Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:1.11.1.7 (peroxidase)
65,474 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe a patient with basophilic leukaemia following a 2-year period with myelodysplastic syndrome (refractory anaemia). The marrow showed 59.4% of blasts with 25.0% of mature and immature basophils. The leukaemic blasts contained granules, positively stained with toluidine blue but negative for peroxidase. The basophilic differentiation was confirmed by ultrastructural analysis demonstrating immature basophil granules. In addition, a morphological transition from immature blasts to more mature basophils was observed. Immunophenotypic analysis of blasts and basophils showed positive for CD5, CD7, CD13, CD33 and CD34. Cytogenetic investigation showed an abnormal karyotype, 46,XY,del(5)(q31q35), in 11% of the cells examined when the initial diagnosis of refractory anaemia was made. However, expansion of the same clone up to 100% was observed concomitantly with transformation to basophilic leukaemia.
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PMID:Transformation into acute basophilic leukaemia in a patient with myelodysplastic syndrome. 773 71

We describe our experience in the identification of 19 cases of AML-M0 categorized among 200 consecutive AML cases. Leukaemic cells from our cases were morphologically marked by agranular basophilic cytoplasm, finely dispersed chromatin and prominent nucleoli. In two cases heavily vacuolated and monocytoid-shaped blasts were also observed. Cytochemistry (MPO, SBB, alpha ANAE, alpha NBE, NASDCAE, AP, PAS) was negative in 14 cases, five cases expressing a very faint cytoplasmic positivity for alpha NBE (not exceeding 30% of the blasts) and alpha ANAE (not exceeding 41%) which was sodium fluoride resistant. In these five cases other monocytic markers (e.g. CD14) were not in favour of myelomonocytic differentiation. All the cases were anti-MPO positive at frequency > 10%. Phenotypic analysis also revealed myeloid features with all the patients having at least one myeloid antigen (CD13, CD33, CD15), Tdt was expressed in nine cases and CD7 in six cases. All cases but one were positive for CD34. Cytogenetic analysis, performed in 16 cases, showed no adequate growth in two cases and no consistent abnormality in four; among the remaining 10 cases no consistent abnormality was observed, the most common finding was trisomy 8 (two cases) and 4 (two cases) and aberrations of chromosomes 2, 3, 5, 7, 9, 12 and 21. No cases of (t9;22), Ph chromosome were observed. Interestingly three out of five patients with faint alpha NBE/alpha ANAE positivity relapsed as typical M4 (one case) or M5a (two cases).
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PMID:Minimally differentiated acute myeloid leukaemia (AML-M0): cytochemical, immunophenotypic and cytogenetic analysis of 19 cases. 781 3

We examined leukemic blasts from 5 cases of AML-M0 diagnosed according to The French-American-British (FAB) classification for expression of immunological markers as well as myeloperoxidase (MPO) using flow cytometry (FCM) and immunocytochemistry (ICC). In one patient, the myeloid antigens, CD13 and CD33, were negative on FCM, but apparently positive in the cytoplasm by ICC, leading to a diagnosis of AML-M0. We examined MPO with anti-MPO monoclonal antibody in four patients by ICC, and could detect 3% or more MPO positive rates in all cases. These findings indicate that immunological studies for MPO and myeloid markers using ICC are very useful for the diagnosis of AML-M0. Two of 5 patients achieved CR, but they relapsed soon or after one year, respectively. The treatment outcomes suggest that the AML-M0 is an AML subtype with poor prognosis.
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PMID:[Immunocytochemistry in the diagnosis of acute myeloid leukemia (M0)]. 782 96

Coexpression of myeloid, B-, and T-lineage associated markers was found in a patient with morphologically and cytochemically undifferentiated acute leukemia. Surface marker analysis using two-color immunofluorescence staining characterized blast cells to express CD34, CD38, CD117, and class II antigens, coexpressing TdT, CD4, CD7, CD13, CD19, and CD33. Cytoplasmic expression of myeloperoxidase, CD3, and CD22 could not be demonstrated. Monosomy for chromosome 7 was found by cytogenetic analysis. The absence of clonal rearrangements of immunoglobulin or T-cell receptor genes was shown by Southern blot analysis. Using a 3H-thymidine incorporation assay, DNA synthesis of leukemic blasts could be stimulated by IL-3, IL-6 and G-CSF in vitro. The present case did not offer specific criteria of lineage commitment. Corresponding to an equivalent counterpart in normal hematopoiesis, the involved cell population may reflect an early, most immature developmental stage within a multipotent progenitor cell compartment.
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PMID:Acute leukemia coexpressing myeloid, B- and T-lineage associated markers: multiparameter analysis of criteria defining lineage commitment and maturational stage in a case of undifferentiated leukemia. 786 61

