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)

This report describes 4 cases of T-cell-associated CD7-positive acute myeloid leukemia (AML). Myelo-peroxidase staining of blasts was negative in 2 cases but became positive during their courses. In all cases, the myeloid determinants CD13 and/or CD33 were associated with CD7 expression. Other B-lymphoid (CD10, CD19) or T-lymphoid (CD2) markers were negative. In three cases, dual fluorescence analyses showed co-expression of CD7 and CD13 (CD33). Clinically, compared with CD7+AML, these CD7+AML patients presented higher leukocyte and blast counts in peripheral blood. All patients achieved complete remission with chemotherapeutic regimens for AML, but 3 relapsed within a short time. Systemic lymphadenopathy was found in 2 cases, and interestingly, the surface markers of the lymph-node in one case were CD7+CD33-. These cases of CD7+AML may represent a distinct subgroup that arises from particular, less different myeloid precursors, and may have poor prognosis.
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PMID:[Four cases of CD7-positive acute myeloid leukemia]. 845 Jun 9

Leukemic transformation in essential thrombocythemia (ET) is rare. We describe a patient with ET which transformed to megakaryoblastic leukemia with myelofibrosis after treatment with melphalan for 8 years. His course after transformation smouldered for 20 months without antileukemic chemotherapy. A 61-year-old man was referred by a local doctor to Niigata University Hospital due to nasal bleeding in June 1984. Complete blood count (CBC) was as follows; hemoglobin 12.4 g/dl, platelets 268.8 x 10(4)/microliters, and white blood cells 11,900/microliters, with differentials of 39% PMN, 1% basophils, 2% eosinophils, 4% monocytes, and 13% lymphocytes. Bone marrow examination revealed hyperplasia of megakaryocytes without increase of reticulin fibers. Neutrophil alkaline phosphatase activity and karyotype of marrow cells were normal. ET was diagnosed. He was followed up by local doctor. The platelet count was controlled at a level of approximately 40 x 10(4)/microliters with melphalan for eight years. In January 1992 he developed pain in his lower extremities. He was admitted to our hospital on May 29, 1992. CBC was as follows; hemoglobin 8.9 g/dl, platelets 14.3 x 10(4)/microliters, and white blood cells 3,500/microliters, with differentials of 25% PMN, 5% monocytes, 28% lymphocytes, and 24% blasts. Bone marrow aspiration was unsuccessful and bone marrow biopsy revealed increases in fibroblasts and collagen fibers. Circulating blasts were positive for CD4, CD7, CD25, CD13, CD33, CD34, and HLA-DR and partly positive for CD41 and CD36. In ultrastructural cytochemistry blasts were positive for platelet peroxidase but negative for myeloperoxidase. Cytogenetic study revealed 46, XY, +der (1) t(1:7) (p11;q11) in all of five metaphases. He was diagnosed with megakaryoblastic leukemia accompanied by myelofibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Essential thrombocythemia in transformation to smouldering megakaryoblastic leukemia with myelofibrosis]. 853 33

During the immunodiagnosis of 517 cases of acute myelogenous leukemia (AML) entered into the Medical Research Council (MRC) AML 10 trials, we have observed the CD34 precursor cell antigen more frequently in AML of M2 morphology, especially in the 84% of cases with the t(8;21) chromosomal translocation, than in any other French-American-British classification group. CD34 expression was then quantified (using QIFI and Quantum Simply Cellular beads [Flow Cytometry Standards, Research Triangle Park, NC] and CD34+ standard cells). When CD34 antibody-binding capacity (ABC) of normal bone marrow (BM) precursors and leukemic blasts was compared, it was shown that AML M2 cases with t(8;21) not only had the highest percentages of CD34+ blasts, but in > 80% of CD34+ cases the individual blasts expressed higher than normal levels of CD34 antigen (> 60 x 10(3) ABC per cell). In addition, in 73% of this group CD34 antigen was overexpressed in an asynchronous combination with cytoplasmic myeloperoxidase (MPO). Other signs of asynchrony included high CD34 expression with CD15 and/or CD56, as well as aberrant combinations of CD13 with terminal deoxynucleotidyl transferase (TdT) and CD19. These findings demonstrate that asynchrony is identifiable in virtually every case of AML with t(8;21), although it does not always involve the same antigens. M2 cases with t(8;21), mostly CD34+, had a 100% remission rate and 71% 5-year survival rate; other patients with CD34+ or CD34- AML showed 69% and 84% remission rates and 31% and 36% 5-year survival rates, respectively. Consequently, individual markers such as CD34 should be interpreted in relation to other features such as chromosomal changes. These simple methods, which are well suited to quantify the expression of ligands, are a useful contribution to diagnosis: 60% to 65% of M2 cases with t(8;21) are rapidly identified by CD34 overexpression alone. This aberration, together with the other signs of asynchrony seen at presentation, can be used to search for residual leukemia after therapy.
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PMID:Leukemia-associated changes identified by quantitative flow cytometry. IV. CD34 overexpression in acute myelogenous leukemia M2 with t(8;21). 856 43

