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)

APO-1 is a cell surface molecule that induces apoptosis when ligated with the monoclonal antibody anti-APO-1. Expression of APO-1 and response to anti-APO-1 was investigated in a number of Epstein-Barr virus (EBV)-positive and -negative Burkitt lymphoma (BL) cell lines, in EBV-immortalized lymphoblastoid cell lines, and in cells from fresh BL biopsies. APO-1 was not expressed in EBV-negative cell lines and in EBV-positive BL cell lines with a phenotype corresponding to BL tumor biopsy cells (CD10+, CD21-, CD23-, CD30-, CD39-, CDw70-, CD77+). Accordingly, fresh BL cells obtained from three BL biopsies were APO-1 negative. EBV-positive BL cell lines that had acquired a lymphoblastoid phenotype (CD10-, CD21+, CD23+, CD30+, CD39+, CDw70+, CD77-) upon prolonged in vitro cultivation, as well as normal B-lymphoblastoid cell lines, expressed a high density of APO-1. APO-1 may, therefore, be regarded as a B-cell activation marker. APO-1 expression is not the only prerequisite for anti-APO-1-induced apoptosis because 6 of 7 APO-1-expressing EBV-positive BL cell lines were not sensitive to anti-APO-1, whereas all lymphoblastoid cell lines were killed by anti-APO-1. The sensitivity of lymphoblastoid cell lines to anti-APO-1-mediated apoptosis may open a new therapeutic approach for the treatment of EBV-induced lymphoproliferative lesions in immunocompromised individuals, because these are composed of cells with a lymphoblastoid phenotype.
 ...
PMID:Expression of the APO-1 antigen in Burkitt lymphoma cell lines correlates with a shift towards a lymphoblastoid phenotype. 137 49

Studies on normal bone marrow and Daudi Burkitt lymphoma cells were performed to determine the efficacy of selective, in vitro chemopurging with methylprednisolone (MP). We found that MP reduces the number of lymphoma cells without significant damage to bone marrow cells. This information is important because we need to improve the existing in vitro purging regimens used to cleanse autologous marrows of metastatic disease before transplantation into cancer patients who have received high-dose chemotherapy. Normal human bone marrow (NBM) and Daudi lymphoma cells were treated in parallel with various purging regimens, NBM death was evaluated using soft-agar culture, while Daudi cell death was evaluated using one-week liquid culture. A protocol of 2.0 mg/mL of MP for four hours demonstrated optimal selectivity. When treatment was followed by cryopreservation, a 1.7 log purge of Daudi cells was increased to 2.3 logs while preserving 36% of committed NBM precursors. We repeated these experiments on a simulated contaminated marrow to model closely the mixture of normal and malignant cells found in advanced, metastatic disease. We evaluated this mixed system by flow cytometric immunoanalysis using the two-color CD10/CD20 markers to detect residual, viable Daudi cells. Our initial results were reproducible in this mixed-cell system, further supporting the evidence for effective in vitro purging of bone marrow using MP.
 ...
PMID:Assessment of methylprednisolone purging efficacy on Daudi burkitt lymphoma cells from normal bone marrow. 189 5

The expression of receptors for proliferation and differentiation factors was analyzed by indirect immunofluorescence on 29 Burkitt lymphoma (BL) cell lines previously classified into 3 groups on the basis of their reactivity with 8 monoclonal antibodies (MAbs), including anti-CALLA, BL13 and TU1. BL13 and HB5 antibodies recognize different epitopes of the EBV/CR2 receptors. The determinant recognized by BL13 has been previously shown to be expressed only on cell lines of the first two groups, supposed to derive from the germinal center and to be negative on a third group of lines of putative BM origin and established from sporadic cases of BL. In contrast, and as expected from its reactivity on normal B cells in the BM or in the lymph nodes, HB5 antibody reacts with all BL lines except one. The receptor for transferrin is expressed on the 29 lines. Two new MAbs, Bac-1 and B1H5, could recognize respectively receptors for BCGF1 and BCGF2. Bac-1 reacts with 15 of 17 BL lines belonging to the first two groups and 7 of 12 BL lines of the third group; 14 of 15 EBV + lines express Bac-1. No BL line expresses B1H5. The IL2 receptor is weakly expressed on 5 EBV + cell lines and one EBV (-) line. All delta are BCGF1-positive. The almost constant expression of BCGF1 receptor on EBV + cell lines is the only strict relation between the expression of receptors for growth factors and their characteristics (i.e. EBV association, translocation, ethnic origin and clinical presentation). The maturation stage or the origin of BL cell lines in relation to the expression of growth factor receptors and the functional significance of these receptors will be discussed.
 ...
PMID:EBV-negative and -positive Burkitt cell lines variably express receptors for B-cell activation and differentiation. 302 6

