Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.11.1.7 (peroxidase)
 65,474 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A novel human myeloid cell line, designated HSM-1, has been established from the pleural effusion of a patient with granulocytic sarcoma (GS) who had been followed as having primary myelofibrosis for 10 years. When he was diagnosed as having granulocytic sarcoma in dermal tissues, no evidence of malignant transformation into leukaemia was found in both the peripheral blood and bone marrow. The established cell line was positive for myeloperoxidase, Sudan black B, Naphthol AS-D chloroacetate esterase. Surface marker analysis revealed that HSM-1 expressed CD4, CD13, CD11a, CD11b, Leu8, CD49b, CD49d, CD49e, CD29 and HLA-DR. To clarify why the unusual myeloid tumours developed in non-haematopoietic tissues, we examined the capability of HSM-1 to bind to skin fibroblast layers. The HSM-1 cells were found to bind to both bone marrow stromal layers and skin fibroblast layers. Among the other myeloid cell lines tested, none was found to bind to skin fibroblast layers. These findings suggest that the GS cell line may be derived from a haematopoietic precursor cell which can bind to skin fibroblasts and is localized in non-haematopoietic tissues resulting in the formation of extramedullary myeloid metaplasia. HSM-1 is a useful tool for analysing the characteristics of granulocytic sarcoma and homing receptors for haematopoietic stem cells.
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PMID:Establishment of a novel granulocytic sarcoma cell line which can adhere to dermal fibroblasts from a patient with granulocytic sarcoma in dermal tissues and myelofibrosis. 141 99

A patient with CML showed monoblastic crisis which started with extramedullary tumor formation in a rib before medullary involvement. She was diagnosed as having CML in 1984 at the age of 57. In February 1990, she was admitted to Furukawa City Hospital because of extramedullary blastic crisis beginning at the right 5th rib. At that time, the bone marrow revealed 4.6% blasts. On March 5, after one course of chemotherapy, she was transferred to our hospital for radiotherapy. Hematological findings were WBC 10,100/microliter with 10% blasts, Hb 10.9 g/dl, platelet 3.7 x 10(4)/microliters. Bone marrow aspiration was unsuccessful. The blasts in the peripheral blood were negative for peroxidase and chloroacetate esterase; but positive for naphtylbutyrate esterase. The leukemic cells were positive for CD13, CD33, and had phagocytic activity. Chromosomal analysis revealed 46XX with Ph1 chromosome and some additional anomalies. Southern blot analysis of tumor cells shows BCR rearrangement. These findings suggest that the blasts were immature monocytic cells, and we conclude that this is a rare case of extramedullary monoblastic crisis of CML.
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PMID:[A case of monoblastic crisis of CML beginning with extramedullary tumor formation in a rib]. 143 21

Seven of 368 cases of acute myeloid leukemia (AML) could not be subclassified by routine morphologic, cytochemical and immunologic analyses during the period January 1989 to December 1990. Further investigations including ultrastructural examination, anti-myeloperoxidase and myeloid specific antigen analysis were carried out in all these patients and they were classified as AML-MO, as per the FAB criteria. Morphologically these blasts resembled ALL-L2/AML-M1. Cytochemically they were negative for Sudan black, myeloperoxidase, periodic acid-Schiff, and non-specific esterase. On initial immunophenotypic analysis, they could not be classified into B, T or myeloid lineages. Further investigations revealed CD13 and CD33 positivity in 4 of 6 patients. Anti-myeloperoxidase was positive in 6 of 6 patients and ultrastructural examination revealed myeloperoxidase-positive blasts in 6 of 7 cases. Cytogenetic analysis done in one patient revealed 60% abnormal metaphases. Six of 7 cases were treated with aggressive chemotherapy. One patient achieved complete remission but relapsed after 6 months, whereas others were resistant to treatment. Hence we conclude that an aggressive investigative and therapeutic approach is required to identify and treat AML-MO.
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PMID:Minimally differentiated acute myeloid leukemia: a morphologic, cytochemical and ultrastructural study. 144 Sep 42

