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)

We report a case of 33-year-old Japanese female who had B-cell lymphoblastic lymphoma with Burkitt's lymphoma (BL)-like morphologic feature. Both breasts were involved and the resected tissue showed starry sky macrophages and a proliferation of lymphoblasts containing lipid droplets. The nucleus of the lymphoblast was oval or indented. The neoplastic cells examined expressed TdT, CD10, CD14, CD38, and WH14 (a marker of pre-B cell leukemia/lymphomas). Southern blotting analysis showed a rearrangement of the immunoglobulin heavy chain gene and germline configurations of T-cell receptor gene and c-myc 3rd exon gene. The immunophenotype and genotype of this neoplasm were different from those of previously reported BLs, but identical to those of B-cell lymphoblastic lymphoma. This case, therefore, was regarded as B-cell type lymphoblastic lymphoma containing lipid droplets.
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PMID:A case of lymphoblastic lymphoma with aberrant morphologic feature. 764 66

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.
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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

Two cell lines were originated from the peripheral blood (PB-LAM) and bone-marrow (BM-LAM) of a patient with Burkitt-type acute lymphoblastic leukemia and AIDS. 26 and 7 clones were isolated from PB-LAM and BM-LAM respectively by limiting dilution. All of these had surface IgM lambda and the CD10 marker with low to absent CD23, CD30, CD39 and surface adhesion molecules. Furthermore, they shared the same chromosomal abnormalities (trisomy 7 and t(8;14) translocation) and the same rearrangements of immunoglobulin L and H chain and of c-myc gene loci. These features are those most frequently found in Burkitt's lymphoma (BL) cells and were different from those of the parental cell lines, which, besides cells identical to those of the malignant clones, also contained normal lymphoblastoid cells. Therefore, the cloning procedure used selected for the growth of cells with malignant features. EBV latent antigens were detected in all clones by Western blotting and their pattern of expression resembled that usually observed in BL cells. All the clones were positive for the EBV genome by Southern blotting and had monomorphic EBV-fused termini as determined by using cDNA probes specific for sequences at either end of the viral genome. However, the clones derived from PB-LAM had EBV fused termini of a different size from that of the clones derived from BM-LAM. The presence of different EBV-fused termini in otherwise monoclonal malignant cells indicate that EBV infection was possibly a late event in lymphomagenesis following rearrangement of the c-myc and the Ig gene loci.
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PMID:Cytogenetic rearrangement of C-MYC oncogene occurs prior to infection with Epstein-Barr virus in the monoclonal malignant B cells from an AIDS patient. 838 76

The combination of chromosomal translocations associated with bcl-2 rearrangement [t(14;18)] and c-myc rearrangement [t(8;14), t(8;22), or t(2;8)] has infrequently been detected in lymphoproliferative disorders. We have recently identified four cases of a B-cell malignancy exhibiting this dual translocation. In addition to t(14;18), one case had t(8;14) and three had the t(8;22). One case presented as de novo acute lymphoblastic leukemia (ALL-L2), two as de novo high grade lymphomas and the fourth evolved to a "blastic" phase from a previously documented follicular lymphoma. Immunophenotyping and molecular analysis was performed on three of the cases: all were negative for terminal deoxynucleotidyl transferase (TdT) but were CD10 positive. Two of the three cases with t(8;22) were negative for surface immunoglobulin (SIg) and positive for HLA-DR. Rearrangement of the oncogene bcl-2 was identified in a single case by polymerase chain reaction (PCR) only. Similar to cases reported in the literature, all patients had a poor clinical outcome despite aggressive therapy. Dual translocation lymphoid malignancy has a relatively characteristic morphology and the diagnosis should be considered when there is a history of an antecedent low grade lymphoma or when there is discordance between the "blastic" morphology and the immunophenotype (TdT- and/or SIg+). Confirmation requires demonstration of the characteristic translocations. Recognition of this entity has significant clinical implications that may require consideration of alternate treatment strategies.
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PMID:Combination of t(14;18) and a Burkitt's type translocation in B-cell malignancies. 840 Nov 80

