It is surprising, and even disappointing, that there have been very few meetings and published volumes resulting from these meetings that focus attention upon all of the groups of DNA tumor viruses. Historically, separate meetings were held each year for the adenovirus-SV40-polyoma researchers, the herpes viruses, hepatitis B virus and the papillomaviruses. It was as if these four virus groups were four fields of study developing independently with a literature and culture of their own. When a virologist crossed the field from the adenovirus group to the herpesvirus or papillomaviruses, he or she was lost to their former group because of the structure of separate meetings and remote literature. This, of course, has resulted from historical accident and is being rectified by the rapid progress made in our understanding of how these viruses contribute to the causation of cancer in animals and humans. It was pre cisely because of these factors that it was time to hold a meeting and publish its proceedings on the subject of transforming proteins of DNA tumor viruses. For the first time, DNA tumor viruses were defined as all of the virus groups that can contribute to cancer in animals with the exception, unfortunately, of the . poxviruses. The purpose of the meeting was to bring together scientists who rarely attend meetings together but actually work on the same problems with different viruses.
Inhaltsverzeichnis
I: The Transforming Protein of Simian Virus 40: Large T antigen and Its Interactions with the Cellular Protein p53. - Structure and Function of SV40 Large T Antigen: Communication Between Functional Domains. - A Genetic Analysis of the Zinc Finger of SV40 Large T Antigen. - Effects of Amino Acid Phosphorylation on the DNA Binding Properties of Large T Antigen. - SV40 T Antigen Catalyzed Duplex DNA Unwinding. - Control of Transcription In Vitro from Simian Virus 40 Promoters by Proteins from Viral Minichromosomes. - Dissection of the T Antigen/mouse p53 Complex and Its Inhibitory Effects on Viral Origin-Directed DNA Replication In Vivo and In Vitro. - Interactions Between SV40 and Cellular Oncogenes in the Transformation of Primary Rat Cells. - Metabolic Stabilization of p53 in SV40 Transformed Cells Correlates with Expression of the Transformed Phenotype but is Independent from Complex Formation with SV40 Large T Antigen. - SV40 Large T Antigen Induces a Protein Kinase Responsible for Phosphorylation of the Cellular Protein p53. - Evidence for Threshold Effects in Transformation of Pancreatic ß-Cells by SV40 T Antigen in Transgenic Mice. - The Biological Activity of Early SV40 Antisense RNA and DNA Molecules. - II: Polyomavirus Middle T Antigen. - Mechanism of Activation of Complexed pp60src by the Middle T Antigen of Polyomavirus. - Further characterisation of the Complex Containing Middle T Antigen and pp60src. - The Mutagenic and Immortalizing Potential of Polyomavirus Large T Antigen. - III: Transforming Functions of Papillomaviruses. - Structure, Activity, and Regulation of the Bovine Papillomavirus E5 Gene and Its Transforming Protein Product. - Functional and Sequence Similarities Between HPV-16 E7 and Adenovirus E1A. - Two Independently Transforming Functions of HumanPapillomavirus 8. - Human Papillomavirus Early Gene Products and Maintenance of Cervical Cancer Cells In Vitro. - IV: Transformation by Adenoviruses. - Adenovirus Terminal Protein Mediates Efficient and Timely Activation of Viral Transcription. - Transcriptional Activation of Adenoviral Early Genes. - Suppression of Cellular Gene Activity in Adenovirus-Transformed Cells. - Recombination Between Adenovirus DNA and the Mammalian Genome. - V: Herpesviruses: The Cellular and Molecular Biology of Epstein-Barr Virus. - Epstein-Barr Virus DNA Replication. - Characterization of the BNLF-1 Oncogene of Epstein-Barr Virus. - Genes for Synthesis of Deoxythymidylate Monophosphate in T-Cell Lymphoma-Inducing Herpesviruses of Nonhuman Primates. - VI: Hepatitis B Virus and Liver Cancer. - Analysis of Hepatitis-B Virus Gene Functions in Tissue Culture and In Vivo. - Transactivation by Hepatitis B Virus may Contribute to Hepatocarcinogenesis.
