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REVIEW: Virus-Associated Human Tumors: Cervical Carcinomas and Papilloma Viruses

F. L. Kisseljov

Institute of Carcinogenesis, Blokhin Russian Cancer Research Center, Kashirskoe Shosse 24, Moscow, 115478 Russia; fax: (7-095) 323-5733; E-mail: f.kis@cityline.ru

Received September 17, 1999
The latest experimental data on the role of viruses in the origin of human tumors are discussed. This group of viruses consists of T-cell leukemia virus type 1 (HTLV 1), herpes viruses (HHV 8 and Epstein--Barr virus), hepatitis B virus, and human papilloma viruses. The most typical feature of this group of viruses is a very long latent period from the initial infection to the development of the disease that varies between 10 and 40 years. The mechanism of malignant cell conversion is specific for each viral type but is mainly associated with a disruption of functions of cellular genes participating in the control of cell division and proliferation. It can be a direct inactivation of tumor suppressor genes by their interaction with viral gene products (papilloma viruses), or a trans-activation of cellular genes modulating cell proliferation by viral gene products (hepatitis B virus and HTLV 1). Viruses play an initiative role and additional genetic changes in the genome of infected cells are necessary for complete expression of the oncogenic potential of the viral genes. Only these cells will give rise to a monoclonal cell population with uncontrolled proliferation. New approaches for the creation of vaccines against cancers associated with hepatitis B virus and papilloma viruses (hepatocellular carcinomas and cervical tumors, respectively) are in progress. These vaccines have been found to be effective in prevention of the disease in the experimental models and are now beginning to be used for human vaccination.
KEY WORDS: tumors, cervical cancer, transformation, mechanisms, papilloma viruses, transforming genes, oncogenes, tumor suppressor genes