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)

Indirect immunofluorescence staining with a large battery of monoclonal antibodies of primary and autologous metastatic lesions removed from seven patients with melanoma has detected heterogeneity in the expression of various types of melanoma-associated antigens (MAAs), of distinct determinants of the high molecular weight melanoma-associated antigen (HMW-MAA), of the two subunits of Class I HLA antigens, and of the gene products of the HLA-D region. Among the 10 MAAs tested, the HMW-MAA had the highest frequency and the Mr 87,000 MAA the lowest. Furthermore, the HMW-MAA displayed the lowest heterogeneity. These findings, in conjunction with the restricted tissue distribution of the HMW-MAA, its lack of susceptibility to antibody-mediated modulation, and the high affinity of the available anti-HMW-MAA monoclonal antibodies, indicate that this antigen may be a useful marker for radioimaging and immunotherapy in patients with melanoma. The common acute lymphoblastic leukemia antigen was detected only in five lesions. Class I HLA antigens were detected in a larger number of lesions than HLA-DR antigens, which had a significantly higher frequency than HLA-DQ antigens. The degree of antigenic heterogeneity did not appear to correlate with the histopathological features of the lesions and/or with the clinical course of the disease. The results of the present study indicate that immunodiagnostic and immunotherapeutic approaches to melanoma should rely on the use of combinations of monoclonal antibodies to distinct MAAs.
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PMID:Heterogeneous expression of melanoma-associated antigens and HLA antigens by primary and multiple metastatic lesions removed from patients with melanoma. 315 50

Fifty-eight pediatric patients with non-T acute lymphoblastic leukemia (ALL) were diagnosed and evaluated at the Sambur Center of Pediatric Hematology Oncology. At least six subtypes of non-T ALLs were identified, corresponding to the various stages of B-cell differentiation, by utilizing an extensive panel of monoclonal antibodies directed against T- B- and myeloid-cell differentiation antigens. Moreover, leukemic cells expressing the phenotype of early B cells could be driven to differentiate along the B- cell lineage to express CALLA and BL antigens and cytoplasmic and/or surface immunoglobulins (IgM). A unique phenotype of non-T ALL was also identified. These leukemic cells expressed B cell antigen exclusively, i.e., HLA/DR and B4 (CD19). Myeloid-cell antigens, however, were expressed on these cells spontaneously after a 24-hour incubation in culture medium in vitro. In addition, leukemic cells of four patients with a phenotype of HLA/DR, CD19, and CD10 expressed antigens of the T-cell lineage: CD7 (3AI) and CD2 (leu 5), and/or of the myeloid cell lineage (My7). These results provide confirming evidence for the wide scope of the heterogeneity of ALL. It stresses the validity of accurate classification of leukemia to identify biologically and clinically unique subtypes of ALL, which bears specific prognostic parameters; and designates therapeutic protocols.
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PMID:Heterogeneity of childhood acute lymphoblastic leukemia (ALL): monoclonal antibodies phenotyping and induction of differentiation in vitro. 326 67

Bone marrow transplantation (BMT) is an intensive mode of treatment for acute leukemia of childhood. Indication are types and stages of leukemia with a poor prognosis following chemotherapy, such as acute nonlymphocytic leukemia (ANLL) in first complete remission (CR) of the disease, and acute lymphocytic leukemia (ALL) following relapse of the disease, in second CR. On the basis of our own experience and of analysis of published data it can be stated that allogeneic BMT, grafting bone marrow cells from a healthy HLA-identical sibling of the patient, has a long-term therapeutical effect which is superior to that of chemotherapy alone: in cases of ANLL, grafted in first CR, a long-term disease-free survival of 55 to 67% was obtained, and in cases of ALL, grafted in second CR, this was between 38 and 64%. The potential effect of autologous BMT, i.e. with own bone marrow of the patient, sampled during CR of the disease, cannot yet be evaluated properly, because the follow-up period of this mode of treatment is too short. It is worth while to investigate the potential beneficial effect of autologous BMT, e.g. for children with ALL in second CR, who lack a HLA-identical donor. Also the potential contribution of bone marrow purging, e.g. for CALLA-positive lymphocytes, should be investigated in relation to the relapse risk after autologous BMT for common ALL.
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PMID:[Contribution of bone marrow transplantation to the treatment of children with leukemia]. 328 86

