"This is a good review of how viruses can hijack a host cell and induce unrestrained cellular replication. It will serve as a good reference and review for scientists working in this field as well as those developing vaccines and therapies for tumor-promoting viruses." from Rebecca T. Horvat (University of Kansas, USA) writing in Doodys read more ...

Small DNA Tumour Viruses Edited by: Kevin Gaston ISBN: 978-1-904455-99-8 Publisher: Caister Academic Press Publication Date: March 2012 Cover: hardback "a good reference and review" (Doodys)

"Cancer biology researchers interested in the transforming viruses will find the information contained in Small DNA Tumour Viruses to be highly applicable in terms of its strong molecular biology coverage. Virologists focused on this group of viruses will find this book invaluable for its multiple perspectives and concise summary of a large body of research in this area." from MedicalScienceBooks.com read more ...

Small DNA Tumour Viruses Edited by: Kevin Gaston ISBN: 978-1-904455-99-8 Publisher: Caister Academic Press Publication Date: March 2012 Cover: hardback "invaluable for its multiple perspectives and concise summary of a large body of research" (MedicalScienceBooks.com)

from Sergei Boichuk and Ole Gjoerup writing in Small DNA Tumour Viruses:

Incoming viral genomes, aberrant viral replication structures or individual viral proteins are potential triggers of DNA damage responses (DDRs). In an emerging theme, viruses interfere with, and frequently commandeer, DDR and repair signaling pathways to promote the viral life cycle. Here we review the diverse mechanisms that small DNA tumour viruses utilize to deregulate DDR pathways. Adenoviruses (Ad) encode gene products that specifically degrade the MRN (Mre11, Rad50, Nbs1) damage sensor or sequester it in nuclear tracks. This causes an inhibition of both ATM and ATR responses. Failure to inactivate MRN leads to attenuation of viral replication and concatemerization of the viral genome, thus preventing efficient packaging. Conversely, polyomaviruses, like SV40, as well as human papillomaviruses (HPVs) appear to exploit the DDR, since they use components of it to positively regulate their life cycle, while generally inhibiting downstream checkpoint responses. SV40, mouse polyomavirus and HPV activate ATM signaling and benefit from it. Complexities of the interplay between small DNA tumour viruses and the DDR are continuously evolving and illuminate both critical aspects of the viral life cycle as well as basic cellular mechanisms operating in a non-viral setting.

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from Scott B. Vande Pol writing in Small DNA Tumour Viruses:

Papillomavirus E6 oncoproteins are small zinc-binding proteins with a bewildering array of biological activities, including modulation of apoptosis, cellular transcription, host cell differentiation, growth factor dependence, DNA damage responses, and cell cycle progression. How can such a tiny protein do so much? This review examines insights from studies of oncogenic human papillomavirus E6 and bovine papillomavirus E6 to illuminate the mechanism by which E6 proteins interact with cellular binding partners. The origins of E6 and the history of its investigation are presented with the discovery of the major interaction partners that mediate E6 effects on DNA damage responses, cellular transcription, and modulation of keratinocyte differentiation.

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from Leonardo G. Alonso, Lucía B. Chemes, María L. Cerutti, Karina I. Dantur, and Gonzalo de Prat-Gay writing in Small DNA Tumour Viruses:

The human papillomavirus E7 oncoprotein is the main transforming agent of this important pathogen. Although its primary action is binding and targeting the retinoblastoma tumour suppressor protein, over two decades of research has shown a much more complex mode of action where multiple cellular partners and cellular events take place before ultimate progression to carcinogenesis. In this chapter we describe the HPV16 E7 protein in biochemical terms in an attempt to understand some of the various interactions in which this protein participates. We describe its multiple equilibria and conformational species in solution and show that these can explain some of its puzzling promiscuous binding activities and we review the few interactions that have been addressed by biochemical and mechanistic approaches to date. We finally discuss the cellular localization of E7 conformers, how they influence its antigenic capacity, and how they can be exploited in therapeutic applications.

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from Amy S. Gardiner, Abigail I. Wald and Saleem A. Khan writing in Small DNA Tumour Viruses:

In recent years, microRNAs (miRNAs) have been found to play important roles in the regulation of gene expression in mammalian cells. MiRNAs regulate many processes, including cell cycle progression, cell differentiation and organogenesis. Human cells encode approximately 1,000 miRNAs, and their expression has been shown to be altered in a variety of human cancers. Human papillomaviruses (HPVs) are DNA tumour viruses that are associated with cancers, especially cancers of the cervix and oropharynx. Recently, several studies have shown altered expression of miRNAs in HPV-associated cervical and oral cancers. In this article, we discuss the role of HPVs and their oncogenes in altering cellular miRNA expression, possible targets of such miRNAs, and how miRNA changes may contribute to the pathogenesis of HPV-associated cancers.

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from Laura White and G. Eric Blair writing in Small DNA Tumour Viruses:

Adenovirus (Ad)-based vectors have been frequently used as gene therapy vectors due to their ability to infect a wide range of dividing and non-dividing cells, their efficient growth to high titres in complementing cell lines and ease of genome manipulation. However, the transition of Ad vectors from in vitro studies to clinical application has been limited by sub-optimal efficacy and robust inflammatory responses elicited upon administration. In recent years it has become clear that multiple innate and adaptive responses limit the efficacy and safety of Ad vectors. In this review, we focus on the current understanding of the immune response to Ads with a particular focus on the innate immune response, and how this information can be used to design safer and more efficacious vectors.

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