We have established a novel human megakaryoblastic cell line, designated as MEG-A2, from a patient with megakaryoblastic crisis of Philadelphia (Ph) chromosome positive chronic myelogenous leukemia. MEG-A2 cells showed positive phenotypes for periodic acid Schiff and alpha-naphthylbutyrate esterase reactions, but were negative for myeloperoxidase and naphthol ASD chloroacetate esterase reactions. Flow cytometric analyses of cell surface markers revealed that MEG-A2 cells had a low level of GP IIb/IIIa expression as well as apparent expressions of CD4, CD7, CD13, CD33 and CD34 antigens, but no expression of GP Ib nor glycophorin A. Stimulation with phorbol 12-myristate 13-acetate (PMA) dramatically increased the expression of megakaryocyte-related markers such as HPL-3, J15, Pit-1, Y2/51 and AN51 in MEG-A2 cells. The PMA-stimulation also induced expression of platelet peroxidase (PPO) in MEG-A2 cells on electromicroscopic observation. Proliferative responses to granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-3 (IL-3) or erythropoietin were observed, and the expression of GP IIb/IIIa was increased by stimulation with GM-CSF, IL-3, erythropoietin and interleukin-6 (IL-6). Protein S mRNA expression was seen in cultured cells on Northern blot analysis. Expression of platelet factor 4 mRNA was induced in PMA-stimulated cells, and a marked accumulation of protein was observed in the culture medium. In conclusion, a new cell line, MEG-A2, belongs to the relatively immature megakaryocytic lineage and has markedly increased megakaryocytic characteristics with PMA stimulation.
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PMID:Establishment and characterization of an immature human megakaryoblastic cell line, MEG-A2. 786 73

The human leukemic cell line NB4 was derived from a patient with acute promyelocytic leukemia and is characterized by a specific 15;17 chromosomal translocation. We analyzed the response of NB4 and HL-60 cells to the biomodulators all-transretinoic acid (ATRA), vitamin D3 (Vit D3) and the protein kinase C agonists bryostatin 1 (Bryo 1) and phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA). HL-60 cells were used for comparison being arrested at the myeloblastic-promyelocytic stage, but lacking the t(15;17) abnormality. In most experiments Vit D3 was only weakly or not at all effective. The other three reagents effectively slowed or stopped the proliferation of the cells in suspension. Associated with this proliferation arrest was the cell differentiation along the myeloid cell lineages: ATRA modulated morphological features indicative of granulocytic differentiation; Bryo 1 and TPA caused also distinct morphological changes. The inducers up-regulated the expression of CD11b (without changing the surface expression of other markers, e.g. CD13, CD14, CD15, CD33, CD68, HLA-DR) and completely down-regulated the originally strong expression of myeloperoxidase and c-myc at the mRNA level. Thus, ATRA- or protein kinase C activator-induced differentiation involved changes associated with maturational processes. Induction of terminal differentiation of leukemic cells by physiological or pharmacological modulators may be able to control the growth of the malignant cells and has therapeutic implications.
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PMID:Modulation of gene expression in the acute promyelocytic leukemia cell line NB4. 790 56

A case of acute myeloid leukemia (AML) with an unusual phenotype which was negative for a panel of myeloid antigens determined by flow cytometry, but was strongly positive for myeloperoxidase has recently been reported. We herein describe a case of AML with this unusual phenotype at diagnosis; relapse occurred with the acquisition of CD13 and CD33 expressions. Morphological features of the blasts at relapse seemed to be more compatible with myeloblasts than those at diagnosis. These phenotypic and morphological changes are suggestive of asynchronous differentiation, clonal evolution or clonal change of leukemic cells.
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PMID:Acquisition of CD13 and CD33 expression at relapse on acute myeloid leukemia cells with an unusual phenotype: MPO+CD13-CD33-. 790 35

