Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.11 (CD10)
 9,792 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A novel erythroid cell line, RM10, was established from a long-term bone marrow culture of a patient with chronic myelogenous leukemia (CML). RM10 cells were positive for periodic acid Schiff (PAS), but negative for peroxidase and dual esterase. RM10 cells had la, pre B (CD10), myeloid (CD13, CD14, CD33) and erythroid (glycophorin A) markers, but had no other lymphoid, megakaryocytic, or mesenchymal cell markers. RM10 cells spontaneously synthesized hemoglobin, which was markedly enhanced with hemin. Isoelectric focusing of the cell lysates and northern blot analysis of the total cellular RNA revealed hemoglobin synthesis in the cells. Using 125I-labeled recombinant human erythropoietin (Epo), two classes of Epo receptors were demonstrated in the RM10 cells. However, Epo did affect neither growth nor erythroid differentiation of the cells. RM10 cells rapidly differentiated to monocytic cells in the presence of 12-0-tetradecanoylphorbol-13-acetate, and simultaneously expressed glycoprotein IIb/IIIa. RM10 cells had Philadelphia chromosome (Ph), and expressed p210bcr-abl using immunoprecipitation with anti-c-abl and anti-phosphotyrosine antibodies. These results indicate that the RM10 cells have the characteristics of multipotential hemopoietic cells originating from Ph-positive CML and that high affinity Epo receptor class is not a sufficient condition for Epo responsiveness.
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PMID:A novel CD10-positive erythroid cell line, RM10, established from a patient with chronic myelogenous leukemia. 216 10

The fine structural distribution of the enzyme-neutral endopeptidase EC 3.4.24.11 (enkephalinase) was examined by immunoradioautography (using an iodinated monoclonal antibody) and peroxidase immunocytochemistry (using the same probe in nonradioactive form) in the neostriatum of the rat. At the light microscopic level, both techniques revealed a heterogeneous distribution of immunoreactive enkephalinase in the caudoputamen, characterized by the presence of patches of intense immunolabeling prominent against a relatively strong immunoreactive matrix, a pattern reminiscent of mu opioid receptors radioautographically labeled in the same region. Pilot experiments indicated that fixation of the brain with a mixture of 4% paraformaldehyde, 0.05% glutaraldehyde, and 0.2% picric acid did not modify the distribution and only slightly reduced the intensity of striatal enkephalinase antigenicity, provided that the post-fixation period did not exceed 1 hr. In the neostriatum of animals fixed according to this protocol, enkephalinase immunoreactivity was found by electron microscopic immunoradioautography to be exclusively confined to neuronal and glial membrane interfaces. Immunoperoxidase cytochemistry confirmed the association of immunoreactive enkephalinase with the plasma membrane of neurons and, to a lesser extent, of astrocytes and oligodendrocytes. Both immunoradioautographic and immunoperoxidase techniques revealed a predominant association of the enzyme with neuronal perikarya and dendrites. The morphological features of the labeled perikarya, together with the presence of immunoreactive dendritic spines, suggested that some of these neurons corresponded to striatofugal medium spiny neurons. Immunoreactive enkephalinase was also detected at the level of myelinated and unmyelinated axons and axon terminals. These axons could potentially have originated from intrinsic striatal neurons or from the substantia nigra. Statistical analysis of silver grain distribution in electron microscopic immunoradioautographs indicated that immunoreactive enkephalinase was not preferentially concentrated at the level of specific membrane interfaces, but rather, was more or less uniformly distributed on the surface of neurons and/or glial cells. A similarly diffuse localization of the enzyme was apparent in peroxidase-reacted material, though the latter technique also revealed a microheterogeneity in the deposition of the reaction product along the labeled membranes. Finally, quantitative analysis of immunoradioautographs clearly indicated an absence of enkephalinase enrichment at the level of synaptic junctions. The similarity between the light and electron microscopic distribution of enkephalinase observed in the present study, and that previously reported for mu opioid receptors, lends support to the concept that this ectoenzyme may be involved in the inactivation of endogenous opioids in the mammalian neostriatum.
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PMID:Electron microscopic localization of immunoreactive enkephalinase (EC 3.4.24.11) in the neostriatum of the rat. 220 54

