Human tumor-associated viruses and new insights into the molecular mechanisms of cancer. Oncogene Suppl 2:S31-S42

Cell Growth Regulation Section, Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892-4330, USA.
Oncogene (Impact Factor: 8.46). 12/2008; 27 Suppl 2:S31-42. DOI: 10.1038/onc.2009.351
Source: PubMed


The study of acute-transforming retroviruses and their oncogenes and of the multiple mechanisms deployed by DNA viruses to circumvent the growth-suppressive and proapoptotic function of tumor suppressor genes has provided the foundation of our current understanding of cancer biology. Unlike acute-transforming animal viruses, however, human tumor-associated viruses lead to malignancies with a prolonged latency and in conjunction with other environmental and host-related cooperating events. The relevance of viral infection to human cancer development has often been debated. We now know that at least six human viruses, Epstein-Barr virus (EBV), hepatitis B virus (HBV), hepatitis C virus (HCV), human papilloma virus (HPV), human T-cell lymphotropic virus (HTLV-1) and Kaposi's associated sarcoma virus (KSHV) contribute to 10-15% of the cancers worldwide. Hence, the opportunity exists to fight cancer at the global scale by preventing the spread of these viruses, by the development and distribution of effective and safe antiviral vaccines, and by identifying their oncogenic mechanism. Here, we discuss the molecular events underlying the neoplastic potential of the human tumor-associated viruses, with emphasis on the enigmatic KSHV and its numerous virally hijacked proangiogenic, immune-evasive and tumor-promoting genes. The emerging information may facilitate the development of new molecular-targeted approaches to prevent and treat virally associated human malignancies.

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    • "R.Y.L. Wang et al. / Virology 443 (2013) 236–247 242 of HCV, playing a key role in the initiation of viral replication (Okamoto et al., 2006, 2008). In addition, Hsp90 participates in transcriptional regulation of oncogenic viral genes of Epstein-Barr virus (EBV) and gamma-herpesvirus, resulting in the regulation of cell signaling pathways (Elgui de Oliveira, 2007; Martin and Gutkind, 2008). In the case of EBV, Hsp90 promotes the LMP-1- induced Akt phosphorylation, resulting in the suppression of apoptosis in EBV-infected lymphoma cells (Jeon et al., 2007), and modulates the expression of EBNA1, an EBV-encoded viral protein that is involved in many EBV functions, including gene regulation, Fig. 5. Pharmacological inhibition of Hsp90β-VPs binding and EV71 assembly. "
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    Virology 05/2013; 443(2). DOI:10.1016/j.virol.2013.05.001 · 3.32 Impact Factor
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    • "Regarding HPV, more than 130 HPV types have been identified and are classified into low-and high-risk groups depending on their likelihood of inducing cervical cancer [12]. Of the individuals infected with HPV, 10–20% will develop cancer of the cervix, anus, vulva, penis and of the head and neck area and oropharynx [1] [4] [13]. HPV is associated with nearly all the carcinomas of the uterine cervix with 70% of the cervical cancers associated with the high-risk HPV types 16 and 18 [12]. "
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    • "Although in some cases the evidence for causation is less than compelling, other bacterial and parasitic infections have been suggested to be involved in other cancers (Burnett-Hartman et al, 2008; Samaras et al, 2010). Several in-depth reviews exist on infections in general and viral infections in particular as cancer-causing agents (Vousden & Farrell, 1994; zur Hausen, 1999; Parkin, 2006; Boccardo & Villa, 2007; Carrillo-Infante et al, 2007; Martin & Gutkind, 2009; Ziegler & Buonaguro, 2009; Ott et al, 2010; Saha et al, 2010). It is not the intention of this article to replicate the depth of coverage offered elsewhere. "
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