During the past two decades immunophenotyping has yielded significant new information regarding the biological heterogeneity of ALL and has provided a solid basis for a biologically oriented and reliable classification of this disease. At present, lineage commitment of acute leukaemias can be achieved in more than 98% of cases by applying a standardized panel of mAbs to pan-B-cell (CD19, cyCD22), pan-T-cell (cyCD3, CD7) and pan-myeloid antigens (CD13, CD33, MPO) that are expressed either on the surface or in the cytoplasm of the earliest progenitors of the respective cell lineage. Further subclassification of ALL based on the analysis of antigens more closely associated with different maturational stages of B- and T-cell lineage has proven useful for the identification of biologically and clinically distinct entities in both B-cell precursor and T-lineage ALL. Immunophenotyping in about 2800 patients recruited for the German multicentre trials has shown that children and adults differ markedly in frequency distribution of immunological subgroups, with a higher adult incidence of immature B-cell precursor (i.e., pre-pre-B ALL) and T-lineage ALL immunophenotypes (i.e., pre-T ALL). Detailed immunological analyses using a broad panel of mAbs have recently documented typical ALL cases inappropriately expressing myeloid antigens (My+ ALL) as well as morphologically/cytochemically defined acute myeloid leukaemia (AML) with lymphoid-associated markers (Ly+ AML). Based on our own results and a critical review of published data, leukaemic blasts in 5-20% of ALL patients disclose My+ ALL, whereas a coexpression, mostly of T-cell-associated antigens, can be identified in 10-25% of AML cases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Immunophenotyping of acute lymphatic leukemia: diagnostic aspects and clinical relevance]. 802 15

We report here an uncommon case of neonatal acute leukaemia that presented concomitant with serological evidence of rubella infection. The clinical course was aggressive and the patient died 5 days after diagnosis from septicaemia. Leukaemic blasts had a mixed lineage immunophenotype co-expressing a constellation of B-lymphoid (CD19, cytCD22, TdT) and myeloid (CD13, CD33, CD14, anti-MPO) markers, as well as multiple adhesion molecules and markers associated with early lympho-myeloid progenitor cells (CD34, CD7, HLA-DR). A previously unrecorded discordant expression of different CD10 and CD34 epitopes was identified using different monoclonal antibodies. The karyotype was 46,XX t(4;11)(q21;q23) and molecular analysis confirmed rearrangement of the trithorax-related oncogene HRX at 11q23. There was a clonal biallelic rearrangement of the immunoglobulin heavy-chain gene. The features of this rare case have implications for possible aetiological events leading to leukaemia.
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PMID:Neonatal mixed lineage acute leukaemia. 803 18

Reports of treatment of patients with minimally differentiated acute myeloid leukemia (AML-M0) are limited, heterogeneous, and controversial. We verified the prognosis of this subtype by analyzing the results of 189 consecutive patients with de novo AML. Fifteen cases fitting the criteria of AML-M0 were identified. No clinical features distinguished them from other patients with AML. The median age was 61 years (range 27 to 70), with a leukocyte count ranging from 0.6 to 185 x 10(9)/L. In all cases the leukemic cells expressed CD34 and reacted with at least one of the antibodies to early myeloid antigens, ie, CD13, CD33, or myeloperoxidase. Immunophenotypic analysis also showed positivity for CD7 in seven samples and the multidrug-resistance P-glycoprotein (P-170) in six. Cytogenetic analysis was abnormal in 12 of the 13 patients in whom an adequate number of mitoses could be evaluated. No single abnormality prevailed, the most common findings being trisomy 8 (three cases) and aberrations of chromosome 7 (two cases). Antileukemic treatment differed according to age, but for remission induction, all patients received a combination of cytosine arabinoside and an anthracycline or mitoxantrone. The prognosis of patients with AML-M0 was remarkably poor as compared with the other French-American-British subtypes. Whereas the overall rate of complete remission (CR) was 58% with a median survival of 63 weeks, only 6 of the 15 patients with AML-M0 achieved a CR, and the median survival of this group was 16 weeks (range 3 to 39). The major determinant of treatment failure was unresponsiveness to chemotherapy, as only one patient died of infection during the hypoplastic phase. The CR duration of responders was short, ranging from 3 to 22 weeks, and no second remissions were observed. We conclude that conventional combination chemotherapy yields disappointing results in AML-M0. The reason for this may be the convergence of various unfavorable prognostic factors, such as (1) the high incidence of cytogenetic abnormalities; (2) the lack of differentiation features and the expression of immaturity markers such as CD34 and CD7; and (3) the frequent expression of P-170. Nonconventional therapeutic approaches should be developed to alter the prognosis of this form of leukemia.
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PMID:Analysis of treatment failure in patients with minimally differentiated acute myeloid leukemia (AML-M0). 812 53


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