Abstract
Chromosomal localization of human papillomavirus (HPV) 16 and 18 on human cervical carcinomas and epithelial cell lines obtained after HPV transfection has uncovered a nonrandom association of viral integration and specific genome sites. Fragile sites appear to be preferential targets for viral integration because of their structural and functional characteristics through which chromosomal anomalies, alterations in protooncogene activity, and gene amplification can occur. Individually or in association, such changes lead to the acquisition of an unlimited cell growth potential but not tumorigenicity. Genetic instability and uncontrolled cell division resulting from HPV integration increase the cell's susceptibility to other exogenous carcinogenic factors that may complete the process of neoplastic development.
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