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.
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PMID:Expression of the APO-1 antigen in Burkitt lymphoma cell lines correlates with a shift towards a lymphoblastoid phenotype. 137 49

HIV-related non-hodgkin lymphomas currently occur in 5 to 8% of AIDS patients. AIDS-related lymphomas are high-grade tumors with the morphologic characteristics of either small noncleaved cell lymphomas of the Burkitt type or large cell centroblastic and immunoblastic lymphomas. Mixed features may be found, making classification difficult. Useful methods for characterizing AIDS-related non-hodgkin's lymphomas include immunophenotypic studies using B-cell differentiation and activation antigens (HLA-DR, CD10, CD19, CD20, CD21, CD22, CD23, CD38), evaluation of expression of surface immunoglobulins (IgS), activation and proliferation (CD25, CD30, CD71, Ki67), and identification of T-cell markers (CD1, CD2, CD3, CD4, CD5, CD7, CD8). Cases studied were of the B-cell type. Comparison with morphologic features revealed that Burkitt's lymphomas were monoclonal and expressed B-cell markers (CD10, CD19, CD20, CD22, CD38) and surface immunoglobulins, especially IgM kappa. This immunophenotype is similar to that of large cell or centroblastic non-hodgkin's lymphomas, suggesting that Burkitt lymphomas originate from centrofollicular cells. Immunoblastic non-hodgkin's lymphomas were monotypic or polytypic and expressed CD10 and CD38 antigens but not the other B-cell antigens Furthermore, a very large number of cells stained positively with the Ki67 antibody demonstrating that most lymphoma cells were undergoing cycling.
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PMID:[Non-Hodgkin's lymphoma and AIDS: histopathologic features]. 144 58

To provide baseline information on the immunoarchitecture of normal bone marrow, we studied cryostat-cut, frozen, and paraffin-embedded, fixed tissue sections prepared from 21 core biopsies of normal bone marrow obtained during bone marrow harvests for transplantation. A large panel of antibodies was applied that included, for frozen tissue, Leu-6 (CD1), T11 (CD2), Leu-3a (CD4), Leu-1 (CD5), Leu-2a (CD8), J5 (CD10), My7 (CD13), Leu-11 (CD16), B4 (CD19), B1 (CD20), B2 (CD21), Tac (CD25), My9 (CD33), T200 (CD45), NKH-1 (CD56), kappa and lambda chains, beta F1, Ki-67, HLA-DR, TQ1, and keratin, and for fixed tissue, leukocyte common antigen (CD45), L26 (CD20), LN1 (CDw75), LN2 (CD74), LN3, LN4, LN5, MB1 (CD45R), MB2, MT1 (CD43), MT2 (CD45R), UCHL1 (CD45R0), BM1, Ki-1 (CD30), Leu-M1 (CD15), lysozyme, KP1 (CD68), actin, S100, neuron-specific enolase, vimentin, and keratin. On fresh-frozen sections CD19 and CD2 were the most reliable and sensitive markers for B and T cells, staining 5% and 9% of marrow cells, respectively. Immunoglobulins generally showed heavy background staining, which frequently precluded an accurate assessment. The CD4 to CD8 ratio in the bone marrow was reversed from that of peripheral blood. On fixed tissues, leukocyte common antigen was found in 14% of the marrow cells, corresponding roughly to the lymphocyte population. L26, a pan-B-cell marker, stained 3% of the marrow cells. Among the other B-cell markers, LN1 and MB2 stained a large number of cells (40% to 70%), indicating reactivity with cells of the myeloid or erythroid series in addition to lymphocytes. Among the T-cell markers, UCHL1 and MT1 stained 66% and 50% of the cells, respectively, which could be explained by their cross-reactivity with myeloid cells. Nonspecific myelomonocytic markers (Leu-M1, KP1, and lysozyme) also showed reactivity in a high percentage of cells. No particular architectural distribution patterns of B or T lymphocytes were noted in either frozen or fixed bone marrow specimens. The results of this study provide normal baseline data for the immunohistologic application of hematopoietic and lymphoid markers on frozen or fixed bone marrow biopsy specimens.
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PMID:Immunoarchitecture of normal human bone marrow: a study of frozen and fixed tissue sections. 159 93

