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)

The immunophenotype of leukaemia cells from 60 patients with acute myeloid leukaemia (AML) was analysed with the APAAP technique using a panel of anti-myeloid and lymphoid associated monoclonal antibodies (McAb). Cells from all cases, including three with negative cytochemical features, were labelled by at least one of the anti-myeloid McAb CD13, anti-myeloperoxidase (anti-Mpo), and/or CD14. The most sensitive marker was CD13, since it was positive in 90% of cases. In two out of three AML cases defined as M0-AML, CD13 was expressed in the cytoplasm but not on the membrane; in these three cases peroxidase (Mpo) was not detected by conventional cytochemistry, but could be demonstrated in all of them using the McAb anti-Mpo. The simultaneous expression of CD14 and CD68 McAb was often confined to the M4 and M5 FAB AML subtypes (92% cases) as compared to the others: M1, M2, M3 (18% cases). Lymphoid antigens were rarely positive (TdT+: 13%, CD7+: 15%, CD19+: 5%) and none of the AML cases were CD3+ or CD10+. By contrast, CD4 was expressed in blasts from 44% of cases and this was not restricted to AML with a monocytic component (M4, M5) but also found in other subtypes. There were no significant differences in the clinical or prognostic features according to the positivity or negativity with TdT and CD4. By contrast, expression of CD7 was associated with refractoriness to the treatment or short complete remission duration, although the number of patients is too small to draw firm conclusions. Our findings support the clinical and diagnostic relevance of immunophenotypic studies in AML.
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PMID:The value of detecting surface and cytoplasmic antigens in acute myeloid leukaemia. 132 89

Interleukin-3 (IL-3)-dependent murine FDCP-mix cells have multilineage differentiation capacity; they are nonleukemic, have a normal karyotype, and are nonimmortalized. These cells coexpress on their cell surface the "early" B-lineage marker B220/CD45R and the myeloid marker Mac-1/iC3b receptor (CR3), transcribe germline T-cell receptor gamma genes, and express the macrophage lineage growth factor receptor gene c-fms as a predominant 8.4-kb transcript. They do not detectably express at the stable mRNA or protein level other lymphoid precursor cell genes including CD2, TdT, lambda 5, and BP1. Induction of granulocyte/macrophage differentiation in these cells closes down expression of the lymphoid genes and activates stable expression of genes specific to the myeloid lineage, including myeloperoxidase. Expression of the c-fms gene at the mRNA level is upregulated and the dominant stable transcript is now in the 4.1-kb form typical of the macrophage lineage. These data provide a plausible explanation for the coexpression of lymphoid and myeloid lineage markers on human leukemic cells of stem cell or progenitor cell origin and have implications for the programming of lineage potential in normal multipotential hematopoiteic progenitor cells.
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PMID:Multilineage phenotypes of interleukin-3-dependent progenitor cells. 137 32

The diagnosis of acute undifferentiated leukemia (AUL) is made when the leukemic cells do not have cytologic or cytochemical features of myeloid cells, and do not express myeloid antigens (CD13, CD14, CD33, CD41 etc.) or lymphoid antigens (CD2, CD3, CD19, CD20, Sm Ig etc.). Most of these cells are reported to be positive for CD7, CD34, TdT and HLA-DR, either alone or in combination. Cell lineage can be suspected in most AUL cells by genotypic analysis, phenotypic analysis after culturing with TPA, or peroxidase activity by ultrastructural or immunohistochemical analysis, which indicates the heterogeneity of AUL. The patients with AUL appear to have a poor prognosis with conventional chemotherapy.
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PMID:[Immunophenotyping analysis of acute undifferentiated leukemia]. 151 41