The ultrastructural, light microscopical and immunological features of twelve cases of acute childhood leukemia are described. Nine cases were unclassifiable by light microscopy, morphology and cytochemistry, and three were difficult to classify because of a low percentage of Sudan-Black B positive blasts. By means of electron microscopy (including peroxidase cytochemistry), two main groups were seen: 1. Acute myeloid leukemia, in which could be distinguished a) a more differentiated myeloid leukemia, b) a leukemia with megakaryoblastic involvement and c) a minimally differentiated acute myeloid leukemia with granules present and 2. lymphoblastic leukemia. One case could not be classified. The first group included two possible cases of a hybrid leukemia with CD19 or CD10 positivity as well as ultrastructural peroxidase activity. We conclude that electron microscopy aids to further classification of minimally differentiated and hybrid acute leukemias.
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PMID:Electron microscopy: a contribution to further classification of acute unclassifiable childhood leukemia. 235 May 92

During the diagnostic investigation of 750 acute leukemias, nine cases were morphologically, cytochemically, and phenotypically undifferentiated. In seven of these cases the blasts were class II+, CD34+ and TdT+, in one were class II+, TdT+, CD7+ while in the remaining leukemia blasts expressed class II only. Cytoplasmic and membrane CD22, CD3, CD13, and Ig as well as membrane CD19, CD10, CD37, CD2, CD33, CD14, glycophorin C, and CD61 were absent. The further characterization of these rare leukemias yielded the following results. The TCR-beta, -gamma and -delta genes were in germline configuration in seven cases studied while IgH genes were rearranged on both alleles in two cases and germline in the other five. By ultrastructural analysis peroxidase activity was detected on unfixed cells in a minority of blasts from four of seven cases. In two of the peroxidase-positive cases a small proportion of blasts also reacted with an anti-myeloperoxidase monoclonal antibody. In one of the peroxidase-negative cases, 7% of blasts were labeled by the antibody, suggesting the presence of peroxidase in its proenzyme form. Importantly, the two cases with Ig gene rearrangements did not have cytochemically or immunologically detectable peroxidase. Three of the nine patients were treated as ALL while six received AML chemotherapy. In five patients complete remission was achieved while the other four died from infections during remission induction. Four patients are still in remission 7, 12, 24, and 30 months after diagnosis while one patient relapsed after 12 months. In conclusion, we have characterized the genotypic and ultrastructural features of subtype of acute leukemia in which blasts expressed immaturity markers and lacked lineage associated antigens. In contrast to previously reported "unclassifiable" cases, the leukemias were phenotypically homogeneous and showed a good response to chemotherapy.
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PMID:Phenotypic, genotypic, cytochemical, and ultrastructural characterization of acute undifferentiated leukemia. 239 82

In February 1986, a 68-year-old woman was diagnosed as having acute myeloblastic leukemia (FAB-M1). At the time of diagnosis, 86.0% of the bone marrow cells were myeloblastoid, and 15% of these myeloblastoid cells were positive to myeloperoxidase. Surface marker analysis by flow cytometry disclosed granulocyte-associated antigen (MY7) and also lymphocyte-associated antigen (CALLA) on the leukemic cells. Chromosomal banding studies of bone marrow cells revealed trisomy 11 in 6 of 19 metaphases examined and normal karyotype in the others. Complete remission was attained after intensive combination chemotherapy, and has remained for 38 months. Only 19 patients with trisomy 11-associated acute nonlymphocytic leukemia (ANLL) including the present case have been reported. Morphologic analyses have revealed that the frequency of FAB-M1 is high. However, except for the present case, surface marker findings were apparent in only one M5a patient, in whom monocyte-macrophage-associated antigen was detected. Accordingly, careful surface marker studies will be needed to clarify the frequency of acute mixed lineage leukemia in such patients.
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PMID:[Trisomy of chromosome 11 in a case of common ALL antigen-positive acute myeloblastic leukemia (FAB-M1)]. 253 25