In this paper a microplate method is described for diagnosing acute leukemia and for investigating the reactivity of monoclonal antibodies (MoAbs) against membrane antigens in combination with rabbit or murine antibodies to nuclear terminal transferase (TdT). The speed of this method facilitates the investigation of fresh leukemic cells from individual patients and assesses the cytolytic efficacy of the relevant MoAbs in the presence of complement (C'). Lymphoblasts (TdT+) are mixed in equal proportions with known numbers of "inert" cells, eg, RBC or nonleukemic bone marrow (BM). Following incubation with MoAbs and C' the ratio of residual TdT+ cells and inert cells is determined on cytospin preparations. Initially, percentages of TdT+ cells are counted in a unit volume of 5,000 inert cells, followed by the scanning of greater than 2 X 10(4) inert cells on entire slides. With this method more than 4 log cytoreduction of TdT + cells is detected. The method is also applicable for studying the cytolysis of malignant B cells by using mostly monoclonal lg expression rather than TdT for the identification of residual B cells. Ten representative patients selected from a group of greater than 100 are reported. In some cases cytoreduction of greater than 4 log with no identifiable residual TdT + cells is achieved by a single C'-fixing MoAb: anti-CD10 (RFAL3) in common acute lymphoid leukemia (ALL) and anti-CD7 (RFT2) in T cell ALL (T-ALL). Other cases require cocktails of anti-CD10, anti-CD19, and anti-CD24 in common ALL or anti-CD7 and anti-CD8 in T-ALL. In T-ALL a few TdT + cells remain that exhibit the features of normal TdT + BM cells (CD7-, HLA-DR+). This is particularly noticeable when patients are studied in partial remission or if nonleukemic BM is used as a source of inert cells. The methods described here contribute to establishing a range of MoAbs (ie, of IgM class) and techniques for efficient purging and to comparing the efficacy of "clean-up," in remission, of common ALL, T-ALL, and B cell malignancies.
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PMID:Leukemia diagnosis and testing of complement-fixing antibodies for bone marrow purging in acute lymphoid leukemia. 353 26

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

To determine whether acute lymphoblastic leukemia (ALL) is a clonal disease and to define the pattern of differentiation shown by the involved progenitor cells, we studied the glucose-6-phosphate dehydrogenase (G6PD) types in the cells of 19 girls heterozygous for this X chromosome-linked enzyme. Lymphoblast immunophenotypes were those of HLA-DR+, CALLA+ ALL (six patients); HLA-DR+, CALLA- ALL (four patients); pre-B cell ALL (two patients); T cell ALL (four patients); and undefined ALL (three patients). Malignant blast cells at diagnosis from ten patients displayed a single G6PD type, indicative of clonal disease. In contrast, both A and B G6PD in ratios similar to those found in skin were observed in morphologically normal blood cells from the same patients. The leukemic cells of three patients were examined at both diagnosis and relapse; in each instance the same G6PD type was found, consistent with regrowth of the original leukemic clone at relapse. Results of studies of cells from nine additional patients tested only at relapse were similar. Our results indicate that childhood ALL is a clonally derived disease involving progenitor cells with differentiation expression detected only in the lymphoid lineage.
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PMID:Evidence for clonal development of childhood acute lymphoblastic leukemia. 386 37

Sixty-five cryopreserved leukemic samples from children diagnosed and treated as having acute lymphocytic leukemia (ALL) were retrospectively examined for the presence of lymphoid and myeloid associated antigens by indirect immunofluorescence using monoclonal antibodies. Expectedly, the majority of these specimens expressed antigens known to be expressed on lymphoid, and not myeloid malignancies. These included the common acute lymphoblastic leukemia antigen (CALLA), the p32 B-cell associated antigen, and T-cell associated antigens. Leukemic cells from the 8 remaining patients expressed antigens known to be present on both myeloid and lymphoid leukemias. These included HLA/DR, and the antigens identified by BA-1 and BA-2. Cells from 2 of these 8 patients reacted with antibodies that define antigens present on normal and malignant myeloid cells. Both specimens reacted with 1G10, an anti-granulocyte antibody, and one reacted with 5F1 which reacts with monocytes, nucleated red blood cells, megakaryocytes and platelets. One of these patients relapsed while receiving ALL therapy, and the morphology of her leukemic cells became characteristic of acute monocytic leukemia (AMoL). The second patient failed ALL therapy but responded to standard acute nonlymphocytic leukemia (ANLL) therapy, clearing her peripheral blasts. Thus these studies confirm that cell surface phenotyping with monoclonal antibodies can recognize ALL cells that express myeloid rather than lymphoid associated antigens and demonstrate that the malignant cells display a clinical behavior consistent with the diagnosis of ANLL.
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PMID:Immunodiagnosis of childhood ALL with monoclonal antibodies to myeloid and lymphoid associated antigens. 388 8