Forty-three Burkitt lymphoma (BL) lines were examined for the expression of 5 monoclonal antibody (MAb)-identified B-cell-specific markers and immunoglobulin production. All (13) EBV-negative BL lines were CALLA+ LB-1-, whereas 30 EBV-carrying lines showed a more heterogeneous pattern. In the EBV-negative lines, the follicle mantle zone markers BA-1 and 35.1C5 were expressed concordantly, at a different level in each line. This coordination was disrupted in EBV-carrying lines. In the EBV-negative lines, there was also an inverted correlation between the expression of 35.1C5 and the germinal center marker BLA, suggesting that some etiologically important event, perhaps the translocation, had fixed the cells at different stages of their transition from one zone to the other. This inverted relationship was also disrupted in the EBV-carrying lines, suggesting that EBV can interfere with the maturation program of the BL cell. This conclusion was also supported by a comparison between 5 EBV-negative BL lines and their EBV-converted sublines. All converted lines have undergone marker changes, but the degree and nature of these changes was different for each EBV-BL line. Both the coordinated expression of BA-1 and 35.1C5 and the inverted relationship between CALLA and LB-1 were disrupted in several other convertants. We have reexamined our previous finding (Ehlin-Henriksson and Klein, 1984) that the majority of the variant translocation-carrying BL lines were CALLA- LB-1+, in contrast to the majority of the typical translocation carriers that were mostly CALLA+ LB-1-. All II EBV-negative lines were CALLA+ LB-1-, irrespective of the type of translocation. Among the EBV-carrying lines, 4 of 17 typical (8;14) translocation carriers were CALLA- LB-1+, whereas 7 of the 12 variant translocation-carrying lines were CALLA- LB-1+. The remaining two expressed both antigens to some extent. The difference is statistically significant at the 0.03 level.
 ...
PMID:Expression of B-cell-specific markers in different Burkitt lymphoma subgroups. 302 73

Twenty-six lines derived from 22 Burkitt lymphoma patients were examined for cytoplasmic vs. surface immunoglobulin and the expression of the monoclonal-antibody-detected BLA, CALLA and LB-I antigens. Six of the lines carried the variant translocations 8;2 or 8;22 (three each), 17 lines had the typical 8;14 translocation, I was translocation-negative (BJAB) and 2 were not examined cytogenetically. Depending on their immunoglobulin and surface marker expression, the BL lines could be subdivided into several subgroups. There was a strong inverse correlation between the expression of the CALLA and the LB-I marker. All BLA-lines were CALLA-, whereas the CALLA+ lines could be either BLA- or BLA+. All six variant translocations belonged to the CALLA-BLA-LBI+ category. Only one set of three lines, derived from the patient with the 8;14 translocation, belonged to the same subgroup. This suggests that the typical vs. the variant translocation freezes the BL cell at a different stage of differentiation. The variant translocation-carrying subtypes represent probably a somewhat more advanced stage of differentiation.
 ...
PMID:Distinction between Burkitt lymphoma subgroups by monoclonal antibodies: relationships between antigen expression and type of chromosomal translocation. 623 Dec 53

Monoclonal antibodies generated against normal and leukemic human leukocytes were tested for their differential reactivity with leukemia and lymphoma cell lines as well as with circulating lymphoid and myeloid leukemic cells by means of immuno-scanning electron microscopy (immuno-SEM). Anti-T (OKT3), anti-mu-chain, anti-CALLA (J5), anti-BA-1, anti-BA-2, and anti-nonlymphoid (Mol) monoclonal antibodies were covalently conjugated to polystyrene latex microspheres (immunolatex), using a two-step glutaraldehyde reaction, and subsequently incubated with the various cell types. Cultured B-type Burkitt lymphoma cells (Daudi) and chronic lymphocytic leukemia (CLL) cells displayed extensive labeling with monoclonal anti-mu, anti-B1, and anti-BA-1 immunolatex conjugates, while cultured malignant T cells (HD-Mar) showed positive labeling with OKT3 immunolatex alone. Cultured myelomonocytic cells (GDM-1) and cells obtained from patients with acute myeloblastic (AML) and monoblastic leukemia (AMoL) labeled only with anti-Mol immunolatex, while cultured promyelocytic cells (HL-60) displayed far less labeling with this conjugate. Common-type acute lymphoblastic leukemia (C/ALL) cells were labeled predominantly with the J5 (anti-CALLA) and anti-BA-2 immunolatex conjugates. Evidence is presented indicating that immuno-SEM employing monoclonal antibodies is a reproducible technique which may be used in the study of leukocyte maturation and may provide additional information in the classification of poorly differentiated leukemias.
 ...
PMID:Utilization of monoclonal antibodies and immuno-scanning electron microscopy for the positive identification of human leukemic cells. 658 Nov 72