A case of acute leukaemia is reported in which blast cells expressed some B-related antigens (namely the CALLA antigen) and no peroxidase activity at the optical level; however, some mature granular cells contained Auer rods. Simultaneous characterization of ultrastructural morphology, cytochemistry and immune phenotype was performed. There was an apparent mutual exclusion in the expression of myeloperoxidase activity and the CALLA antigen, and a heterogeneity in the CALLA expression among the blastic population. These results disagree with the hypothesis of a true biphenotypic leukaemia and demonstrate a complete heterogeneity between the lymphoblastoid cells and the myeloid ones. The interest of such a simple combined method in a case of putative hybrid acute leukaemia is emphasized.
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PMID:Interest of simultaneous ultrastructural characterization of morphology, cytochemistry and immune phenotype in a case of putative hybrid acute leukaemia. 253 24

Pretreatment peripheral and/or bone marrow blasts from 14 patients with acute unclassifiable leukemia (AUL) expressing myeloid related cell-surface antigen (CDII) or megakaryocyte-platelet related cell-surface antigen (OKM6), were isolated for further analysis in this study. Among 11 cases of CD11+AUL, despite a lack of myeloperoxidase (MPO) activity, one patient's blasts possessed Auer rod in a basophilic cytoplasm and another one's blasts expressed MPO maintaining the same surface phenotype after 20 months of his clinical course. The blast from 2 cases possessed both myelomonocytic and monocyte-specific antigens on the cell-surface, whereas the remaining nine cases completely lacked monocyte-specific antigen which is detectable by monoclonal antibodies, Mo2, My4 and Leu M3 (CD14). In addition, we revealed the presence of MPO protein in the cytoplasm of 3 cases of AUL patients by cytoplasmic immunofluorescence test utilizing monoclonal antibody (MA1). Following these results, the former was diagnosed as acute myelomonocytic leukemia (AMMoL) and the latter as acute myelogenous leukemia (AML) by immunophenotypic analysis using flow cytometry (FACS IV) and cytoplasmic immunofluorescence test. We have also described three cases of acute megakaryocytic leukemia which were demonstrated by the presence of megakaryocyte-platelet-related cell-surface antigens detected by utilizing flow cytometry and monoclonal antibodies in addition to both the PPO activity which was shown by ultrastructural cytochemistry, and the emergence of differentiation antigens while culturing these leukemic cells. The blast of 1 case possessed both platelet GPIb and GPIIb/IIIa cell-surface antigens detected by 5F1 (CD36), AN51 (CDw42), and J15, P2 and HPL2 (CDw41), respectively, whereas the remaining two cases almont lacked the GPIb cell-surface antigen. Hence, the former was diagnosed as immature (pro) megakaryocytic leukemia and the latter as acute megakaryoblastic leukemia from the viewpoint of immunophenotypic analysis as will be discussed in this article. These leukemic blasts did not express both T-cell lineage antigens which are detectable by monoclonal antibodies, T6 (CD1), T11 (CD2), T3 (CD3), T4 (CD4), T1 (CD5), Tp40, Leu9 (CD7), T8 (CD8), and B-cell lineage antigens which are detectable by monoclonal antibodies, B4 (CD19), B1 (CD20), B2 (CD21) and J5 (CD10).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Flow cytometric analysis of myeloperoxidase negative acute unclassifiable leukemias by monoclonal antibodies. Acute myelogenous and acute megakaryocytic leukemia]. 254 Dec 76

