By Satvir S. Tevethia, Fred Rapp (auth.), Michael G. Hanna Jr., Fred Rapp (eds.)
It has lengthy been suspected, and lately proven, that there's an etiologic courting among numerous viruses and of course happening neoplasias. Virus precursors within the kind of nucleic acids or antigens have always been linked to yes neoplasias. notwithstanding, the function of those virus-specified precursors in etiology continues to be imprecise. contemporary stories of virus-associated neo plasias have ended in advances in molecular suggestions, that have yielded increas ingly delicate assays for detection of virus-specific nucleic acids, and that have enabled the disruption of virus debris with out concomitant loss in antigenicity of the elements. those methods have, in flip, ended in molecular probes that permit extra definitive review of the host reaction to its virus and to the tumor phone with which the virus or its precursors are linked. reviews of the immune reaction and standing of the host have supplied very important informa tion approximately carcinogenesis and the instruments for seroepidemiological reports of quite a few cancers. those seroepidemiological stories have established that a number of human cancers, e. g. , Burkitt's lymphoma and nasopharyngeal carcinoma, are most likely virus-induced, and that antibodies which are diagnostic and prog nostic for those ailments are detectable. the realization that tom cat leukemia is a ailment transmitted horizontally through a pandemic resulted basically from immunologi cal experiments.
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Additional info for Contemporary Topics in Immunobiology: Immunobiology of Oncogenic Viruses
T antigen is heat labile and resistant to deoxyribonuclease and ribonuclease, but it is susceptible to trypsin. It has a molecular weight of about 70,000 (Del Villano and Defendi, 1973). , 1975) and binds preferentially to SV40 DNA at the origin of replication (S. , 1975) suggest an important role in DNA regulation. This possibility is strengthened by the fact that T antigen is not produced at normal levels by virus mutants which are defective in viral DNA synthesis (Tegtmeyer and Ozer, 1971). The presence of T antigen in the transformed cells has been used to follow the development of SV40-induced tumors in vivo.
1975). , 1974). Mutants in a second complementation group of DNA-minus ts mutants transform rat embryo cells more efficiently than the wild type at elevated temperatures (Ginsberg et al. 1974). This result suggests that a viral gene product normally prevents transformation. This possibility and the observation that no adenovirus-transformed cells containing the entire genome have been identified suggest that transformation may require the integration of the left-hand end of the viral genome and the selective loss of other viral sequences.
The transformation of rat cells by nononcogenic human adenoviruses (which are transplantable under certain conditions in the syngeneic animals) indicates that the apparent nononcogenicity of these transforming human adenoviruses may be due to a strong immunological reactivity of the host to antigens associated with these transformed cells. Transformation of hamster or rat cells by highly or weakly oncogenic human adenoviruses often leads to tumor production by the transformed cells in the appropriate host (for reviews, see Casto, 1973; Tooze, 1973).