Epstein-Barr virus (EBV) negative and EBV carrying Burkitt lymphoma (BL) lines that remain phenotypically similar to the in vivo tumor cells (operationally defined group I BLs) express high levels of CD10 and CD77, and lack immunoblastic markers such as CD23 and CD39, and the cell adhesion molecules CD11a, CD18, CD54 and CD58. This cell phenotype is associated with poor stimulatory capacity in allogeneic mixed lymphocytes cultures (MLC) [Avila-Carino et al. Int. J. Cancer 40, 691-697 (1987)] EBV carrying BL lines tend to drift spontaneously towards an immunoblastic phenotype in parallel with up-regulation of six EBV-encoded nuclear antigens (EBNA-2 to -6) and two membrane proteins (LMP-1 and -2). These viral antigens are characteristically expressed in all EBV transformed lymphoblastoid cell lines (LCLs) of normal B cell origin and can be induced in group I BL lines by treatment with the DNA demethylating agent 5-azacytidine (5-azaC) [Masucci et al. J. Virol. 65, 1558-1567 (1989)]. We have now studied the effect of 5-azaC on the induction of allogenic T cell proliferation by three EBV negative (Ramos, BL28 and BL41) and four EBV carrying BL lines (Rael, Eli, Chep and Mutu) which stably express a group I phenotype. Pre-treatment with 4-15 microM 5-azaC had no effect on the EBV negative cells but increased the stimulatory capacity of all four EBV carrying lines. LMP-1 was the only viral antigen regularly induced suggesting that its expression may be required for the increase of allostimulation. This was corroborated by the observation that LMP-1 transfection increased 35-70-fold the stimulatory capacity of Rael cells. The cell adhesion molecule CD54 was the only cellular marker selectively up-regulated in all cell lines with increased stimulatory capacity.
 ...
PMID:Selective induction of allostimulatory capacity after 5-azaC treatment of EBV carrying but not EBV negative Burkitt lymphoma cell lines. 768 32

Activated c-myc gene was introduced into the cells of three normal Epstein-Barr virus (EBV)-positive lymphoblastoid B cell lines (LCL). The cells were monitored for the appearance of new phenotypic and functional features compared with the control LCL cells transfected with plasmid that did not contain the c-myc gene. The LCL-expressing c-myc constitutively did not arrest growth in low serum concentration. However, the cell number in the cultures failed to increase because of substantial cell death. Death was due to apoptosis as demonstrated by flow cytometric analysis of propidium iodide-stained cells, by typical DNA laddering in gel electrophoresis, and by the inspection of Giemsa-stained cell smears. Apoptosis was also induced by exposing the transfected cells to antibodies directed to the immunoglobulin mu chain (a-mu-ab) irrespective of the serum concentration in the culture. Exposure of the cells to CD40 ligand (CD40L) or CD40 monoclonal antibody prevented cell apoptosis. Upon transfection with c-myc, the LCL cells acquired a vacuolated morphology that was never observed in control cells. Moreover, the expression of CD10 and CD38 was upregulated, while that of CD39 and especially CD23 was downregulated. Unlike that observed in certain Burkitt lymphoma (BL) cell lines that share the same surface phenotype (CD10+CD38+CD23-CD39-), the c-myc-transfected cells expressed lymphocyte function-associated (LFA) 1, LFA-3, and intercellular adhesion molecule 1 and grew in large clumps rather than single-cell layers. Expression of CD10 and CD38 was particularly evident on the cells undergoing apoptosis, thus suggesting a correlation between the presence of these markers and the apoptotic process. Cells placed in conditions favoring in vitro apoptosis displayed downregulation of Bcl-2 protein. Bcl-2 expression was, however, upregulated when the cells were exposed to CD40L. These data indicate that the B cells expressing c-myc constitutively acquire some of the features of normal centroblasts and of BL cells, including the expression of CD10 and CD38, and the propensity to undergo apoptosis, which can be prevented by exposure to CD40L. Therefore, these cells can serve as a model system to study both BL lymphomagenesis as well as the process of B cell selection occurring in the germinal centers.
 ...
PMID:Transfection of the c-myc oncogene into normal Epstein-Barr virus-harboring B cells results in new phenotypic and functional features resembling those of Burkitt lymphoma cells and normal centroblasts. 783 23

