Chapter title |
Role of Epstein-Barr virus in Burkitt's lymphoma.
|
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Chapter number | 9 |
Book title |
Epstein-Barr Virus and Human Cancer
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Published in |
Current topics in microbiology and immunology, January 2001
|
DOI | 10.1007/978-3-642-56515-1_9 |
Pubmed ID | |
Book ISBNs |
978-3-64-262568-8, 978-3-64-256515-1
|
Authors |
Takada, K, K. Takada, Takada, K. |
Abstract |
We established an in vitro system representing BL-type EBV infection, which is characterized by expression of EBNA1, EBER, BARF0, and LMP2A, and absence of EBNA2 and LMP1 expression (Shimizu et al. 1994; Komano et al. 1998). Comparison of EBV-positive and -negative Akata cell clones revealed that EBV contributes to the malignant phenotype and resistance to apoptosis. This is clear evidence that EBV is not a passenger and plays a role in BL. Moreover, we found that EBERs are responsible for these phenotypes (Komano et al. 1999). In the transfection study, EBER-expressing Akata cell clones restored the malignant phenotype, resistance to apoptosis and upregulated expression of bcl-2 protein to a level comparable to the restoration rate of EBER expression compared with EBV-reinfected cell clones. Many RNAs are known to have catalytic functions; however, there has been no report describing an oncogenic RNA. This is the first paper that provides evidence that RNA polymerase III-transcribed virus-encoded small RNAs affect the malignant phenotype and resistance to apoptosis. Like Akata cells (Takada et al. 1991), all the BL cells possess a chromosomal translocation involving the c-myc locus, which results in constitutive activation of the c-myc gene (Klein 1981). In mammalian cells, deregulated expression of c-myc has been shown to contribute not only to tumorigenesis (Land et al. 1983) but also to induce apoptosis (Askew et al. 1991; Evan et al. 1992; Milner et al. 1993). Therefore, BL cells are predisposed to c-myc-induced apoptosis. Our data imply that EBV infection would upregulate expression of bcl-2 protein to protect cells from c-myc-induced apoptosis, and to allow c-myc to exert its oncogenic functions (Vaux et al. 1988; Brito-Babapulle et al. 1991; Bissonnette et al. 1992; Fanidi et al. 1992; Karsan et al. 1993; Mohammad et al. 1993; Oltvai et al. 1993; Marin et al. 1995). In this way bcl-2 might cooperate with c-myc in the development of BL (Fig. 5). |
Mendeley readers
Geographical breakdown
Country | Count | As % |
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Unknown | 12 | 100% |
Demographic breakdown
Readers by professional status | Count | As % |
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Student > Bachelor | 3 | 25% |
Researcher | 2 | 17% |
Student > Doctoral Student | 2 | 17% |
Student > Master | 2 | 17% |
Other | 1 | 8% |
Other | 1 | 8% |
Unknown | 1 | 8% |
Readers by discipline | Count | As % |
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Medicine and Dentistry | 3 | 25% |
Agricultural and Biological Sciences | 3 | 25% |
Biochemistry, Genetics and Molecular Biology | 2 | 17% |
Psychology | 1 | 8% |
Immunology and Microbiology | 1 | 8% |
Other | 0 | 0% |
Unknown | 2 | 17% |