In order to compare primary gastro-intestinal (GI) B-cell lymphomas histomorphologically and immunophenotypically with orthologous steps of B-cell differentiation within the mucosa-associated lymphoid tissue (MALT) of the GI tract, a comprehensive panel of well characterized leucocyte differentiation antigens was composed. It comprised immunoglobulin constituents CD5, CD10, CD11c, CD20, CD23, CD24, CD30, CDw32, CD38, CD39, CDw75, CD76, and vimentin. These antigens yield characteristic immunoprofiles for the following B-cell compartments of the MALT, per se closely linked to cytologically distinct B-cell phenotypes: mantle zone (MZ), extrafollicular compartment (EF), follicle center (FC), and plasma-cell compartment (PC). An unselected series of 31 MALT B lymphomas (13 of low and 18 of high grade malignancy) was classified histologically in routine preparations and subsequently characterized immunohistochemically using fresh frozen tissue, monoclonal antibodies (MAbs) against the antigen panel listed above, and an indirect immunoperoxidase method. The final classification considered both morphology and immunoprofile of tumor cells. Ten tumors were "typical" in both respects: 2 closely corresponded to MZ, 5 to EF, 2 to FC and 1 to PC. The remaining 21 cases were characterized as "atypical" because of anaplastic cytology and/or abnormal co-expression and/or loss of antigens. A hybrid EF/FC phenotype was most frequently observed together with centrocyte-like or centrocytic anaplastic cytology of tumor cells. We conclude that MALT B-cell neoplasia comprises a broad spectrum of histo- and immunophenotypes ranging from well differentiated forms closely mimicking normal B-cell development to highly abnormal tumors which cannot be subclassified.
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PMID:Histomorphologic and immunophenotypic spectrum of primary gastro-intestinal B-cell lymphomas. 170 53

Sixteen cases of primary anterior mediastinal B-cell lymphoma were characterized by morphologic, immunophenotypic, and clinical profiles. Twelve were men and four were women. The median age was 42 years. Virtually all tumors were of large cell type. Three main morphologic categories were identified, with one rare exception. In some tumors, the cells were compatible with centrocytes and centroblasts (four). Others had cells readily identifiable as centroblasts (six). Both these groups had a variable proportion of cells with multilobed nuclei. A third group was composed mainly of unclassifiable cells with multilobed nuclei (five). All had discernible sclerosis of varying intensity. A wider range of morphologic features and different sex distribution was noticed in comparison with previously reported clear cell features and younger women. The dominant phenotype of these B-cell lymphomas was CD19+, CD22+, CD37+, CD21-, CD30-, CD10-, CD5-, and Ig-negative. The finding of CD21-, Ig-negative phenotype, as observed by the authors and others, overlaps with some high-grade lymphomas of follicular center cell origin but is thought to bear similarity to a noncirculating population of thymic medullary B-cells. The tumors attained large size without peripheral dissemination and responded to chemotherapy as well as radiotherapy.
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PMID:Primary anterior mediastinal B-cell lymphoma. A clinicopathologic and immunohistochemical study of 16 cases. 201 57