TdT positive cells in rat thymus belong to distinct subsets as shown by light and electron microscopic immunocytochemistry. Using polyclonal antibodies to calf TdT and peroxidase labeled goat anti-rabbit IgG it has been possible to identify several subpopulations of TdT positive thymocytes. Large blasts corresponding to thymocytes at early maturational stages, are strongly positive for TdT which is diffusely distributed in both the nucleus and the cytoplasm. Smaller cells which correspond presumably to more advanced stages of maturation display nuclear TdT only, or are negative. Ultrastructural analyses of TdT indicate that the localization of the enzyme is related to the morphological features of the cells and TdT expression corresponds to maturational stages of T-cells.
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PMID:Ultrastructural localization of Terminal deoxynucleotidyl Transferase (TdT) in rat thymocytes. 158 13

We report a patient with Ph1-positive acute lymphoblastic leukemia (ALL) having i(17q) in whom bony lesions were the initial clinical manifestation. The patient was a 53-year-old male who began to have pains in his left hip early in March 1985. Relevant findings on admission included: WBC 21,300/microliters; blast cells 73.5%; peripheral blood blast cells, peroxidase (-), PAS (-) and esterase (-); cytoimmunologic markers, Ia(+) cells 49.1%, CD10(+) cells 67.1%, CD20(+) cells 75.1%; positivity for TdT, and Ph1(+); and i(17q) upon chromosomal analysis. These findings led to a diagnosis of ALL with Ph1(+),i(17q). This case seems to represent an exceedingly rare instance of Ph1(+),i(17q) ALL in which the differential diagnosis between blast transformation of CML and Ph1(+) ALL was initially difficult to make.
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PMID:Ph1-positive acute lymphoblastic leukemia associated with an isochromosome 17q. 174 60

Twenty-six cases of acute myeloid leukemia (AML) with cytochemical and immunophenotypic data were studied prospectively for immunoglobulin and T-cell receptor gene rearrangement. Dysmyelopoiesis was seen in 100% and Auer rods in 18%. Sudan black B was positive in 83% of the cases, peroxidase in 76%, nonspecific esterase in 74% (fluoride-inhibited in 82%), chloroacetate in 70%, acid phosphatase and PAS in 100%, and immunoperoxidase stains for platelet glycoprotein IIIa and factor VIII in 0% of the cases studied. Flow cytometry revealed myeloid phenotype in 19 of 20 cases. In four cases 5-86% of cells were TdT positive. Heavy-chain gene rearrangement was demonstrated in three cases (12%) and kappa light chain gene rearrangement in one; clinically significant rearrangement of the T-cell receptor gene was not found. Rearrangements of immunoglobulin genes are found occasionally in AML; these may represent nonspecific findings or coexistent lymphoid differentiation in AML.
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PMID:Prospective gene rearrangement studies and multiparameter analysis of acute myeloid leukemia. 190 18

Most cases of acute leukemia with deletions of chromosome 5q (5q-) are acute myelogenous leukemia. 5q- in acute lymphoid leukemia is rare. We studied a case of acute leukemia with 5q- using morphologic, cytochemical, immune and molecular techniques. Morphologic and cytochemical techniques were consistent with ALL (FAB L-2, PAS+, MPO-, ASD-). TdT was present. Immune studies suggested a T-cell phenotype (CD5+, CD7+); however, there was no rearrangement of the T beta-cell receptor gene. Surprisingly, the leukemia cells also expressed the CD13 myeloid antigen. Dual staining analysis showed co-expression of lymphoid and myeloid antigens on most cells. Based on these data and a review of previous reports we suggest that acute leukemia associated with the 5q- abnormality can occur in an immature stem cell resulting in a hybrid leukemia.
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PMID:Hybrid leukemia and the 5q-abnormality. 204 86