Acute leukemias have been classified on French-American-British (FAB) criteria depending on the morphocytochemical features of blasts. Immunophenotyping and clonal rearrangement analysis of lineage-associated genes can decide a frozen stage of the hematopoietic differentiation process in blasts from acute leukemias. B-lineage acute lymphoblastic leukemia (ALL) and T-lineage ALL are systematically classified according to the sequential expression of differentiation-associated antigens. In acute myelogenous leukemia (AML), several new entities are proposed: AML-M0 is an AML without cytologic maturation, in which the myeloid commitment should be demonstrated by myeloperoxidase-positive microgranule on immunohistochemical staining or electron-microscopy, or by positive reaction for CD13 or CD33 antigens. CD7-positive AML is considered to be one of immature subtypes of AML, rather than hybrid leukemia. Thus, immunological studies on blasts enable us to discriminate a subgroup of leukemias, which will perhaps contribute to the improvement of treatment approach.
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PMID:[Immunophenotypic analysis in acute leukemia]. 151 38

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

Granulocyte colony-stimulating factor (G-CSF) receptors on the gated leukemic blast cells from newly diagnosed patients with acute leukemia or crisis of chronic myelogenous leukemia were investigated using flow cytometric detection. Surface marker analysis and cytochemical studies were conducted simultaneously to characterize the blast cells. Among 24 leukemia cases examined, G-CSF receptor-positive blast cells were detected in all 11 cases of acute myeloblastic leukemia even though the percentage range of positive cells was widely variable. On the other hand, they were not detected on the blast cells from patients with peroxidase-negative acute lymphoblastic leukemia with no myeloid surface antigens. However, G-CSF receptors were demonstrated in significant amounts on blast cells from 5 of 8 cases of peroxidase-negative acute leukemia expressing both myeloid and lymphoid surface antigens (biphenotypic leukemia). The percentage of blast cells positive for G-CSF receptors was significantly smaller in biphenotypic cases [33 +/- 14% (SD)] than in acute myeloblastic leukemia cases [65 +/- 22%] (P less than 0.01). The percentage expression of CD13 antigen by blast cells was significantly related to their percentage positivity for G-CSF receptors (rs = 0.50, P less than 0.05). These findings indicate that the distribution of flow cytometrically detectable G-CSF receptors on leukemic cells possessing myeloid characteristics may be related to the maturation process.
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PMID:Granulocyte colony-stimulating factor receptors on human acute leukemia: biphenotypic leukemic cells possess granulocyte colony-stimulating factor receptors. 153 71

The mechanism by which a clone of HL-60 human promyelocytic leukemia cells designated Tf-Gel-1 expresses reduced levels of the transferrin receptor (TfR) was investigated. Tf-Gel-1 was developed by continuous exposure of HL-60 cells to human iron-saturated transferrin covalently linked to the plant toxin gelonin (Tf-Gel); this variant was five- to sixfold more resistant to Tf-Gel than parental HL-60 cells. The amount of cell surface, as well as of solubilized, TfR and the cycling pools of TfR in Tf-Gel-1 cells, as measured by the binding of [125I]Tf, were all decreased to 20-30% of the levels present in parental cells. The growth of Tf-Gel-1 cells was independent of exogenous Fe3+ and was comparable to that of parental HL-60 cells. Despite the lower levels of TfRs, the Tf-Gel-1 clone retained the capacity to alter receptor expression, depending upon the phase of growth and the intracellular iron concentration, and to down-regulate TfRs in response to inducers of differentiation. Southern hybridization of cellular DNA with TfR cDNA did not reveal differences between parental and Tf-Gel-1 cells in the level and arrangement of the TfR gene. Basal and inducible (repressible) levels of TfR mRNA from Tf-Gel-1 cells, as measured by northern hybridization of cellular RNA with TfR cDNA, were comparable to those of parental cells. Metabolic labeling of cells with [35S]methionine, followed by immunoprecipitation of TfRs, demonstrated that the amount of radioactivity incorporated into TfRs in Tf-Gel-1 cells was reduced to a degree that approximated the decrease in [125I]Tf binding. Cell surface TfRs prepared from exponentially growing parental cells labeled with 125I by the solid-phase lactoperoxidase-glucose oxidase method existed as a doublet, with one form being phosphorylated and the other not phosphorylated. In contrast, Tf-Gel-1 cells not only contained diminished amounts of TfRs but also contained only the phosphorylated form of TfRs in the surface membrane. The decrease in the surface membrane concentration of the TfR in Tf-Gel-1 cells was specific for this glycoprotein, since the levels of other cell surface antigens, such as CD13, CD15 and CD45, were normal in Tf-Gel-1 cells. A reduction in the incorporation of [3H]mannose into the acid-insoluble fraction of cells and an increase in sensitivity to ricin suggested that Tf-Gel-1 cells possessed an aberration in carbohydrate metabolism.
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PMID:Characterization of the defect in a variant of HL-60 promyelocytic leukemia cells with reduced transferrin receptor expression. 154 69

