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

It has been suggested that the malignant transformation, in some of the acute leukemias, may involve totipotent stem cells resulting in a biphenotypic leukemia expressing both myeloid, and lymphoid characteristics. We describe here a hybrid cell acute leukemia, in a 16-day-old infant, in whom leukemic cells coexpressed myeloid and lymphoid B cell antigens. Blast cells in the bone marrow showed L2 morphology according to the French American British (FAB) classification, with positive periodic-acid Schiff, and nonspecific esterase staining. Sudan black, and specific esterase were negative. Terminal deoxynucleotidyl transferase, was strongly positive in 5% of blasts, and faintly reactive with the rest. Karyotypic analysis demonstrated a translocation of t(11:17);(q23;p13). Immunoglobulin gene analysis revealed rearrangement of the heavy chain genes. The blasts' phenotype was HLA/DR+ B4+ My7+ My9+ common acute lymphoblastic leukemia antigen (CALLA) B1- T11-. Dual immunofluorescence staining using anti My7, and My9 fluorescein isothiocyanate, and anti B4 pycoerythrin conjugated monoclonal antibodies, and flow cytofluorometry, revealed a labeling pattern of 25% B4+; 10% to 15% My7+; 17% My9+; and 50% of cells coexpressing B4 My7, and My9 antigens. These results provide evidence for a hybrid leukemia with lymphomyeloblasts being part of a single clone, which may indicate the origin of this leukemic clone from a pluripotent (lymphoid/myeloid) stem cell.
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PMID:Undifferentiated leukemia of infancy with t(11:17) chromosomal rearrangement. Coexpressing myeloid and B cell restricted antigens. 310 33

Leukemic cells of a 19 year old patient with prolymphocytic leukemia of T-cell type (T-PLL) were characterized by surface markers and immunologic functions. Phenotypic analysis using a large panel of monoclonal antibodies corresponding to the clusters (CD) of differentiation antigens established on the Leukocyte Typing Workshops I and II revealed a unique T-cell phenotype not yet reported in the literature: CD1 (T6)-, CD2 (T11)+, CD3 (T3)+, CD4 (T4)-, CD5 (T1)-, CD6 (T411)+, CD7 (Leu9)+, CD8 (T811)-, CD10 (J5)-, CD11 (M22)+, CD12 (M67)-, CD13 (My7)-, CD14 (Mo2)-, CD16 (Vep13, 3G8, Leu11)+, CD18 (MHM23)+, CD19 (B4)-, CD20 (B1)-, CD25 (TAC)-, MHC-class II (HLA-DR, HLA-DQ)-, NKH1A+, Leu7-. Despite the expression of surface structures associated with natural killer (NK) function (CD16, CD18, NKH 1 A) the T-PLL cells were inactive in NK assays in vitro. Low in vitro ADCC activity was detectable. This unusual T-PLL phenotype might help to identify a new distinct T-cell differentiation stage.
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PMID:T-cell prolymphocytic leukemia (T-PLL) with unique surface phenotype. 310 23

The immune phenotype of the infiltrating cells in 13 positive patch tests from 8 cases of contact dermatitis and 1 case of poison ivy was studied. An indirect immunoperoxidase technique was used in conjunction with monoclonal antibodies directed against mature T cells (Leu-1, T11), helper T cells (Leu-3A), suppressor/cytotoxic T cells (Leu-2A), killer and natural killer cells (HNK 1), B cells (B1), Langerhans cells (HLA-DR), and the common acute lymphoblastic leukemia antigen (CALLA), (J5). The majority of infiltrating mononuclear cells were Leu-1+, T11+, Leu-3A+, Leu-2A-, HLA-DR+, T9-, T10-, HNK-, B1-, J5-. Occasional T6+ cells were observed in the epidermis (including spongiotic microvesicles) and also isolated in the dermis and within the dermal mononuclear infiltrates. The phenotype was compared with cutaneous T-cell lymphoma, a disease in which contact allergy and antigenic persistence may play a role.
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PMID:Immunophenotype of lymphoid cells in positive patch tests of allergic contact dermatitis. 315 92