We describe a patient with primary myelodysplastic syndrome (MDS) evolving into acute nonlymphocytic leukemia (ANLL) who had two cytogenetically unrelated abnormal clones. A 68-year-old man presented with refractory anemia with excess of blasts (RAEB) and developed overt ANLL. Two cytogenetically independent clones, one with 5q- and the other with 20q-, were observed when the patient developed ANLL. The clones carrying both 5q- and 20q- were not detected. Leukemic blast cells were positive for peroxidase, naphtol ASD chloroacetate esterase, CD13, CD33, CD34 and HLA-DR, but negative for alpha-naphthyl butyrate esterase, CD14, CD10, CD19, CD20, CD1, CD2, CD3, CD5 and CD7. Although there have been a few reports describing the presence of multiple cytogenetically unrelated clones in one patient with MDS, this is the first case report that the 5q- and 20q- anomalies are derived from independent clones.
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PMID:Two karyotypically unrelated clones with 5q- and 20q- in a primary myelodysplastic syndrome patient evolving into acute nonlymphocytic leukemia. 859 Jul 73

A novel human leukaemia cell line (Kasumi-4) was established from the peripheral blood of a 6-year-old girl suffering from chronic myelogenous leukaemia (CML) in blast crisis. The Kasumi-4 cells had the following characteristic features: undifferentiated blasts which were positive from CD34, CD33 and CD13 surface markers, but negative for myeloperoxidase platelet peroxidase, CD36, CD41 and CD42; chromosome abnormalities of t(9;22;11) (q34;q11;q13), inv(3)(q21q26); and elevated expression of EVI1 gene which is located at chromosome band 3q26. Megakaryocytic maturation was not observed in the liquid culture following the addition of TPA, IL3, IL-6 or GM-CSF, b2-a2 type of BCR-ABL chimaeric messenger RNA was detected by RT-PCR analysis. This the first leukaemia cell line with a three-way translocation containing the the Ph chromosome and the second cell line with an inv(3)(q21q26). This cell line appears to be useful for studying the mechanisms of leukaemogenesis involving these chromosomal abnormalities and related oncogenes.
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PMID:Establishment of a myeloid leukaemia cell line (Kasumi-4) with t(9;22;11)(q34;q11;q13), inv(3)(q21q26) and the EVI1 gene activation from a patient with chronic myelogenous leukaemia in blast crisis. 861 78

A novel human leukemia cell line (Kasumi-3) was established from the blast cells of a 57-year-old man suffering from myeloperoxidase-negative acute leukemia. The cell line had five distinctive features, as follows. 1) Flow cytometric analyses showed cell surface expression of CD7, CD4, CD13, CD33, CD34, HLA-DR and c-Kit. This phenotype is compatible with that of acute myelocytic leukemia cells with the M0 subtype in the French-American-British classification. 2) Kasumi-3 cells carried chromosomal abnormalities of t(3;7)(q27:q22), del(5)(q15), del(9)(q32), and add(12)(p11). The breakpoint of 3q27 was located near the EVI1 gene, and a high level of expression of the EVI1 gene was observed. 4) Kasumi-3 cells treated with TPA showed maturation to monocytic lineage. 5) Treatment with either interleukin (IL)-2, IL-3, IL-4, granulocyte-macrophage colony-stimulating or stem cell factor induced the proliferation of Kasumi-3 cells. Thus, the Kasumi-3 cell line shows the characteristic features of undifferentiated leukemia. It should, therefore, be useful both for studying the biological characteristics of acute myelogenous leukemia M0 subtype and for investigating the role of the EVI1 gene in leukemogenesis.
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PMID:Establishment of an undifferentiated leukemia cell line (Kasumi-3) with t(3;7)(q27;q22) and activation of the EVI1 gene. 861 29

FAB proposals for the diagnosis of AML-M0 represent the formal recognition of a distinct entity which has been described over the past few years by several authors and called minimally differentiated acute myeloid leukemia. By definition, AML-M0 includes acute leukemias which do not fit morphological and cytochemical criteria for the diagnosis of AML, and for which myeloid lineage assignment can be made by immunological assay showing positivity for MPO, CD13, and CD33 and negativity for lymphoid markers. Involvement of an early myeloid progenitor in the leukemic process is a possible theory hypothesized to explain the existence of such a form. Validity of this assumption has been based on the observation that AML-M0 frequently bears "stem cell" markers such as CD34, HLA-DR, Tdt, CD7, and promiscuous IgH/TCR gene rearrangements, which are thought to occur in uncommitted cells. Finally, AML-M0 very frequently carries cytogenetic abnormalities common to MDS or secondary AML, such as -5/5q- or -7/7q- deletions and or complex karyotype. In our experience, AML-M0 is also very often associated with the MDR phenotype, which in turn has been found strictly linked to "stem cell" features, especially in MDS. These biological aspects, altogether, translate into a very unfavorable prognosis, confirming even from a clinical point of view that AML-M0 is a distinct entity. In conclusion, "stem cell" markers, MDR phenotype, complex chromosome lesions, frequent occurrence in elderly patients, and intrinsic chemoresistance characterize AML-M0 and indicate the need for tailored treatments, possibly involving the use of MDR modulators and/or differentiating agents.
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PMID:Minimally differentiated acute myeloid leukemia (AML-M0): a distinct clinico-biologic entity with poor prognosis. 862 74

