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The Symposia, 1933 — 2003

1979:   Viral Oncogenes, Vol. XLIV

Organizer: James Watson

Table of Contents

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What a difference a few years and a technique or two can make! At the time of the 1974 Symposium on Tumor Viruses, recombinant DNA techniques were only just being adopted and were restricted to analysing small genomes like those of viruses. But as Jim Watson pointed out in his foreword, between the 1974 and 1979 Symposia, two techniques–DNA sequencing and Southern blotting–together with improvements in cloning techniques, had led to the analysis of eukaryotic genomes, and to a better understanding of the genes of tumor viruses.

In contrast to the optimism many at the Symposium must have been feeling, Howard Temin opened the Symposium volume with a thoughtful and distinctly sobering essay. Beginning with a review of some of the limitations of viral oncology, Temin went on to point out that environmental factors were probably the main cause of cancers, and that viruses were not involved in the great majority of cancers. He raised many questions about cancer and discussed the relationship between viral and nonviral cancers, and whether studies of tumor virus genes will be helpful.

The participants clearly thought so; following reviews by Lionel Crawford on DNA tumor viruses and Peter Duesberg on retroviruses, they were able to fill some 1300 pages in the Symposium volume. Strikingly, but not surprisingly given the recent discovery that src had protein kinase activity, there were no fewer

than 18 papers on src. But there were other interesting reports. For example, Crawford’s group described the association of the cellular 53K protein (later named p53) with the SV40 large T antigen, and protein-protein interactions became a recurring theme in understanding the actions of oncogenes. On the retrovirus side, Hayward presented his findings on the locations of endogenous Avian Leukosis viruses, a prelude to demonstration that the virus integrated at the same genomic site in tumors of the same type and in so doing activates an endogenous gene, myc.

Temin hoped that: “...tumor virsues may provide simple agenets to study the processes and the molecules invopllved in all oncoogenesis and in much differentiation”. He was right, as the flood of research on the genetics of cancer, cell cycle control and growth regualtion that came over the next 15 years showed.

Peter Sherwood

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