Latent Epstein-Barr virus (EBV) infection and growth transformation of B lymphocytes is characterized by EBV nuclear and membrane protein expression (EBV nuclear antigen [EBNA] and latent membrane protein [LMP], respectively). LMP1 is known to be an oncogene in rodent fibroblasts and to induce B-lymphocyte activation and cellular adhesion molecules in the EBV-negative Burkitt's lymphoma cell line Louckes. EBNA-2 is required for EBV-induced growth transformation; it lowers rodent fibroblast serum dependence and specifically induces the B-lymphocyte activation antigen CD23 in Louckes cells. These initial observations are now extended through an expanded study of EBNA- and LMP1-induced phenotypic effects in a different EBV-negative B-lymphoma cell line, BJAB. LMP1 effects were also evaluated in the EBV-negative B-lymphoma cell line BL41 and the EBV-positive Burkitt's lymphoma cell line, Daudi (Daudi is deleted for EBNA-2 and does not express LMP). Previously described EBNA-2- and LMP1-transfected Louckes cells were studied in parallel. EBNA-2, from EBV-1 strains but not EBV-2, induced CD23 and CD21 expression in transfected BJAB cells. In contrast, EBNA-3C induced CD21 but not CD23, while no changes were evident in vector control-, EBNA-1-, or EBNA-LP-transfected clones. EBNAs did not affect CD10, CD30, CD39, CD40, CD44, or cellular adhesion molecules. LMP1 expression in all cell lines induced growth in large clumps and expression of the cellular adhesion molecules ICAM-1, LFA-1, and LFA-3 in those cell lines which constitutively express low levels. LMP1 expression induced marked homotypic adhesion in the BJAB cell line, despite the fact that there was no significant increase in the high constitutive BJAB LFA-1 and ICAM-1 levels, suggesting that LMP1 also induces an associated functional change in these molecules. LMP1 induction of these cellular adhesion molecules was also associated with increased heterotypic adhesion to T lymphocytes. The Burkitt's lymphoma marker, CALLA (CD10), was uniformly down regulated by LMP1 in all cell lines. In contrast, LMP1 induced unique profiles of B-lymphocyte activation antigens in the various cell lines. LMP1 induced CD23 and CD39 in BJAB; CD23 in Louckes; CD39 and CD40 in BL41; and CD21, CD40, and CD44 in Daudi. In BJAB, CD23 surface and mRNA expression were markedly increased by EBNA-2 and LMP1 coexpression, compared with EBNA-2 or LMP1 alone. This cooperative effect was CD23 specific, since no such effect was observed on another marker, CD21.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Epstein-Barr virus latent membrane protein (LMP1) and nuclear proteins 2 and 3C are effectors of phenotypic changes in B lymphocytes: EBNA-2 and LMP1 cooperatively induce CD23. 215 87

Using serial frozen sections, monoclonal antibodies and an indirect immunoperoxidase method, 13 fibroadenomas (FA) and 3 cystosarcomas phyllodes (CSP) were analyzed for the expression of Egp34, HEA319-antigen, leucocyte differentiation antigens CD10, CD30, CD57, CD72, CDw75, and CD77, epidermal growth factor receptor (EGFR), estrogen (ER) and progesterone receptor (PR), and transferrin receptor (CD71). Egp34, CDw75, HEA319 antigen, CD10, and CD30 turned out to be consistently expressed in different cell types constituting FA and CSP and revealed that in malignant CSP the myoepithelial compartment acquires the ability to invade the stroma. Phenomenologically, the variable mode of expression of CD57 in myoepithelial cells, of CD77 in ductal epithelium, and of CD72 in both epithelial and stromal cells is suggestive for reflecting differences in their functional state but cannot be further interpreted at present. Expression of PR and ER was restricted to duct cells and was relatively independent, non-systematical. However, expression of ER and EGFR was inverse. This was also true for EGFR and CD71 in both duct cells and myoepithelial cells of FA. In contrast, stromal cells of FA were able to co-express EGFR and CD71 in the absence of PR and ER. This suggests a hormone-independent stimulation of the stromal cell compartment, possibly leading to local proliferation as the primary event in tumorigenesis of FA. In malignant CSP, however, the main proliferating cell is an abnormally mobile, HEA319 antigen-, CD10- and CD30-positive myoepithelial cell found to co-express ERFR and CD71 which is abnormal for this cell type but encountered in (myo-)fibroblasts of FA.
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PMID:Antigenic profile of mammary fibroadenoma and cystosarcoma phyllodes. A study using antibodies to estrogen- and progesterone receptors and to a panel of cell surface molecules. 217 50

