By J. Michael Bishop, Harold E. Varmus (auth.), Frederick F. Becker (eds.)
The impression of easy examine on oncology has been quite striking within the fresh look for the reason for malignancy. both awesome is our appreciation of the reason for tumors in response to statement. Even within the earliest period of the examine 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 was once viral. the advance of molecular biology, supported through technical advances and conceptual knowing of macromolecular motion, ended in an explosive bring up in reports of animal oncogenic viruses. For a decade, new findings emerged from study laboratories revealing the big number of such brokers, the complicated ity in their interactions with cells, and the tantalizingly attainable mechanisms wherein they may reason malignant transformation of the mobile. time and again, clues emerged which prompt the intervention of viral brokers in human tumors. A breathless pleasure pervaded either the medical and public groups as hugely publicized findings quickly each other. the buzz used to be no much less medical than it was once sensible, for implicit within the inspiration of the viral oncogen is the potential for particular virostatic or virotoxic brokers or of immunization.
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Additional resources for Cancer a Comprehensive Treatise 2: Etiology: Viral Carcinogenesis
4:454. , AND MORGAN, H. , 1970, Mechanism of oncogenic transformation by Rous sarcoma virus. 1. Intracellular inactivation of cell-transforming ability of Rous sarcoma virus by 5-bromodeoxyuridine and light,]. 5:470. ) 226:1209.
Binding of agglutinin to transformed cells restores their growth pattern to that of normal cells (Burger and Noonan, 1970), but efforts to implicate the binding sites in the mechanisms which control cell growth have been inconclusive. The increased agglutination of transformed cells was originally ascribed to the presence of more binding sites for lectins, but this explanation is now in doubt (Cline and Livingston, 1971; Ozanne and Sambrook, 1971; Arndt-Jovin and Berg, 1971; for a dissenting opinion, see Noonan and Burger, 1973).
References AARONSON, S. , AND DUNN, C. , 1973, High-frequency C-type virus induction by inhibitors of protein synthesis, Science 183:422. AARONSON, S. , TODARO, G. , AND SCOLNICK, E. , 1971, Induction of murine C-type viruses from donal lines of virus-free BALB/3T3 cells, Science 174: 157. , AND DARNELL,]. , 1972, Evidence that all messenger RNA molecules (except histone messenger RNA) contain poly(A) sequences and that the poly(A) has a nuclear function,]. Mol. Biol. 71:21. , AND TEMIN, H. , 1970, Carcinogenesis by RNA sarcoma viruses.