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Titlebook: DNA Tumor Viruses; Oncogenic Mechanisms Giuseppe Barbanti-Brodano,Mauro Bendinelli,Herman Book 1995 Springer Science+Business Media New Yo

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978-1-4899-1102-5Springer Science+Business Media New York 1995
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Simian Virus 40 Large T Antigen Induces Chromosome Damage that Precedes and Coincides with Completeated the involvement of abnormal chromosomes in oncogenesis and even postulated the existence of “chromosomes which inhibit division.” Such early work laid the foundation for the theory that tumorigenesis is a series of genetic mutations. In the early 1980s, actual mutations in growth regulatory gen
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Transformation by Polyomaviruses,nd growth properties of susceptible cells. From its humble beginnings, the polyomavirus tumor biology field has mushroomed into several new directions, most notably into tumor suppressors. These new branches are now buzzing with activity and touching or merging with other established disciplines inc
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Association of BK and JC Human Polyomaviruses and SV40 with Human Tumors,nd monkeys and transform cells . to a neoplastic phenotype. For all these reasons, BKV and JCV have been considered possible candidates in the etiology of human tumors. Association of BKV, but not of JCV, with human tumors has been described, although a formal proof for an etiological role of BKV in
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Immortalization of Keratinocytes by Human Papillomaviruses,ed to the host immune system. In 1907, Ciuffo demonstrated that the infectious agent for the common wart persisted in filtered homogenates and, thus, clearly established that it was not either a bacterium or protozoan.. Subsequently, it was determined that common warts are associated with HPV-1 and
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Vaccines against Human Papillomaviruses and Associated Tumors,n progress. Systems for production of the necessary antigens have been available for some time, and the problems of producing papillomavirus-coded proteins in adequate amounts and of acceptable quality have largely been overcome. For a long time the fact that HPVs could not be grown ., and that viru
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