Large-cell variants are uncommon in mantle cell lymphoma (MCL). Here we describe the pathologic and clinical findings in five patients with large-cell lymphoma related to MCL (L-MCL), and compare them to a group of classic small-cell MCL (s-MCL) cases. Histologically, the MC origin of the large cells was evinced by their association with a small mantle cell component in the same tissue, or their distribution in a classic mantle zone pattern, or their development in a patient with previous s-MCL. The large cells were either pleomorphic mantle cells (case 1) or transformed blast-like cells (case 2-5). The median nuclear diameter, median nuclear area and proliferation index of L-MCLs and s-MCLs, were statistically different. Immunophenotypic characterization of four specimens of L-MCL and 10 of s-MCLs with a large panel of antibodies showed the classic findings of MCL, i.e. the IgM+ D+/-, CD5+, CD10-, CD23- phenotype in all cases except two (one CD5- and one CD23+), and the association with a loose follicular dendritic cell network. Two of four L-MCLs and 5/10 s-MCLs demonstrated rearrangements of the bcl-1 gene by Southern blot or by polymerase chain reaction (PCR); 2/4 L-MCLs and 1/9 s-MCLs had p53 mutations on single-strand conformation polymorphism analysis; none of the 14 specimens showed rearrangement of bcl-2 by PCR or bcl-6 and c-myc by Southern blot. All patients with 'transformed' histology (versus 37% of all others) died of lymphoma; their survival (15-18 months; median 17) was much shorter than that of all the others (28-117+ months; median 43) (P=0.0035). All three patients with p53 anomalies, two of whom had tumours with transformed histology, died of their disease in a short time (15, 18 and 28 months). In contrast, the presence of bcl-1 rearrangements did not have prognostic implications. This study documents the existence of large-cell variants of MCL and the poor prognosis associated with the 'transformed' cytologic type and/or p53 abnormalities.
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PMID:Large-cell variants of mantle cell lymphoma: cytologic characteristics and p53 anomalies may predict poor outcome. 863 52

The cDNA for the mouse 5HT5A receptor has been functionally expressed in the unicellular yeast Saccharomyces cerevisiae. The NH2-terminal end of the receptor gene was fused to the Bacillus macerans (1-3, 1-4)-beta-glucanase signal sequence to ensure proper membrane insertion and to the c-myc epitope to permit immunological detection of the heterologously expressed protein. In the resulting episomal yeast expression plasmid pCNNmm5HT5A the modified 5HT5A gene is under the transcriptional control of the endopeptidase B gene promoter (PRB1). After transformation of the vector into the protease deficient S. cerevisiae strain cI3-ABYS-86, recombinant clones were examined for the presence of functional receptor by radioligand binding using [3H]LSD. Whole cells as well as crude membrane preparations of recombinant clones showed saturable binding of the receptor with a KD of approximately 2.2 nM. The pharmacological properties for the heterologous expressed receptor, estimated by ligand-displacement studies using certain serotonin agonists and antagonists, were comparable to those reported for the receptor expressed in mammalian systems. Western blot analysis of membranes prepared from a recombinant clone using the monoclonal antibody 9E10, directed against the c-myc epitope of the modified receptor, revealed an apparent molecular mass of about 43 kDa for the receptor expressed in S. cerevisiae. Glycosylation of the receptor was analysed by EndoH digestion. A heat shock of recombinant yeast significantly increased the number of specific binding sites per cell and also improved the affinity of the receptor. Immunogold electron microscopy was used to study the localization of the heterologously expressed protein within the yeast cells.
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PMID:Pharmacological and biochemical characterization of the mouse 5HT5A serotonin receptor heterologously produced in the yeast Saccharomyces cerevisiae. 886 64

We experienced a case of Burkitt's lymphoma showing an unusual surface phenotype, CD5 expression, at an early stage of the disease. Initially, this patient showed massive abdominal para-aortic lymph node swelling which rapidly developed into leukemic change. Based on the clinical course and cytogenetic features of lymphoblasts in the bone marrow, which showed t(8;14) and c-myc gene rearrangement, the patient was diagnosed with Burkitt's lymphoma. Combination chemotherapy induced short-term remission, but central nervous system (CNS) involvement developed, followed by a regrowth of lymphoma cells in the bone marrow. The bone marrow at the end stage showed monotonous expansion of large cells with conspicuous vacuolation in the basophilic cytoplasm. The initial lymphoma cells showed pan-B markers and were CD5 positive but weakly CD10 positive; however, the lymphoma cells obtained from the bone marrow at the terminal stage did not express CD5. The chromosomal t(8;14) was seen, and identical rearrangement of immunoglobulin heavy chain joining gene and c-myc gene were detected by Southern blot analysis in the bone marrow lymphoblasts throughout the clinical course. This case is evidence that remarkable transformation of CD5-positive lymphoblasts to CD5-negative lymphoblasts occurred in an identical clone of Burkitt's lymphoma.
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PMID:An aggressive case of Burkitt's lymphoma with t(8;14) and c-myc rearrangement transformed from CD5+ B-cell lymphoma. 943 79

