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)

Acute leukemias (ALs) with phenotypic and genotypic features of several hematopoietic lineages are difficult to classify and may represent the transformation of multipotent stem cells. We have studied immunological features of 200 cases of acute leukemia (109 acute myelogenous leukemia, AML, and 91 acute lymphoblastic leukemia, ALL, according to FAB criteria), including 17 (8.5%) classified as biphenotypic by a scoring system based on the number and specificity of unexpected lineage antigens and which gives more weight to cytoplasmic markers such as myeloperoxidase, CD3, and CD22, and less to other membrane markers. Sixty-eight AML and 42 ALL cases were also examined for rearrangements of the immunoglobulin (Ig) and T-cell receptor (TCR) beta, gamma, and delta genes, and these included 12 biphenotypic AL. The expression of myeloid antigens in ALL was seen in 25% of the cases. All B-lineage ALL had rearrangements and/or deletions of the Ig genes whereas TCR beta, gamma, and delta genes were rearranged in 21%, 52%, and 71%, respectively. TCR delta, gamma and/or beta were rearranged in T-ALL and four out of 13 cases had Ig gene rearrangement. Lymphoid-associated antigens were expressed in 40% of AML cases; those most frequent expressed were CD7 (17%), CD2 (15%), CD19 (10%), and CD10 (7.5%). Evidence of Ig and/or TCR gene rearrangements was detected in 12% of AML cases. There was no correlation between the isolated expression of terminal deoxynucleotidyl transferase (TdT), B, and T-cell antigens with Ig and TCR gene rearrangements. However, in cases of AML defined as biphenotypic because they expressed two or more lymphoid antigens there was a statistically significant correlation between gene rearrangements and lymphoid score (p < 0.001). Our findings support the concept of biphenotypic leukemia as a distinct entity in which there is frequent correspondence between phenotypic and genotypic changes.
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PMID:Lineage commitment in biphenotypic acute leukemia. 850 86

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

Thirty-four patients with chronic myeloid leukemia in blast crisis (CML-BC) were evaluated for lineage differentiation with immunological markers and the presence of ultrastructural peroxidase. Eighteen (52.9%) were found to have myeloid blast crisis. Cytochemically, myeloperoxidase (MPO) could be detected only in six patients on light microscopy while in the remaining 12 patients, myeloid differentiation was confirmed only by demonstration of MPO either at ultrastructural level or by the reactivity with anti myeloperoxidase (anti MPO) antibody. Six (17.6%) had lymphoid blast crisis as identified by lymphoid specific markers (CD19; CD10; CD7; CD4) along with the absence of myeloid markers. Heterogenous blast cell populations with mixed lineage differentiation were seen in 4 (11.7%) patients. These cases showed both lymphoid (CD19, CD10) and myeloid (anti MPO and ultrastructural MPO) characteristics. A single case of megakaryoblastic blast crisis was identified with positivity for CD41 and CD42 along with the presence of platelet peroxidase at the ultrastructural level. Five cases (14%) of CML blast crisis remained unclassifiable. These results suggest that blast crisis in CML show an arrest of differentiation at an early stage when compared to de novo acute leukemias. This is particularly evident from the fact that MPO could only be demonstrated ultrastructurally or with anti MPO antibody in the majority of patients with myeloid differentiation. It is expected that utilisation of molecular studies including immunoglobulin and T-cell receptor gene rearrangement and m-RNA expression for myeloperoxidase will provide a better insight into the level of differentiation for the presently unclassifiable cases of CML-blast crisis.
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PMID:Immunophenotype and ultrastructural studies in blast crisis of chronic myeloid leukemia. 853 24

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 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

