Download Cancer a Comprehensive Treatise 2: Etiology: Viral by J. Michael Bishop, Harold E. Varmus (auth.), Frederick F. PDF

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

The impression of easy learn on oncology has been fairly awesome within the contemporary look for the reason for malignancy. both extraordinary is our appreciation of the reason for tumors in accordance with statement. Even within the earliest period of the examine of infectious ailments, it used to be proposed that tumorous development 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 via technical advances and conceptual realizing of macromolecular motion, resulted in an explosive elevate in reviews of animal oncogenic viruses. For a decade, new findings emerged from study laboratories revealing the large number of such brokers, the complicatedĀ­ ity in their interactions with cells, and the tantalizingly attainable mechanisms through which they may reason malignant transformation of the cellphone. time and again, clues emerged which advised 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 thrill used to be no much less medical than it used to be functional, for implicit within the idea of the viral oncogen is the opportunity of particular virostatic or virotoxic brokers or of immunization.

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Additional info for Cancer a Comprehensive Treatise 2: Etiology: Viral Carcinogenesis

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Is the site of integration a determinant of the extent to which viral genes are expressed? Are proviruses which are integrated in multiple copies arranged in tandem, or are they integrated separately? These issues are now accessible to experimental test, but no persuasive data are available. 3. , 1973c; also, unpublished data of H. E. Varmus). A few of the infected nonpermissive cells will convert to a neoplastic state. , 1973c). The mechanism which blocks expression of viral information in these cells is not known.

E. V ARM US In summary, the application of molecular biology to the search for RNA tumor viruses in Homo sapiens is limited by both the specificity of most available reagents and the conceptual problems engendered by present animal models. The investigator must contend with the fact that the demonstration of viral genes in human cells does not necessarily implicate those genes in oncogenesis. The apparent ubiquity of endogenous, often cryptic C-type viruses in ostensibly normal cells, coupled with uncertainties regarding the role of these viruses in either experimental or natural oncogenesis, requires that molecular studies be conducted in conjunction with biological and genetic analyses of both known and yet to be discovered cancer viruses.

The template for synthesis of provirus) can be recovered from the host nucleus very shortly after infection (Dales and Hanafusa, 1972). , 1973, 1974), or (3) that the viral RNA observed in the nucleus is not participating in the replicative cycle. The properties of viral DNA prior to integration have not been extensively characterized. It is at least in part duplex DNA composed of chains approximately 7500 nucleotides in length and therefore presumably transcribed from single subunits of the viral genome (unpublished data of R.

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