Mutations in the PEX gene are responsible for X-linked hypophosphatemic rickets. To gain insight into the role of PEX in normal physiology we have cloned the human full-length cDNA and studied its tissue expression, subcellular localization, and peptidase activity. We show that the cDNA encodes a 749-amino acid protein structurally related to a family of neutral endopeptidases that include neprilysin as prototype. By Northern blot analysis, the size of the full-length PEX transcript is 6.5 kilobases. PEX expression, as determined by semi-quantitative polymerase chain reaction, is high in bone and in tumor tissue associated with the paraneoplastic syndrome of renal phosphate wasting. PEX is glycosylated in the presence of canine microsomal membranes and partitions exclusively in the detergent phase from Triton X-114 extractions of transiently transfected COS cells. Immunofluorescence studies in A293 cells expressing PEX tagged with a c-myc epitope show a predominant cell-surface location for the protein with its COOH-terminal domain in the extracellular compartment, substantiating the assumption that PEX, like other members of the neutral endopeptidase family, is a type II integral membrane glycoprotein. Cell membranes from cultured COS cells transiently expressing PEX efficiently degrade exogenously added parathyroid hormone-derived peptides, demonstrating for the first time that recombinant PEX can function as an endopeptidase. PEX peptidase activity may provide a convenient target for pharmacological intervention in states of altered phosphate homeostasis and in metabolic bone diseases.
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PMID:Cloning of human PEX cDNA. Expression, subcellular localization, and endopeptidase activity. 959 14

A 39-year-old man was admitted with massive ascites. Specimens of ascitic fluid contained numerous cells with a FAB-L3 appearance, and small noncleaved cell lymphoma morphology. These cells expressed CD10, CD19, CD20, CD38, CD45, HLA-DR, and IgM antigens, and were positive for IgM and c-myc protein in cytoplasmic immunostaining tests. Clonal rearrangements of IgH and c-myc genes were detected by Southern blot analysis. No mass lesions were found by physical examination, and systemic computed photography did not reveal enlargement of lymph nodes, spleen, or liver. Bone marrow aspiration showed no infiltration of malignant cells. Ga scintigraphy indicated hot lesions only in the abdomen. These findings suggested that Burkitt's lymphoma had developed in the peritoneal cavity as a primary lymphomatous effusion. Chemotherapy with methotrexate, cyclophosphamide, vincristine, doxorubicin, etoposide, and dexamethasone was effective, and the patient has been free from the disease for 1 year since completion of consolidation treatment with autologous peripheral blood stem cell transplantation.
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PMID:[Burkitt's lymphoma occurring as a primary lymphomatous effusion]. 1084 64

Primary cutaneous B-cell lymphomas (CBCLs) should be clearly separated from non-Hodgkin's B-cell lymphomas with secondary cutaneous involvement and from cutaneous B-cell pseudolymphomas. The majority of CBCLs are characterized by a homogeneous clinical presentation and behavior, with good response to local radiotherapy, low tendency to extracutaneous spread, and excellent prognosis. According to the European Organization for Research on the Treatment of Cancer classification of primary cutaneous lymphomas, CBCLs with an indolent behavior are divided into 2 subgroups: follicular center cell lymphoma and immunocytoma/marginal zone lymphoma, due to putative histologic similarities with their purported nodal counterparts. In addition, a third subgroup with intermediate prognosis (large B-cell lymphoma of the leg) is identified. Conversely, the identification of distinct subgroups is disputable from a strictly histologic, immunophenotypic, and genotypic point of view, and has neither correlation with the clinical course nor the prognosis of the disease. Moreover, the majority of CBCLs show a uniform immunophenotype (CD5-, CD10-) and genotype (lack of bcl-1/bcl-2 and c-myc gene rearrangement) of neoplastic cells. Therefore, we favor the use of the term Skin-Associated Lymphoid Tissue (SALT)-related B-cell lymphomas, due to the close similarities between CBCLs and mucosa-associated lymphoid tissue (MALT) lymphomas, and the evidence for an acquired B-cell arm of SALT.
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PMID:The skin-associated lymphoid tissue-related B-cell lymphomas. 1089 14


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