We have studied the molecular characteristics of the T cell receptor (TcR) genes in 16 patients with CD7+ early T cell acute lymphoblastic leukemia (T-ALL), defined as being positive for CD7 but negative for CD3/4/8, myeloperoxidase (MPO), and CD19/20. Using gene analysis, rearrangement was demonstrated in one patient for immunoglobulin heavy chain (IgH) gene, five for TcR-beta gene, and four for TcR-gamma gene. Fifteen patients (94%) had rearranged band(s) involving the joining region of the TcR-delta chain gene. In nine cases these were the only rearrangements, whereas in six cases TcR-beta and/or TcR-gamma gene rearrangements were found as well. The D delta 2(D delta)J delta 1 rearrangement was demonstrated in 87.5% (14/16) of cases. D delta 2(D delta)J delta 3 was recognized in one patient, D delta 2D delta 3 was found in three, and V(D)DJ using only V delta 2 and V delta 3 was recognized in two patients. We found no V2D delta 3, V3D delta 3, or V1(D)DJ delta rearrangement patterns. Five of nine cases with DDJ delta were positive for cytoplasmic CD3 epsilon(CyCD3 epsilon). Our data suggest that DDJ delta joining occurs at an early stage during T cell differentiation, followed by rearrangements of V delta to the DDJ delta complex. Furthermore, our findings suggest that DDJ delta recombination occurs earlier than expression of CyCD3 epsilon protein products. DDJ delta rearrangements have never been observed in non-T cell malignancies, such as precursor-B-ALL or acute myeloid leukemia. Therefore, detection of DDJ delta rearrangement in the TcR-delta locus is a useful tool to establish lineage and clonality of leukemic cells in the most immature stages of T cell development.
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PMID:High prevalence of T cell receptor D delta 2(D delta)J delta rearrangement in CD7-positive early T cell acute lymphoblastic leukemia. 861 42

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

CD7-positive acute myeloid leukaemias (CD7+AML) represent a distinct biological and clinical subtype of AML. The results of previous studies suggested that CD7 expression on myeloid leukaemic blasts might result from leukaemic transformation and maturation arrest of haemopoietic precursors at the stage of early myeloid differentiation when CD7 was transiently expressed. However, CD7+ myeloid progenitors have not yet been directly documented in normal human haemopoietic tissues. In this study, haemopoietic cells from 16 human fetal livers with a gestational age of 16-28 weeks were studied. Double myeloperoxidase (MPO) and CD7-positive cells could be demonstrated on 0-4% (mean 1.8%) of total fetal liver mononuclear cells (FLMC) by double cytochemical reaction of MPO and immunocytochemical staining of CD7. Simultaneous expression of CD7 and myeloid antigens (CD13 and/or CD33) could also be detected on 2.2-15.6% (mean 9.3%) of FLMC by dual-colour immunofluorescence flow cytometry analyses. CD13 and/or CD33 positive (CD13/33+) myeloid cells were positively selected by immunomagnetic bead separation system to a purity of 86.5-99.1% (mean 96.0%) of which < or = 3.3% were CD3+ cells and < or = 1.2% were CD19+ cells. Coexpression of CD7 was detected on 8.7-34.5% (mean 17.3%) of this CD 13/33+ cell population, but it was induced to decrease significantly after short-term in vitro culture with the differentiation-inducing agent phorbol ester (TPA). Coexpression of CD7 and CD13/33 could also be shown on a minor population of adult bone marrow and cord blood mononuclear cells (mean 3.9% and 1% respectively). In conclusion, the normal putative counterparts of blasts from CD7+ AML could be demonstrated in human haemopoietic tissues. The fact that CD7 expression tended to be lost after TPA stimulation suggested that CD7 was transiently expressed in early myeloid differentiation.
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PMID:Putative normal counterparts of leukaemic cells from CD7-positive acute myeloid leukaemia can be demonstrated in human haemopoietic tissues. 879 Jan 49

A novel human leukaemic cell line, designated CTS, was established from the peripheral blood of a 13-year-old girl suffering from acute myeloblastic leukaemia (AML) in relapse. CTS cells expressed CD7, CD13, CD33, CD34 and HLA-DR antigens, and showed ultrastructural myeloperoxidase activity. In addition, CTS cells showed DNA rearrangements of the immunoglobulin heavy chain gene and the light kappa chain gene, and deletions of the T-cell receptor delta 1 gene. Cytogenetic analysis revealed a human female diploid karyotype with a t(6;11)(q27;q23) chromosomal translocation. Molecular studies demonstrated a DNA rearrangement of the MLL gene, the expression of a truncated 11.0 kb MLL mRNA and the detection of the MLL/AF-6 fusion transcript in CTS cells. To our knowledge, this cell line is the first report of a human leukaemic cell line with a t(6;11) chromosomal translocation. CTS cells showed no significant proliferative response to the cytokines, IL-2, IL-3, IL-6, IL-11, GM-CSF, G-CSF, EPO, SCF, but were induced to differentiate to the T-cell, B-cell, erythroid or megakaryocytic lineage in the presence of particular cytokines. This CTS cell line may provide a useful tool in the study of the oncogenesis of mixed lineage leukaemia with 11q23 abnormalities and for the analysis of growth and differentiation of pluripotent stem cells.
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PMID:A novel human leukaemic cell line, CTS, has a t(6;11) chromosomal translocation and characteristics of pluripotent stem cells. 890 86


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