Human Papillomavirus 16 DNA and Epithelial Cell Immortalization

  • Joseph A. DiPaolo


Papillomaviruses have had a unique position in carcinogenesis studies. As early as 1907 Ciuffo1 demonstrated that the infectious agent for the common wart persisted in filtered homogenates and thus was not due to a bacterial or protozean etiology. These findings raised the possibility that warts were caused by newly recognized submicroscopic entities that are now referred to as viruses. Shope and Hung2 later isolated and characterized the first oncogenic DNA virus, referred to as cottontail rabbit papilloma. Subsequently, Rous and associates3,4 demonstrated that when Shope papilloma virus was injected in rabbits, progression from papillomas to carcinomas would be accelerated by the application of either coal tar or a well characterized carcinogenic polycyclic hydrocarbon, 3-methylcholanthrene. This rabbit-virus model also responded to X-irradiation5 which was shown to contribute to progression of papillomas to carcinomas. A decade later, it was realized that X-irradiation of juvenile laryngeal papilloma (HPV 6/11) resulted in carcinomas6. Today, treatment is by surgery or laser. Human papilloma viruses (HPV) are strongly associated with anogenital cancer, including cervical cancer. HPV’s have been associated worldwide with 15% of the human cancers, most notably cancer of the uterine cervix, penis, vulva and anal region. HPV type 16, 18, 31, 33 and 39 have been identified in cervical cancer; over 90% of these neoplasias can be classified as positive. Current epidemiological evidence suggests that incidence of cervical cancer in women is greater in smokers than in non-smokers7.


Cervical Cancer Human Papilloma Virus SW756 Cell Human Papilloma Virus Polycyclic Hydrocarbon 
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Copyright information

© Springer Science+Business Media New York 1988

Authors and Affiliations

  • Joseph A. DiPaolo
    • 1
  1. 1.Laboratory of Biology, Division of Cancer EtiologyNational Cancer Institute, National Institutes of HealthBethesdaUSA

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