Veterinary and Biomedical Sciences, Department of


Date of this Version

October 1995


Published in CLINICAL MICROBIOLOGY REVIEWS, Oct. 1995, p. 549–556 Vol. 8, No. 4. Copyright 1995, American Society for Microbiology. Used by permission.


Approximately 1.6% of all women will develop cancer of the cervix during their lifetime (4). Cervical cancer is the second leading type of cancer in women and accounts for approximately one-sixth of all cancer deaths in females. In many ways, cervical cancer behaves as a sexually transmitted disease. The major risk factors associated with cervical cancer are the early onset of sexual intercourse, multiple sexual partners, and/or sexual contact with promiscuous partners (66, 94). The disease is composed of several pathological stages ranging from cervical intraepithelial neoplasia (CIN) to invasive squamous carcinoma. Substantial evidence suggests that CIN is a precursor of invasive cervical carcinoma (76, 88). Cytological and colposcopic studies have determined that most initial neoplastic events occur within the cervical squamous epithelium adjacent to the endocervical epithelium (the squamocolumnar junction or transformation zone [reviewed in reference 108]). At the junction where columnar epithelium becomes squamous epithelium, there is a temporary state of genetic imbalance that renders the immature cells susceptible to neoplastic events. It is believed that unique developmental aspects of the squamocolumnar junction as well as exogenous factors are necessary for induction of cervical carcinoma.