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 new human cell line, WSU-BL, was established from a malignant ascitic fluid occurring in a patient with Burkitt's lymphoma. The established line grows in a single-cell suspension with a doubling time of 19 hours and expresses L3 morphologic features by the French-American-British classification. Immunologic study revealed that WSU-BL cells express IgM-lambda both in the cytoplasm and on the surface and react with monoclonal antibodies to B-cell antigens (B1, B4, BL3, BL4, HLA-DR, and common acute lymphoblastic leukemia antigen [CALLA]). These cells are negative for T-cell and myeloid/monocyte antigens as well as Epstein-Barr virus nuclear antigen (EBNA). These results suggest that WSU-BL corresponds to an intermediate stage of B-cell differentiation. Both fresh tumor and WSU-BL cells had a hyperdiploid karyotype carrying the 8;14 chromosome translocation. Molecular studies showed that WSU-BL has a rearrangement of c-myc proto-oncogene and expresses c-myc RNA. Phorbol ester 12-0-tetradecanoylphorbol-13-acetate (TPA) and interferon-gamma (IFN-gamma) were able to induce several phenotypic changes on WSU-BL cells. Two-dimensional gel electrophoresis of total cellular protein showed that either TPA or IFN-gamma induced both the synthesis or loss of several proteins. Analysis of the protein patterns indicated that some proteins were uniquely responsive to either TPA or IFN-gamma and others were common to both. This cell line should be valuable for future studies of cell proliferation, differentiation, and oncogenesis concerning this neoplasm.
Cancer 1989 Sep 01
PMID:Establishment and characterization of a new human Burkitt's lymphoma cell line (WSU-BL). 252 86

Serum thymidine kinase (STK) levels have recently been used to detect tumour regression and progression in a number of hematological malignancies. In this study, patients with myeloma were monitored longitudinally for STK and several other potentially useful tumour markers to determine which laboratory parameters are the most useful for differentiating between stable and progressive disease. STK was determined by radioenzyme assay, lymphocyte surface markers were analysed by flowcytometry, plasma cell labelling index (LI) by immunofluorescence with anti BU-1, serum B2-microglobulin (SB2M) by radioimmunoassay and M proteins by radial immunodiffusion. Detailed multiparameter longitudinal investigations of 5 patients and ongoing studies of 70 other patients suggest that STK is a more reliable marker of progressive disease than either SB2M, LI, M-protein or CD10 positive lymphocytes. A rise in STK during the emergence of progressive disease at least paralleled and usually preceded any change in the other parameters which often did not change at all. All samples from patients with progressive disease (n = 29) had a STK above the normal range (0-5U/l) whereas 76% of patients in clear stable disease had a STK within the normal range. All samples (n = 34) from patients with light chain isotype suppression (LCIS) had STK values of less than 12 U/L and 82% of samples (n = 33) from patients without LCIS had a STK above the normal range (0-5U/L). The correlation between STK and LI was r = 0.65; p less than 0.001 (n = 21). The radioenzyme assay for STK is simple, reproducible and a valuable tool for monitoring patients with myeloma and when used in conjunction with other clinical and laboratory investigations, aids in the separation of patients with stable myeloma from patients whose disease is progressive.
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PMID:Serum thymidine kinase as a marker of disease activity in patients with multiple myeloma. 252 40

We have previously isolated a cDNA clone encoding the common acute lymphoblastic leukemia antigen (CALLA) from a normal human kidney library. Analysis of the amino acid sequence deduced from nucleotide sequencing of this cDNA established that CALLA is identical to the recently cloned human neutral endopeptidase (NEP; E.C. 3.4.24.11). Southern blot analysis of SacI fragments of DNA from human-rodent somatic cell hybrids using a 1.6-kb CALLA cDNA probe showed that the CALLA-NEP gene is located on human chromosome 3.
Cancer Genet Cytogenet 1989 Oct 01
PMID:The common acute lymphoblastic leukemia antigen (neutral endopeptidase-3.4.24.11) gene is located on human chromosome 3. 252 24

Several established human glioma cell lines have been previously shown to express the common acute lymphoblastic leukemia antigen (cALLa, CD 10), an important marker in the diagnosis of human acute lymphocytic leukemia (ALL). The amino acid sequence of cALLa is identical to that of neutral endopeptidase (NEP,E.C.3.4.24.11), and cALLa expressed on leukemia and melanoma cell lines is enzymatically active NEP. In the present study, we investigated whether cALLa expressed on glioma cell lines is active NEP. We detected cALLa on 10 out of 13 glioma cell lines using 2 different anti-cALLa MAbs (A12-G4 and FAH99). NEP antigen, as detected by immunostaining with an anti-NEP MAb (135A3), was expressed on the same 10 lines. cALLa-positive, but not cALLa-negative cell lines displayed an endopeptidase activity. This activity could be blocked by phosphoramidon, a specific inhibitor of NEP. Furthermore, mRNAs hybridizing to an NEP-specific probe were present in cALLa-positive glioma cells but not in cALLa-negative cells. Taken together, the results provide strong evidence that cALLa-positive glioma cell lines express endopeptidase activity on the cell surface.
Int J Cancer 1989 Nov 15
PMID:Human glioma cell lines expressing the common acute lymphoblastic leukemia antigen (cALLa) have neutral endopeptidase activity. 253 Nov 22