A 58-year old man was admitted because of general malaise in April 1987. Physical examination revealed systemic lymphadenopathy and hepatosplenomegaly. The white blood cell count was 252, 900/microliters with 82% of blasts. Bone marrow aspiration contained 93.8% lymphoblasts, which were positive for TdT and negative for peroxidase reaction. Immunologic marker studies showed OKT 11 positive and CALLA negative. Cytogenetic analysis revealed a clone with 46, XY, t (9; 22) (q34; q11), del(5) (q15) in 12 of the 13 metaphases. Ph1 positive T-acute lymphoblastic leukemia was considered. After AdVP and following AdVEMP (induction) chemotherapy, complete remission was obtained in August 1987. Cytogenetic study at the remission stage showed complete disappearance of Ph1 positive clone. Treatment with BH-AC DMP protocol at the time of recurrence in November 1987, brought no improvement and he died of respiratory failure. Chromosome study at recurrence showed an additional complex abnormal karyotype (double Ph1, +2, 5q-, -10, -13, -17). DNA analysis revealed rearrangements of bcr gene with deletion of 5' side and of TCR delta gene, without any rearrangements in other immunoglobulin genes. From cytogenetic, immunophenotypic and genetic analysis the patient was diagnosed as having acute lymphocytic leukemia (FAB L1) with Philadelphia chromosome and rearrangements of bcr gene with deletion of 5' side and of TCR delta gene.
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PMID:[Acute lymphocytic leukemia with Philadelphia chromosome and rearrangements of bcr gene and deletion of 5' side and of TCR-delta gene]. 214 50

The patient, an 18-year-old male, was admitted on May 17, 1988, because of high-grade fever, neuralgia and generalized lymphadenopathy. Bone marrow examination revealed a large number of small nests with myeloid blastic cells negative for both peroxidase and TdT activity. Ph1 chromosome and bcr rearranged fragment were positive. On a diagnosis of CML in the accelerated phase, treatment was started with standard BHAC-DMP and vincristine. However, fever still persisted and hematological improvement could not be obtained. From September 20, 1988, mithramycin was given at 25 micrograms/kg every three days. No fever was noted and the NAP score decreased. However, fever reappeared despite the continuing treatment. Combination use of vincristine (1.0 mg/week) and mithramycin (25 micrograms/kg/week) was then begun, and the fever immediately disappeared. After mithramycin administration, a transient marked increase of neutrophils appeared in the peripheral blood, suggesting the induction of differentiation. After then, a complete remission was obtained. A transient disappearance of Ph1 chromosome by the chemotherapy was noticed. He has remained in the chronic phase of CML for one year. In conclusion, combination use of vincristine and mithramycin may be useful in the treatment of the myeloid blast crisis.
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PMID:[Successful treatment of CML in accelerated phase with mithramycin]. 214 52

We report two cases of Philadelphia (Ph1) chromosome positive acute mixed lineage leukemia (AMLL) with breakpoint cluster region (bcr) (M-BCR-1) rearrangement. A 31 year-old-man (case 1) and a 42 year-old-woman (case 2) were admitted to our hospital for further evaluation of leucocytosis with atypical blasts. Each case was diagnosed as having bilineal type of AMLL because: (1) blasts in each case consisted of larger myeloid cells positive for myeloperoxidase and small lymphoid cells positive for PAS, and blasts in case 2 were positive for TdT; (2) blasts in case 1 expressed B lymphoid associated antigen; (3) Southern analysis in each case showed clonal rearrangements of both the immunoglobulin heavy chain and the T cell receptor beta gene. These two cases demonstrated the Ph1 chromosome and rearrangement of the bcr (M-BCR-1) gene, but none of splenomegaly, basophilia, and additional chromosome abnormalities were observed. In addition, after achieving remissions, they didn't revert to chronic phase of chronic myelogenous leukemia (CML) and showed normal neutrophil alkaline phosphatase scores, and the Ph1 chromosome disappeared completely in case 1 and coexisted with the normal chromosome in case 2. These findings suggest that diagnosis of both cases should not be CML blast crisis (BC) but Ph1 positive acute leukemia, and Ph1 positive AMLL may be a distinct clinical entity to be distinguished from CML-BC.
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PMID:[Philadelphia chromosome positive acute mixed lineage leukemia with bcr (M-BCR-1) rearrangement]. 215 95


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