2007
DOI: 10.1007/s12105-007-0020-7
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An Update on Epstein-Barr Virus and Nasopharyngeal Carcinogenesis

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Cited by 10 publications
(12 citation statements)
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“…This supports the idea that EBV infection is involved in an early stage of NPC carcinogenesis [10]. Molecular abnormalities in NPCs are complex and include inactivation of RASSF1A and p16 tumour suppressor genes on 3p21 and 9p21 chromosomal regions by homologous deletion and promoter methylation during low-grade dysplasia stages.…”
Section: Introductionsupporting
confidence: 80%
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“…This supports the idea that EBV infection is involved in an early stage of NPC carcinogenesis [10]. Molecular abnormalities in NPCs are complex and include inactivation of RASSF1A and p16 tumour suppressor genes on 3p21 and 9p21 chromosomal regions by homologous deletion and promoter methylation during low-grade dysplasia stages.…”
Section: Introductionsupporting
confidence: 80%
“…In EBV-associated carcinogenesis, the virus infects B lymphocytes through binding of the major envelope glycoprotein gp350 to the B cell CD21 receptor and binding of a second glycoprotein, gp42, to MHC class II molecules as a co-receptor [10]. The transformation of EBV viral particles [Epstein-Barr nuclear antigens (EBNAs), latent membrane proteins (LMPs) and Epstein-Barr virus-encoded small RNA (EBERs)] from B cells into latently infected lymphoblastoid cell lines, both in lytic and latent cycles, ultimately affects host genome regulation causing dysregulation of apoptosis, genetic instability, and constant proliferation.…”
Section: Introductionmentioning
confidence: 99%
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“…The result includes dysregulation of apoptosis, genetic instability, and constant proliferation [11,12]. These effects can be seen in when the virus is in both lytic and latent cycles.…”
Section: Introductionmentioning
confidence: 99%