Important note: Information in this article was accurate in 1992. The state of the art may have changed since the publication date.
HUMAN PAPILLOMAVIRUS (HPV), CO-FACTORS AND CARCINOGENESIS OF THE UTERINE CERVIX
Serono Symp Publ Raven; 78:31-48 1990. Unique Identifier : AIDSLINE ICDB/92678047 Monsonego J; Inst. Alfred Fournier, Dept. of Cyto-Colposcopy, 25 Blvd. Saint; Jacques, 75014 Paris, France
Abstract:
Recently, a distinct increase has been seen in the incidence of viral anogenital condylomatous lesions in men and women. The epidemiological profile of cancer of the uterine cervix (including intraepithelial cancer) has changed, with an overall decrease in incidence in the past 30 yr, which has occurred mainly in women over 50 yr old, while a progressive increase has been observed in women from 20-40 yr old. Koilocytosis, pathognomonic of HPV infection, is seen in cervical intraepithelial neoplasia (CIN) and in successive stages leading to invasive cancer. HPV and cofactors in cervical carcinogenesis are reviewed, including factors related to local exposure to the virus (columnar ectopy and recurring cervicitis and cervico-vaginitis); factors involved in CIN and invasive epidermoid cancers of the uterine cervix (oral contraception, tobacco use, immunodepression, diseases associated with disorders of immunity, seropositivity for HIV, pregnancy, age at first intercourse, diet, associated sexually transmitted diseases, and viral lesions in the male partner); and oncogenes. Numerous biological, epidemiological, and evolutionary arguments support the view that the association between HPVs 16-18 and possibly others with condylomatous lesions and CIN is insufficient, by itself, to confer tumor characteristics on infected tissues. The host and the cofactors that characterize it also are probable determinants in carcinogenesis. It is not impossible that, in certain circumstances, HPV or cofactors may induce activation of certain oncogenes, the transcription of which may be augmented in certain precursors of cancer of the cervix and amplified in the tumor processes. Certain cofactors may favor viral replication and integration into the host genome, or may induce the liberation of transforming factors. In practical terms, the determination of markers of carcinogenesis that are more specific than HPV should permit better selection of patients for treatment. The determination of activated oncogenes, overexpressed or mutated, in the precursor lesions of cancer of the cervix very probably will constitute a valid marker for the evolution of disease. (108 Refs)
Keywords: Carcinoma, Squamous Cell/*ETIOLOGY Cell Transformation, Neoplastic/GENETICS Cervix Neoplasms/*ETIOLOGY *Cocarcinogenesis Condylomata Acuminata/ETIOLOGY Female Human *Papillomavirus/GENETICS Precancerous Conditions/*ETIOLOGY Risk Factors Tumor Virus Infections/*ETIOLOGY MONOGRAPH REVIEW 920228
M9220893
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Important note: Information in this article was accurate in 1992. The state of the art may have changed since the publication date.