The use of different viral promoters for the expression of the EBNA1 gene product appears to be a critical step in the regulation of Epstein-Barr virus latent gene expression and may reflect the extent of differentiation of B-cell hosts. Low-passage Burkitt lymphoma cell lines resemble immature B cells in that they express CD10 (CALLA) and do not express B-cell activation antigens. In these cells, transcription from a promoter located in the BamHI F fragment of the viral genome results in the exclusive expression of EBNA1, referred to as the latency I pattern of viral gene expression. In contrast, high-passage Burkitt lymphoma cells and lymphoblastoid cell lines resemble activated B cells in that they do not express CD10 but do express activation antigens such as CD23. In these cells, the use of two promoters located in the BamHI W and C fragments of the viral genome leads to the expression of all six EBNA gene products (latency III). We have found that four human B-cell lines, DB, LBW2, LBW14, and Josh 7, stably express a pattern of B-cell differentiation antigens intermediate between those found in latency I and latency III cell lines and characterized by the coexpression of CD10 and CD23. The pattern of EBNA1 promoter usage in these cell lines was examined to determine whether their intermediate cellular phenotype was reflected in their patterns of viral gene expression. DB, LBW2, and LBW14 utilize both the BamHI F promoter region and BamHI W promoter region to transcribe the EBNA1 gene. This stable pattern of mixed promoter usage for the expression of the EBNA gene products in B cells has not previously been described. In addition, these three B-cell lines expressed lower levels of the viral latent gene product EBNA2 than those typically observed in latency III cells. The lower levels of activation of viral and cellular promoters known to be regulated by EBNA2 also correlated with the reduced levels of EBNA2 expression in these cells. These included the viral LMP1 and LMP2A promoters and the cellular CD23B promoter. The fourth B-cell line, Josh 7, expressed EBNA1 mRNAs derived from both the BamHI W promoter and BamHI C promoter, similar to latency III cells. The intermediate cellular phenotype in Josh 7 cells appeared to be due, in part, to a deficiency in the expression of viral LMP1.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Dual EBNA1 promoter usage by Epstein-Barr virus in human B-cell lines expressing unique intermediate cellular phenotypes. 808 80

The recombination activating gene-1 (RAG-1), which is required for immunoglobulin (Ig) gene rearrangement, is expressed in murine B-lymphoid precursors but not in mature B lymphocytes. In order to characterize the temporal relationship of RAG-1 expression to other markers of human B-lymphoid differentiation [cell surface antigens, terminal deoxynucleotidyl transferase (TdT), Ig gene rearrangements], RAG-1 expression was studied in a group of B lineage childhood acute lymphoblastic leukemia (ALL). ALL cells from 21 patients were grouped into three developmentally related phenotypes based on the expression of the differentiation antigens CD19, CD10, and CD20. All 21 leukemias were surface Ig (slg) negative. There were leukemias representing each developmental stage of Ig gene rearrangement. RAG-1 was expressed in 20 of 21 B-lineage ALL, including leukemic cells from each stage of differentiation, as defined by immunophenotype and IgH and IgL gene rearrangement status. RAG-1 was expressed in slg- ALL, regardless of the Ig heavy chain (IgH) or Ig light chain (IgL) gene configuration. RAG-1 was not expressed in two Burkitt lymphomas and Burkitt lymphoma cell lines with slg+ mature B-lymphocyte phenotype. In two cases, RAG-1 was expressed in TdT-negative ALL; conversely TdT was expressed in the one RAG-1 negative ALL. These results suggest that RAG-1 in B-lineage ALL is expressed at all phenotypic and genotypic developmental stages preceding surface immunoglobulin expression, and that TdT and RAG-1 may be regulated by different mechanisms.
 ...
PMID:Recombination activating gene-1 (RAG-1) expression in all differentiation stages of B-lineage precursor acute lymphoblastic leukemia. 844 48


1 2 3 4 5 6 7 8 Next >>