Because clonal rearrangements of the beta-T cell receptor (beta-TCR) gene occur in some patients with B cell chronic lymphocytic leukemia, we studied the arrangement of this gene in fourteen patients with multiple myeloma, a malignancy of the most terminally differentiated B cells. The gene was in germline configuration in peripheral blood lymphocytes (PBLs) and bone marrow samples of thirteen patients. By contrast, it was clonally rearranged in the marrow but not in the PBLs of one patient with stage IIA IgA-lambda myeloma. This patient's bone marrow consisted of 95% morphologically identifiable plasma cells which were CALLA-, OKT10+ (93%), and PCA-1+ (78%). Only 5% of marrow cells were small lymphocytes which contained T cell markers (CD3+ or CD2+). To eliminate the possibility that the small percentage of contaminating T cells contained the gene rearrangement, they were depleted by avidin-biotin immunoadsorption using the Leu4 determinant. Positively selected marrow T cells did not contain beta-TCR gene rearrangements. By contrast, the T cell depleted marrow contained the rearranged gene. This is the first demonstration that rearranged beta-TCR genes can occur in multiple myeloma.
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PMID:Clonal rearrangement of the beta-T cell receptor gene in multiple myeloma. 253 28

Multiple myeloma (MM) is a B-cell malignancy characterized by the accumulation, primarily in bone marrow, of a clone of plasma cells. The nature of the stem cells feeding the tumoral compartment is still unknown. To investigate this special point, we have studied the phenotypes of nine well-known human myeloma cell lines (HMCLs) and compared them with those of normal lymphoblastoid cell lines (LCLs). Twenty-four clusters of differentiation involved in B lymphopoiesis were investigated using a panel of 65 monoclonal antibodies (MoAbs). For each cluster, the percentage of positive cells and the antigen density were determined, giving rise to a "quantitative phenotype". We thus classified the HMCLs into two different groups: those with cytoplasmic mu chains (c mu+) and those without (c mu-). In the first (c mu+) group, comprising seven cell lines, the HMCLs had a phenotype of pre-B/B cells close to that of Burkitt's lymphoma cell lines. They expressed low densities of surface mu chains, without detectable cytoplasmic or surface light chains. Three of them were infected with the Epstein Barr virus (EBV). These c mu+ HMCLs bore most of the B-cell antigens except CD23. They expressed the CALLA antigen (CD10) and lacked the plasma-cell antigen PCA1. In contrast, LCLs expressed surface light chains, high densities of CD23, low densities of PCA1 antigen, and no CD10 antigen. The c mu- HMCLs had a plasma-cell phenotype, lacking most of the B-cell antigens and expressing high densities of PCA1 antigen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Phenotypic analysis of human myeloma cell lines. 253 14

Recently, great interest has been shown in the histological identification of small cell tumours of childhood--nephroblastoma (Wilms' tumour), neuroblastoma, rhabdomyosarcoma and Ewing's sarcoma--using immunohistochemical methods. However, several antigens operationally specific for leucocyte typing in blood and marrow are also expressed on cells of epithelial and neural origin. We undertook phenotypic characterization of 17 non-haemopoietic small cell tumours of childhood using a panel of 30 monoclonal antibodies to leucocyte, epithelial and cytoskeletal antigens using a sensitive alkaline phosphatase-anti-alkaline phosphatase technique on cryostat sections of fresh tumour. Our results demonstrated frequent expression of the leucocyte-associated antigens CD10 (CALLA), CD9 (p24) and CDw32 (FcRII) in these small cell tumours and occasional expression of MHC class II (HLA-DR) and HNK-1 antigens. However, the leucocyte-associated antigens CD45 (leucocyte common), CD22 (pan B-cell), CD11b (C3bi receptor), CD15 (Lewisx) or CDw42 (platelet gp Ib) were not detected on any tumour. Aberrant expression of desmin, neurofilament and UJ13A antigen was found in nephroblastoma and of epithelial-associated markers (CIBr17 and 43-9F) in neuroblastoma. Our results also demonstrated broad reactivity in frozen section with two monoclonal antibodies specific for melanoma (NKI/C-3) or epithelial cells (OM-1) in paraffin sections. Hence, it is necessary to include monoclonal antibodies to CD45 and pan-epithelial antigens, e.g. LP34 (cytokeratin) or HEA125 for the precise immunohistochemical identification of small round cell malignancies of childhood.
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PMID:Phenotypic characterization of non-haemopoietic small cell tumours of childhood with monoclonal antibodies to leucocytes, epithelial cells and cytoskeletal proteins. 254