We report a patient with acute myeloid leukemia (AML) presenting with generalized lymphadenopathy, clinically stimulating aggressive non-Hodgkin's lymphoma. This patient presented with anemia and bulky lymphadenopathy in the oropharyngeal (Waldeyer's ring), submandibular, supraclavicular and inguinal nodal regions. Lymph node biopsy was initially suggestive of a T-cell lymphoblastic lymphoma, based on morphologic features together with positive immunohistochemical staining for CD7 and CD43 (Leu 22). Definitive diagnosis of AML was established when a more detailed immunophenotypic analysis showed expression of the myeloid markers CD13 and CD33, and by the demonstration of rare Auer rods and positive peroxidase staining in bone marrow blast cells. Although this is a rare presentation, AML must always be considered in the clinical and pathologic differential diagnosis of aggressive non-Hodgkin's lymphoma.
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PMID:Acute myelogenous leukemia presenting with bulky lymphadenopathy. Case report and literature review. 863 42

Fourteen patients with hypocellular acute leukemia (HAL) were reviewed. The median age was 72 years, with an equal male-to-female ratio. Severe granulocytopenia with marrow hypocellularity and increased marrow blasts and absence of physical findings were common features. The median peripheral blood blast count was 2%. All except 3 cases of erythroleukemia had marrow blast count that exceeded 30% of all nucleated marrow cells. All cases were classifiable with the FAB criteria. FAB classification revealed a preponderance of the M1 category followed by M2 and M6 types. The majority of blasts were type I and the median myeloperoxidase positivity was 14%. Immunophenotyping of bone marrow cells by flow cytometry in 9 cases showed expression of myeloid antigens (CD13, CD33); 6 cases also expressed CD34 antigen. Significant dysplasia involving erythroid and megakaryocytic lineages was seen in most of the cases. Trilineage dysplasia was observed in 5 cases. Median survival of the entire group was 10.5 months. Eleven patients underwent induction therapy consisting of daunorubicin and cytosine arabinoside +/- 6 thioguanine; 8 patients achieved complete remission (72.6%). Remission duration was 14.5 months. Three patients (27.4%) died secondary to infections during induction therapy. Higher frequencies of trilineage dysplasia and FAB M6 type together with low percentage of peripheral blasts and presence of antecedent hematologic disorders suggest that some of these cases might represent the hypocellular form of acute myeloid leukemia with trilineage dysplasia.
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PMID:Hypocellular acute myeloid leukemia: the Rochester (New York) experience. 865 64

The authors examined the expression of myeloid antigens (MyAg): CD11b, CD13, CD14, CD15, and CD33 in 249 adults with lymphoid neoplasms using flow cytometric analysis. In this study, acute leukemia that was myeloperoxidase negative by light microscopy and had at least one lymphoid antigen was defined as acute lymphoblastic leukemia (ALL). The patients were classified as follows: 6 with unclassified ALL, 35 early B precursor ALL, 32 T-ALL, 25 B-cell chronic lymphocytic leukemia (B-CLL) and its variants, 24 B-cell non-Hodgkin's lymphoma (B-NHL), 7 plasma cell disorders, 8 T-CLL, 2 adult T-cell leukemia, and 10 T-NHL. CD11b and CD15 were present in a wide range of lymphoid disorders irrespective of B/T lineage and maturity. Unclassified ALL and phenotypically immature ALL frequently expressed CD13 and CD33, and occasionally expressed CD14. Among early B precursor ALL, CD13, and/or CD33 were significantly associated with the presence of stem cell marker CD34 and the chromosomal abnormality t(9;22). In addition, ALL with deletion of chromosome 7 commonly expressed CD13 and CD33. Taken together, CD13 and/or CD33 positive ALL may originate from a multipotential stem cell. Among mature neoplasms, CD14 was frequently, and CD13 and CD33 were occasionally expressed in B-cell, but not T-cell tumors. These results suggest that CD13, CD14, and CD33 are preferentially expressed in two types of lymphoid neoplasms, namely undifferentiated ALL and mature B-cell lymphoproliferative disorders.
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PMID:Myeloid antigen, CD13, CD14, and/or CD33 expression is restricted to certain lymphoid neoplasms. 865 52


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