Development of monoclonal antibodies to lymphoid cells has allowed for simple methods for the classification of leukemias. Using the monoclonal antibodies, B1, B4, T1, T11, Ia, CALLA, My7, My9, and a polyclonal TdT reagent, we report a number of unusual phenotypes analyzed by flow cytometry. Two cases of mixed linkage leukemia are reported, one marked with anti-CALLA and My9, the other marked with T11 and Ia. Three rare cases of pediatric CLL are reported. Both were of B cell origin with chromosome transformation. These studies demonstrate the clinical importance of monoclonal antibodies in leukemia classification. The results also show that the so-called rare leukemias may not be as rare as previously thought.
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PMID:The utilization of monoclonal antibodies in the diagnosis of unusual leukemias. 318 Jan 37

Fifty cases of acute leukemia were analyzed by means of flow cytometry. The results obtained were correlated with morphology and routine cytochemistries. The panel selected was useful in classifying an acute leukemia as acute lymphocytic (ALL) or acute nonlymphocytic (ANLL), which is of primary importance for therapeutic considerations. Common ALL (CALLA) (J5) was a good marker for classifying the leukemia as ALL. Monoclonal antibodies (MoAbs) T1 and/or T11 further delineated the lymphoid leukemia as T-cell ALL while MoAbs B4 or B1 delineated the lymphoid leukemia as non-T-cell ALL. Eighteen cases of ALL were diagnosed and consisted of five cases of T-cell ALL and 13 cases of non-T-cell ALL. Both the T-cell ALL cases and non-T-cell ALL cases were found to be heterogeneous and could be further subgrouped by phenotypic expression with additional MoAbs in the panel. A monoclonal antibody panel consisting of My4, My7, My9, Mo1, and Mo2 was useful in characterizing an acute leukemia as ANLL. This panel was less useful in distinguishing myeloid from monocytic subtypes although My4, Mo1, or Mo2 when present, appeared to favor a monocytic component. Of interest, a case of biclonal leukemia with two distinct blast populations on the flow cytogram was discovered. Morphology alone was successful in diagnosing ALL from ANLL in 35 cases (70%). It was not useful in distinguishing non-T-ALL cases from T-ALL cases. The ambiguous cases could be resolved by cytometric means. Flow cytometry has much to offer as a diagnostic aid in the evaluation of acute leukemia.
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PMID:Flow cytometry in the diagnosis of acute leukemia. 325 16

Philadelphia chromosome-positive (Ph1) acute leukemia is a heterogeneous subset of acute leukemia with a poor prognosis. We studied five patients to determine the potential for phenotypic and molecular heterogeneity. Cellular characterization studies included light myeloperoxidase (L-MPO), terminal deoxynucleotidyl transferase (TdT), ultrastructural MPO (U-MPO), and immunophenotyping by flow cytometry using T11, T3, T4, T8, Leu 1, B1, Leu 12, HLA-DR (la), CALLA (J5), OKM1, My4, My7, My8, My9, and My10. DNA was analyzed for rearrangements of the breakpoint cluster region (bcr), immunoglobulin heavy chain, joining region (JH), immunoglobulin kappa light chain constant region (C kappa), and T cell receptor (TcR beta). RNA dot blots were hybridized by using molecular probes for MPO and TdT. We found that four of five cases were acute mixed-lineage leukemia (AMLL). One patient had acute unclassifiable leukemia. Of the four patients classified as having AMLL, three showed myeloid and lymphoid features, with one patient showing myeloid, T cell, and B cell features. The last case showed T cell and B cell features only. In one patient MPO/RNA was positive in spite of insufficient L-MPO or U-MPO to diagnose acute myelogenous leukemia (AML), thereby suggesting significant MPO gene expression before the production of sufficient MPO protein to meet the French-American-British criteria for AML. Three of the five patients showed rearrangement of bcr (cases 1, 2, and 5). Studies of these five patients support the concepts of molecular and phenotypic heterogeneity in Ph1 acute leukemia, demonstrate a high incidence of AMLL in this subset of acute leukemia, and support the use of lineage-associated molecular probes to define lineage at an earlier stage than previously possible.
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PMID:Phenotypic and molecular heterogeneity in Philadelphia chromosome-positive acute leukemia. 333 95