We report the case of a spontaneously regressing lymphocytic lesion on the neck of a 76-year-old man. Routine histopathological examination revealed a heterogeneous infiltrate composed of both lymphoid follicles and preferentially perifollicular and interfollicular sheets of large atypical cells. Immunohistologically, large atypical cells were positive for Ki-1/Ber-H2 (CD30), anti-Il-2 (CD25), Ber T9, anti-HLA-DR, Leu-5b (CD2), T3 (CD3), Leu-3 (CD4), Leu-1 (CD5) and, occasionally, Leu-M1 (CD15); that is, they showed an arrangement and immunophenotype similar to those of perifollicular Ki-1 positive cells in reactive lymphoid tissue. In contrast, antibodies To15 (CD22), anti-immunoglobulins, and anti-CALLA (CD10) stained polyclonal B-cells restricted to lymphoid follicles and small clusters representing remnants of follicles. We suggest that this lesion be termed "follicular lymphoid hyperplasia of the skin with high content of activated T-helper cells."
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PMID:Follicular lymphoid hyperplasia of the skin with high content of Ki-1 positive lymphocytes. 254 99

The diagnostic value of immunohistochemistry using monoclonal antibodies was assessed in 100 liver biopsy specimens. The majority of these cases were hepatic localizations of lymphoid malignancies. Ten normal and reactive inflammatory liver biopsies were used as controls. Some monoclonal antibodies directed against leukocyte antigens revealed unexpected reactivities with normal liver structures: biliary tract (anti-CD10, anti-B MB2) and hepatocytes (anti-B LN1). In 12/17 cases of hepatic involvement by large cell malignancy, immunohistochemistry allowed the diagnosis of non Hodgkin's lymphoma (NHL); the remaining 5 cases were metastatic undifferentiated carcinoma. It was difficult to differentiate small cell liver NHL from reactive inflammatory infiltration. New anti-B (MB1, MB2, 4KB5, LN1 and LN2) and anti-T (MT1 and UCHL1) monoclonal antibodies suitable for use on paraffin sections were of value to phenotype NHL when only fixed material was available. But, information was too limited to distinguish malignant from reactive infiltrates. Immunohistochemistry on frozen sections was often necessary to diagnose inflammatory infiltrates and to phenotype NHL. Most NHL were of B cell origin (11/13 cases) and showed monotypic surface immunoglobulins as well as B cell-associated antigens (CD22+). The expression of the T CD5 antigen by B-cell NHL may have some diagnostic value. When monotypic surface immunoglobulins could not be demonstrated (due to background staining) the expression of this antigen by B lymphocytes was considered to be highly indicative of their neoplastic nature. Hairy cell leukemia exhibited a pathognomonic phenotype on frozen sections (CD11c+, CD22+, CD25+). T NHL were rare (2 cases) and difficult to diagnose due to the lack of clonal markers. The diagnosis of Hodgkin's disease in liver (15/20 cases) was facilitated by using paraffin sections of both monoclonal antibodies anti-CD15 (Leu M1) and anti-CD30 (Ber-H2) which detect fixation-resistant antigens expressed by Sternberg cells.
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PMID:[Immunochemical diagnosis of hepatic localizations in malignant lymphoid hematologic diseases. Study of 80 cases]. 266 Dec 93

Using 14 well-defined (clustered) monoclonal antibodies (MAbs) against B-cell restricted/associated differentiation and activation (CD) antigens and 12 mediastinal clear-cell lymphomas (MCCL), 46 follicular-center-cell lymphomas (FCCL), and 20 non-neoplastic lymph nodes--including toxoplasmic and HIV-associated lymphadenitis--were immunohistochemically examined to determine the histogenesis of MCCL. Antigenically, MCCL was characterized as CD5-, CD10-, CD19+, CD20+, CD21-, CD22+, CD30-, CD37+, CDw40+, and by a frequent expression of CD11c and CD23, while other antigens were inconsistently expressed. The antigenic profiles of MCCL and FCCL showed statistically significant differences in 4/14 distinct antigens. When the neoplastic cells of both tumor groups were compared with morphologically defined normal B-cell types, the overall resemblance of their immunophenotypes was even closer between MCCL and sinusoidal (monocytoid) B cells than between FCCL and follicular-center B cells. We conclude that MCCL is a lymphoma type distinct from FCCL, most probably representing a highly malignant neoplasm corresponding to sinusoidal B-cell reaction.
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PMID:Immunophenotypic similarities of mediastinal clear-cell lymphoma and sinusoidal (monocytoid) B cells. 278 13


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