Abstract
One of the earliest indications that cervical cancer is a sexually transmitted disease comes from the observation of Rigoni-Stern [1] who in 1842 published a statistical paper indicating that “cancer of the uterus” was rare among virgins and nuns and quite common among married women and widows. Although the precise etiology of cervical neoplasia is unknown, the epidemiological profile of the disease makes it almost certain that an infectious agent, as a result of sexual transmission, plays a part in the carcinogenesis [2–4]. In the past few years evidence from various sources, including cytology, histology, and immunohistochemistry, has shown that there is an association between human papillomavirus infection and cervical neoplasia [5–7]. Furthermore, human papillomas have a single host species (Homo sapiens) and multiply in mucosal or differentiated cutaneous epithelium at specific anatomical sites. Today there are over 50 various human papillomavirus genotypes; of these a small number, i.e., 6, 11, 16, 18, 31, 33, and 35, and 52b, are found in intraepithelial and invasive cervical cancer [8–11]. Human papillomaviruses 6 and 11 are associated predominantly with benign lesions (condylomas or low-grade dysplasia), whereas the other types occur in invasive cervical carcinomas. Types 16 and 18 occur in most invasive cervical carcinomas; about 95% of women with cervical cancer are found to be positive for a papillomavirus.
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References
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DiPaolo, J.A., Woodworth, C.D., Furbert-Harris, P.M., Evans, C.H. (1990). Immunomodulation of HPV 16 Immortalized Exocervical Epithelial Cells. In: Gross, G., Jablonska, S., Pfister, H., Stegner, HE. (eds) Genital Papillomavirus Infections. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-75723-5_20
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DOI: https://doi.org/10.1007/978-3-642-75723-5_20
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