A clonogenic assay has been developed that utilizes Burkitt's lymphoma tumor cell lines to detect elimination of up to 5 logs of tumor cell contamination within human bone marrow. Different Burkitt's lymphoma lines bear one or more of a group of markers, including common acute lymphoblastic leukemia antigen gp26 (glycoprotein with a molecular weight of 26,000), B1, surface membrane immunoglobulin, HLA, beta 2-microglobulin, and Ia. Burkitt's tumor cells of the Namalwa line have been mixed with a 20-fold excess of irradiated human bone marrow cells. After treatment with one or more monoclonal antibodies and rabbit complement (RC), mixtures have been grown on a monolayer of irradiated human bone marrow cells and tumor cells enumerated by limiting dilution. Multiple treatments with antibody and RC were more effective than a single treatment in destroying clonogenic tumor cells which bore relevant determinants. Human serum components inhibited the lytic activity of RC in the presence of murine monoclonal antibodies. The total concentration of bone marrow cells proved critical in determining the complete elimination of tumor. Incubation of the Namalwa tumor cell line with RC and the J2 anti-gp26 eliminated more than 3 logs of malignant cells from a 20-fold excess of human bone marrow. Combinations of two monoclonal antibodies were more effective than any single antibody in eliminating Namalwa cells. A combination of three monoclonal reagents was no more effective than a combination of J2 and B1 or J2 and J5 in eliminating Namalwa cells. Treatment of human bone marrow with three antibodies and RC did not, however, produce a selective loss of nonmalignant GM-CFU-C, CFU-E, or BFU-E.
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PMID:Elimination of malignant clonogenic cells from human bone marrow using multiple monoclonal antibodies and complement. 396 24

Lymphoblasts from 59 children with non-T, non-B acute lymphoblastic leukaemia were studied with monoclonal antibodies to four cell-surface proteins. 87% of the children had lymphoblasts positive for HLA-DR, 82% for p30, 75% for p24, and 72% for CALLA. The commonest composite phenotype was HLA-DR+ p30+ CALLA+ p24+. Significant correlations were seen between expression of HLA-DR, p30, and CALLA, but not p24. p30- and CALLA phenotypes were found in patients with high white-blood-cell counts (WBC) and splenomegaly. With standard chemotherapy, disease-free survival from time of remission was shorter in p30- and CALLA- patients than in others. Splenomegaly was associated with poor disease-free survival and provided prognostic information independent of phenotype. High WBC was less significant than phenotype in predicting outcome and was not independent of phenotype.
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PMID:Clinical usefulness of monoclonal-antibody phenotyping in childhood acute lymphoblastic leukemia. 612 6

The expression of HLA-DC/DS antigen detected by the monoclonal antibody Leu 10 was studied in three human precursor and pre-B cell lines (Josh 7, Reh, and Nalm 12). Flow cytometric analysis showed that none of these cell lines stained for the HLA-DC/DS antigen. In the presence of 1.6 X 10(-9) M of 12-O-tetradecanoylporbol-13-acetate (TPA), expression of this antigen was detected. The expression was completed after 168 h of incubation. Iodination of cell surface, immunoprecipitation by Leu 10 antibody, and two-dimensional gel analysis revealed that TPA-treated Josh 7 cells synthesized and expressed a 29,34 kD bimolecular complex with both alpha and beta chains different from those of HLA-DR antigen. Quantitative absorption experiments with cell lysates indicated a greater than 25-fold increase in HLA-DC/DS antigen in TPA-treated cells. With the induction of HLA-DC/DS antigen expression, there are concomitant decreases in the expression of the common acute lymphoblastic leukemia antigen (CALLA) and the enzymatic activity of terminal deoxynucleotidyl transferase. No appreciable changes in HLA-DR and Ig expression were observed. There was also no change in HLA-SB expression as detected by antibody ILR-1. However, DNA synthesis was markedly inhibited by TPA treatment. These results indicate that precursor and pre-B cell lines can be induced to mature in vitro. They also suggest that the expression of HLA-DC/DS antigen which precedes the expression of membrane Ig and follows the HLA-DR expression is relevant to human B cell development and cell interaction.
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PMID:Induction of HLA-DC/DS (LEU 10) antigen expression by human precursor B cell lines. 635 64


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