patient with typical ALL, except for myeloid-associated antigens, achieved complete remission with conventional induction therapy for ALL. By contrast, three of the seven children with ANLL whose blasts expressed the T-11 surface antigen failed ANLL induction therapy. These three patients subsequently achieved remission with ALL therapy.
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PMID:Acute mixed lineage leukemia: clinicopathologic correlations and prognostic significance. 393 24

The cytochemical methods for lysozyme and nitroblue-tetrazolium reduction have been used to study the blast cells of acute myeloid leukaemia. Both proved useful in characterizing the cases with predominant monocytic differentiation. THE DEMONSTRATION OF LYSOZYME ACTIVITY HELPED TO DEFINE TWO MAIN GROUPS: (a) with predominantly lysozyme-negative cells (myeloblastic-promyelocytic), and (b) with considerable numbers of positive cells (monoblastic-monocytic). In addition this test was also of value in the differentiation of other leukaemic disorders. Reduction of nitroblue-tetrazolium was also a feature of monocytic differentiation. The combination of these two methods with those for myeloperoxidase and non-specific esterase activity contributes to the cytological characterization of acute myeloid leukaemia.
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PMID:Lysozyme activity and nitroblue-tetrazolium reduction in leukaemic cells. 451 38


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