The carcinoma of the uterine cervix is the second most common cancer among women worldwide, with its higher incidence in developing countries (1). Strong clinical and experimental evidence demonstrated that the high-risk (HR) types of human papilloma virus (HPV) play a central role in causing cervical cancer, although a role of multiple risk factors has been suggested too. Not only does the epidemiological data indicate the criteria of causality on HPV and cervical cancer, but also there are several studies that identified the viral transforming genes, and their mode of action supports a model of multistep carcinogenesis. It is generally accepted that the development of invasive cervical cancer from intraepithelial neoplasia (cervical intraepithelial neopla-sia [CIN]1-2/3) involves molecular changes and therefore is a preventable if detected and treated early. The vast majority of low-grade squamous intraepithelial lesions (LSILs) regress spontaneously and it is estimated that about 10-20% of high-grade SILs (HSILs) are at risk of progressing into invasive cancer.

Despite the success of screening programs, cervical carcinoma continues to be diagnosed especially in underscreened and unscreened populations. Present research spans the spectrum from understanding the epidemiology of HPV infection, including its natural history, to understanding the molecular biology of cervical cancer. Identification of molecular changes as a result of HPV infection can lead to new therapies to treat existing cervical cancer and, in the long-term, to prevent the disease.

From: Current Clinical Oncology: Molecular Pathology of Gynecologic Cancer Edited by: A. Giordano, A. Bovicelli, and R. Kurman © Humana Press Inc., Totowa, NJ

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