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Deregulated c‐ myc expression in epstein‐barr‐virus‐immortalized b‐cells induces altered growth properties and surface phenotype but not tumorigenicity
Author(s) -
Hotchin Neil A.,
Allday Martin J.,
Crawford Dorothy H.
Publication year - 1990
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910450332
Subject(s) - phenotype , biology , lymphoblast , lymphoma , immortalised cell line , virus , epstein–barr virus , oncogene , cell culture , antigen , cancer research , plasmid , cell , virology , microbiology and biotechnology , immunology , gene , genetics , cell cycle
Endemic Burkitt's lymphoma (eBL) is characterized by the presence of Epstein‐Barr virus (EBV) and a chromosomal translocation which results in deregulation and constitutive expression of the c‐ myc proto‐oncogene. In order to examine the role played by activation of c‐ myc in determining the eBL phenotype, we have introduced into EBV‐immortalized lymphoblastoid cells (LCL) plasmids which permit constitutive expression of c‐ myc . The resulting cells show a reduced serum dependence, reduced homotypic cell aggregation, and changes in surface characteristics. In particular, levels of the cell adhesion molecule, LFA‐1, are greatly reduced. However, the cells continue to express all the EBV latent antigens associated with the LCL phenotype and they remain nontumorigenic. These results suggest that, whilst constitutive expression of c‐ myc may contribute to the malignant phenotype, it is insufficient to induce tumorigenicity.