Acute leukemia was diagnosed in 62 adults and children over a recent 13-month period. Using light microscopy, cytochemical profiles, surface markers, and cytogenetics, 25 cases were classified as acute myeloid leukemia (AML) and 32 as acute lymphoblastic leukemia (ALL). The remaining 5 cases of de novo acute leukemia were unclassifiable. The routine cytochemical battery used on these 62 cases included: myeloperoxidase, sudan black B, nonspecific esterase, and periodic acid-Schiff (PAS). Flow markers utilized were: T3, T4, T5, T8, T10, T11, B1, B4, kappa, lambda, Ia, CALLA, Mo1, Mo2, My4, My7, My8, and My9. TdT was performed by immunoperoxidase and ELISA methods. The five unclassified cases were cytochemically negative and expressed no B- or T-cell-specific antigens, or TdT positivity. The morphologic differential diagnosis was between FAB L-2 and M-1. Karyotypic abnormalities involving chromosomes 3 and 7 were suggestive of myeloid origin in 2 of 4 patients studied. Flow cytometry demonstrated My7 on greater than 50% of blasts from two cases. Myeloperoxidase ultracytochemistry showed reaction product in small primary granules of blasts from all 5 cases. Positive cells contained only 1-2 granules/cell profile. The number of positive cells per case was in the range 10-20%. We conclude from this study that ultracytochemistry is very useful in providing definitive diagnosis and accurate subclassification of some AML FAB M-1 cases, particularly when light microscopic cytochemistry, cytogenetics, and flow cytometric markers are noncontributory. We propose to designate these acute "unclassified" leukemias as AML FAB M-1 "microgranular" type.
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PMID:Acute myeloid leukemia, FAB M-1 microgranular variant: a multiparameter study. 254 66

A 20-year-old man was admitted to our hospital because of fever and knee joint pain on March 20, 1986. Physical examination revealed generalized lymphadenopathy and hepatomegaly. White blood cell count was 32,800 microliters with 74.4% blast cells. Bone marrow was hypercellular with 93.6% blast cells. Blast cells were weakly positive for acid phosphatase and PAS stainings but were negative for peroxidase, sudan black B and esterase stainings. Cell surface marker analysis of blast cells disclosed that they were positive for anti-HLA-DR, CD19, CD24, CD33 and CD38, but were negative for CD10 and CD20. Cytoplasmic immunoglobulin of blast cells was negative and TdT activity by immunofluorescent method was positive. Chromosomal analysis of bone marrow samples revealed normal karyotype. Therefore, this case was diagnosed as having acute lymphoblastic leukemia (L2) and achieved complete remission with LVP therapy consisting of 1-asparaginase, vincristine and prednisolone. Gene analysis of blast cells disclosed germ-line configuration of both the immunoglobulin heavy chain gene and T cell receptor beta chain gene. We speculated that the phenotype of leukemic cells might precede the genotype in some cases of acute leukemia.
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PMID:[Germ-line configuration of the immunoglobulin heavy chain gene in a case of B cell precursor acute lymphoblastic leukemia]. 255 12

A 26-year-old male was admitted to our hospital because of fever and leukocytosis. On admission, a white blood cell count was 28,300/microliters with 46.5% blast cells and 16.0% atypical monocytoid cells, a hemoglobin level 13.7 g/dl, and a platelet count 15.0 X 10(4)/microliters. Bone marrow contained 58.8% of peroxidase-negative blast cells. He was diagnosed as acute lymphoblastic leukemia (ALL L2) according to the FAB classification. Chromosome analysis revealed the marrow cells to contain 45, XY, -7, t(9; 22) (q34; q11). On surface marker analysis, the leukemic cells were positive for both lymphoid (CD10) and myeloid markers (CD13). Two color flow-cytometric analysis showed two distinct populations with CD10 and CD1 3, respectively. Rearrangements of both immunoglobulin heavy chain and T cell receptor beta-chain were observed. The "breakpoint cluster region" on chromosome 22 was not rearranged. On the basis of these findings, we thought this case being acute mixed leukemia. He was refractory to AdVP therapy and BHAC-DMP therapy. He is now under treatment with A-Triple-V therapy.
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PMID:[Philadelphia-positive acute mixed leukemia with monosomy 7]. 255 34


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