Spontaneous lymphoblastoid cell lines (LCLs) were established from the peripheral blood of 10 human immunodeficiency virus (HIV)-seropositive patients in order to investigate whether or not progression of the cells towards a malignant state could be traced. The LCLs studied displayed no differences in their surface phenotype, karyotype, and tumorigenicity in nude mice as compared with a wide panel of control LCLs. Furthermore, no c-myc rearrangement could be detected in any of the LCLs. However, 4 of the 10 LCLs derived from HIV-seropositive patients formed colonies in agar with a cloning efficiency of 0.1-0.9%. This percentage was much lower than that of a control neoplastic B cell line (50%), but consistently higher than that observed for a battery of spontaneous LCLs. The cells of a number of sublines that were derived from the agar colonies expressed new activation markers (CD10 and Bac-1) but did not induce tumors in nude mice or display chromosomal abnormalities. These sublines might comprise cells that have progressed towards a more markedly transformed state.
Int J Cancer Suppl 1989
PMID:Studies on the oncogenic potential of Epstein-Barr-virus (EBV)-infected B cells in AIDS-related disorders. 255 27

In a four year span, between 1983 and 1987, 215 bone marrow and cell culture samples from 125 myeloma patients were immunotyped and coexpression of myelomonocytic and plasma cell antigens occurred in 16 (13%). We employed both immunohistochemical and flow cytometry methods including coplots and double labelling. Three types of myeloma cases were found: (1) those with isolated myeloid antigen coexpression, usually Leu M1 or esterase (BE, CE) positive (11 cases); (2) those with multiple myeloid antigens (Leu M1, M3, M5, MY7, BE, CE) (four cases); and (3) one case beginning as 1 and ending as 2. Isolated myeloid antigen expression was generally associated with typical features of myeloma with survival close to the anticipated median (33 months), while multiple myeloid antigen expression was associated with more aggressive disease and shorter survival duration (median survival 16 months). The latter subgroup also had other poor prognostic factors including high labelling index and common acute lymphoblastic leukemia antigen (CALLA) positivity. Other features found overall were frequent abnormal karyotypes (seven of 12 abnormal) and coexpressed IgA (eight of 16); all IgA+ cases also coexpressed Leu M1. We conclude that there is an unusual and unexpected predilection for coexpression of myelomonocytic antigens in myeloma cells. The reasons are not immediately obvious. Whether the coexpression indicates that myeloma cells truly have latent multilineage potential or just aberrantly coexpress other hematopoietic antigens as a manifestation of malignancy remains to be explained. However, a cell line established from the bone marrow of one patient is a valuable scientific tool allowing detailed analysis of these questions.
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PMID:Myelomonocytic antigen positive multiple myeloma. 264 87

The distribution of the BLA, CALLA (CD 10), AC-2 (CD 39), MHM-6 (CD 23), LB-I, and 351C5 (CD 45R) antigens in 40 non-Hodgkin's lymphomas was demonstrated by immunohistochemical staining of frozen tissue sections. Nine out of 10 centroblastic and centrocytic follicular and diffuse type of lymphomas (CB/CC F/D) and all 10 cases of CB/CC follicular lymphomas were BLA+ and CALLA+. A few cases also showed weak expression of activation antigens (AC-2, MHM-6 and LB-I) and 351C5. In contrast, 3 CC and 3 lymphoblastic (non-Burkitt) lymphomas showed a heterogeneous pattern of distribution with dominating activation antigen expression. A single case of lymphoblastic lymphoma of Burkitt-like type expressed BLA and CALLA but not activation antigens. In reactive follicular center and FCC lymphomas different cell populations appeared to express BLA and activation antigens, respectively. Assessment of staining intensity and proportion of the stained cells indicated that almost all BLA+ cells are CALLA+. CALLA+ BLA- cells were regularly present, in addition. The co-expression of BLA and CALLA in the same cell was confirmed by double immuno-enzymatic staining. By the same technique, BLA+ and CALLA+ cells were shown to be activation-antigen negative.
Int J Cancer 1989 Apr 15
PMID:Immunophenotypic characterization of follicle-center-cell-derived non-Hodgkin's lymphomas. 264 42


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