By J. Michael Bishop, Harold E. Varmus (auth.), Frederick F. Becker (eds.)

The influence of uncomplicated examine on oncology has been relatively outstanding within the contemporary look for the reason for malignancy. both extraordinary is our appreciation of the reason for tumors in keeping with commentary. Even within the earliest period of the research of infectious illnesses, it was once proposed that tumorous progress in animals and birds resulted from "minute" infectious debris. Experiments then supported the speculation, that the etiologic agent in lots of animal tumors used to be viral. the advance of molecular biology, supported through technical advances and conceptual figuring out of macromolecular motion, resulted in an explosive elevate in reviews of animal oncogenic viruses. For a decade, new findings emerged from learn laboratories revealing the big number of such brokers, the complicated­ ity in their interactions with cells, and the tantalizingly attainable mechanisms through which they may reason malignant transformation of the mobilephone. time and again, clues emerged which steered the intervention of viral brokers in human tumors. A breathless pleasure pervaded either the clinical and public groups as hugely publicized findings speedily each other. the thrill used to be no much less clinical than it was once useful, for implicit within the suggestion of the viral oncogen is the potential for particular virostatic or virotoxic brokers or of immunization.

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Either crucial genes are not transcribed into RNA or control factors operate at some point subsequent to transcription. Available data cannot distinguish between these alternatives. , 1973e), illustrate how little is known about the mechanisms which regulate the expression of viral genes integrated into RNA TUMOR VIRUSES 36 J. M. BISHOP AND H. E. V ARMUS cellular DNA. If transcriptional controls are responsible, they must operate on specific portions of the integrated viral genome rather than effecting either complete repression or complete expression.

ACKNOWLEDGMENTS Research in the authors' laboratories is supported by grants from the American Cancer Society (VC-70) and the USPHS (AI 08864, CA 12380, CA 12705, AI 06862, AI 00299), and by Contract No. NOI CP 33293 within the Virus Cancer Program of the National Cancer Institute. H. E. V. is the recipient of a Research Career Development Award (CA 70193) from the National Cancer Institute. We thank B. Bickerstaff and J. Skiles for stenographic and bibliographical assistance. 11. References AARONSON, S.

By contrast, heterologous hosts, either permissive or nonpermissive, generally contain no detectable genes homologous to those of the infecting virus. Consequently, the entire viral genome is newly inserted into host DNA as a consequence of infection (see above). , the particular morphology assumed by the cell (Temin, 1961; Yoshii and Vogt, 1970). , 1973b). , 1973). , temperature sensitive) when induced by viral strains which are conditional mutants in genes for transformation. Mutants of avian sarcoma viruses which are temperature sensitive for transformation have been arranged into four complementation groups (Wyke, 1973), but more recent studies indicate that the observed complementation was due to recombination (Wyke, personal communication).

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