Immunophenotypic analysis of acute leukemias is time consuming and often requires flow cytometric analysis. A 1-hour alkaline phosphatase-labeled streptavidin-biotin immunocytochemical procedure was evaluated as an alternative. Seventeen cases of acute leukemia, including 10 acute lymphocytic (ALL) and 7 acute nonlymphocytic, were phenotyped by the rapid immunocytochemical procedure and the results were compared with standard analyses. In all 17 cases, the diagnoses made using standard cytochemical and immunologic methods were the same as obtained in blinded reviews by rapid immunocytochemical analysis. Nine cases of precursor B-cell ALL were positive for CD19 and/or CD22. Five CD19 + cases of ALL reacted with anti-myeloperoxidase, with one case also positive for CD15. CD15 positivity was confirmed on repeated study as well as with plastic section immunoperoxidase staining. Nine cases of ALL were positive for CD10 and eight were positive for terminal deoxynucleotidyl transferase. One case of ALL marked as T-cell ALL with CD1, CD2, CD3, and CD7. All cases of acute nonlymphocytic leukemia were positive for CD15, CD13, and/or CD33; anti-myeloperoxidase was positive in all but one case of monocytic leukemia. All cases of acute nonlymphocytic leukemia were negative for CD10 and one was positive for terminal deoxynucleotidyl transferase. Acute leukemias apparently may be phenotyped easily and accurately in 1 hour with this immunocytochemical technique, and slides may be stored permanently for review. There was in these 17 cases high correlation of the diagnoses with standard flow cytometric and cytochemical results. This rapid method allows a coordinated evaluation of morphologic features and immunophenotype; the latter features facilitated confirmation of unexpected reactivity of myeloid markers CD15 and MPO-7 in some cases of ALL.
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PMID:Rapid immunocytochemical analysis of acute leukemias. 159 10

A megakaryoblastic cell line (MKPL-1) was newly established from the bone marrow of an adult patient with acute megakaryoblastic leukemia. This cell line grew in single cell suspension with a doubling time of 30 h and consisted of large primitive blasts with persistent development of giant cells carrying multilobed nuclei. MKPL-1 cells were positive for platelet GPIIb/IIIa (CD41) and GPIIIa (CD61), and expressed OKM5 (CD36), MY7 (CD13), and MY9 (CD33) antigens in the absence of erythroid and lymphoid markers. The cytochemical and morphologic characteristics of MKPL-1 were also consistent with those of megakaryoblasts. The cells did not, however, express ultrastructural platelet peroxidase which is considered to be another marker of the megakaryocytic lineage. Cytogenetic analysis of MKPL-1 revealed a model chromosome number of 92 with abnormal chromosomes including those found in the patient's bone marrow cells. Furthermore, MKPL-1 cells were serially transplanted into nude mice for nine passages with production of lethal tumors and leukemic manifestation. Thus, our megakaryoblastic cell line which can be maintained both in vitro and in vivo would be useful for further studies of the biology of megakaryopoiesis and megakaryoblastic leukemia.
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PMID:Acute megakaryoblastic leukemia: establishment of a new cell line (MKPL-1) in vitro and in vivo. 160 96

A 63 year-old woman was referred to our hospital because of fever and increased number of blasts in the bone marrow. On physical examination she had slight hepatomegaly but no splenomegaly. Laboratory tests disclosed a hemoglobin level of 8.5 g/dl; a WBC count of 13,200/microliter with 26% blasts; a platelet count of 51,000/microliter. A bone marrow aspirate was normocellular with 74% blasts and 37% blasts were stained positive for myeloperoxidase. Cell surface markers for HLA-DR, CD10, CD19, CD13, CD33 were positive. Karyotype analysis revealed 46, XX, t (9q+; 22q-) and 45XX, -7, t (9q+; 22q-). Southern analysis showed rearrangement of immunoglobulin heavy chain but not T cell receptor beta gene. Rearrangements in M-BCR were not detected with 5' or 3' bcr probes. After 2 courses of chemotherapy, blasts decreased to 7% with recovery of normal elements and 11 out of 20 metaphases of the bone marrow cells were normal karyotype. These findings suggest that this case was de novo Ph1 positive acute leukemia which demonstrated both lymphoid and myeloid features.
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PMID:[Biphenotypic acute leukemia with Ph1 chromosome, M-BCR-, myeloperoxidase+, and CALLA+]. 164 7


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