Infant leukemia cells with 46XY,t(11; 17)(q23; p13) karyotype and a hybrid pre B myeloid phenotype (HLA-DR, (Ia), B4 and My7-positive and CALLA and T11-negative) and immunoglobulin heavy chain gene rearrangement were maintained in long-term culture for over 10 months. The in-vitro survival and growth of the leukemia cells were strictly dependent upon the presence of their autologous marrow stromal cells. The latter could be replaced by the 14F1.1 clone of preadipocytes derived from mouse bone marrow. Neither heterologous human marrow or foreskin fibroblasts nor fibroblast or endothelial like cell lines from mouse stroma could mimic the effect of autologous stroma or 14F1.1 adipocytes. The leukemia cells maintained their original phenotype throughout the 10-month culture period with either their autologous stroma or the 14F1.1 adipocytes. They could be induced to differentiate in two distinct directions. Phorbol myristate acetate induced adherence of the leukemia cells and development of macrophage properties. In contrast, conditioned medium from a hybridoma producing B-cell growth factor caused aggregation of the leukemia cells and expression of CALLA antigen and surface IgM. This bipotency of the leukemia cells and their dependence upon marrow stroma are properties in common with stem cells.
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PMID:Long-term culture of infant leukemia cells: dependence upon stromal cells from the bone marrow and bilineage differentiation. 352 80

For 60 cases of acute lymphoblastic leukemia (ALL) immunological typing was done concurrently by the avidin-biotin-peroxidase method using cytocentrifuged smears and by flow cytofluorometry for the study of surface antigens. The use of a large panel of antibodies detecting differentiation antigens allowed us to sub-classify 57/60 cases as 43 B-lineage ALLs and 14 T-lineage ALLs. The two types of ALL can be accurately distinguished by the expression of the antigens recognized by the antibodies of the clusters of differentiation CD19 (B4) and CD7 (Leu 9). Almost perfect agreement was obtained between the results of the two methods for antigens DR, CD10 (cALLA;J5) and CD7. A number of discordances were observed with other antigens [CD19 (B4), CD20 (B1), CD22 (To15), CD1 (T6), CD2 (T11), CD4 (T4), CD8 (T8), CD3 (T3), T9, T10]. In spite of these discordances, the avidin-biotin-peroxidase method can predict the lineage involved in most ALLs with a high degree of reliability. Nevertheless, for weakly expressed surface antigens (such as B4 and B1) the immunocytological method is less sensitive than flow cytofluorometry and can only approximately determine the stage of differentiation of neoplastic cells. Furthermore, the existence of cases which are at the same time negative with flow cytofluorometry and positive with immunocytology is consistent with the intracytoplasmic expression of certain differentiation antigens. Thus in the course of lymphoid differentiation, intra-cytoplasmic expression of T3, To15 and possibly J5 precedes their expression at the cell surface.
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PMID:Immunological typing of acute lymphoblastic leukemia: concurrent analysis by flow cytofluorometry and immunocytology. 354 Apr 62

Plasmacytoid T cells in two cases of Castleman's disease were stained with a panel of monoclonal antibodies to hematopoietic cell-associated antigens, using an immunoperoxidase technique on frozen sections. The immunohistologic phenotype of these cells was T4/Leu-3+, HLA-DR+, T1/Leu-1-, T3/Leu-4-, T8/Leu-2-, T11/Leu-5-, B1-, B2-, Leu-14-, Ig-, CALLA-, OKM1-, Leu-M1-. In contrast to plasma cells of B lineage, plasmacytoid T cells were T200+, T10-. The phenotype was similar to that of two previously reported lymphomas of plasmacytoid T cells. Plasmacytoid T cells appear to be a unique subset of lymphoid cells, whose function remains to be established.
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PMID:"Plasmacytoid T cells" in Castleman's disease. Immunohistologic phenotype. 354 85

Expression of lineage-associated surface antigens, was studied in 7 patients with acute undifferentiated leukemia (AUL), 3 patients with acute myeloid leukemia (AML), 4 patients with acute lymphoid leukemia (ALL) and bone marrow from 2 healthy donors, before and after exposure to the differentiating agent 12-O-tetradecanoylphorbol-13-acetate (TPA). The surface antigens were identified by monoclonal antibodies (My4, My8, My9, MO1, B1, CALLA, T11) and formation of EA and EAC rosettes. Adherence to plastic was also assessed. Cells from the AML patients responded to TPA with an increase in myeloid antigen positive cells and other markers of differentiation. Four of the AUL patients showed, also, a large increase in the fraction of cells expressing one or more myeloid markers, in correlation with formation of EAC rosettes. In contrast, the percentage of cells expressing myeloid antigens, did not increase in the 4 ALL patients, or in the normal donors. These findings confirm the heterogeneity of undifferentiated leukemias, and suggest the hypothesis that some AUL's can be induced to express markers of early myeloid cells.
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PMID:Acute undifferentiated leukemia: induction of partial differentiation by phorbol ester. 399 Mar 34


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