Epidemiology and biology of cervical cancer

Authors

  • Wolfgang M.J Schoell MD,

    Corresponding author
    1. Division of Gynecologic Oncology, University of Miami School of Medicine, Miami, Florida
    2. Department of Obstetrics and Gynecology, University of Graz, Graz, Austria
    • Division of Gynecologic Oncology, University of Miami, Sylvester Comprehensive Cancer Center, 1475 NW 12th Avenue (D-52), Miami, FL 33136. Fax: 305-243-4938
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  • Mike F. Janicek MD,

    1. Division of Gynecologic Oncology, University of Miami School of Medicine, Miami, Florida
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  • Ramin Mirhashemi MD

    1. Division of Gynecologic Oncology, University of Miami School of Medicine, Miami, Florida
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Abstract

Worldwide, cancer of the cervix is the second leading cause of cancer death in women: each year, an estimated 500,000 cases are newly diagnosed. Among populations, there are large differences in incidence rates of invasive cervical cancer: these reflect the influence of environmental factors, screening Papanicolaou (Pap) tests, and treatment of pre-invasive lesions. The high-risk human papillomavirus (HPV) subtypes 16, 18, 31, 33, and 51 have been recovered from more than 95% of cervical cancers. We have made great strides in understanding the molecular mechanism of oncogenesis of this virus, focusing on the action of the E6 and E7 viral oncoproteins. These oncoproteins function by inactivating cell cycle regulators p53 and retinoblastoma (Rb), thus providing the initial event in progression to malignancy. Cervical cancers develop from precursor lesions, which are termed squamous intraepithelial lesions (SIL) and are graded as high or low, depending on the degree of disruption of epithelial differentiation. Viral production occurs in low-grade lesions and is restricted to basal cells. In carcinomas, viral DNA is found integrated into the host genome, but no viral production is seen. The well-defined pre-invasive stages, as well as the viral factors involved at the molecular level, make cervical carcinoma a good model for investigating immune therapeutic alternatives or adjuvants to standard treatments. Semin. Surg. Oncol. 16:203–211, 1999. © 1999 Wiley-Liss, Inc.

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