Introduction

Cervical cancer is one of the most common cancers in women worldwide and is globally a leading cause of death among women. Nearly all of invasive cervical cancers are caused by persistent human papillomavirus (HPV) infection and resultant progression of cervical intraepithelial neoplasia (CIN). Common symptoms of cervical cancer include irregular vaginal bleeding or postcoital bleeding, vaginal discharge, and signs of ureteral, venous, or lymphatic compression. Stage is the most important predictor of survival; cervical cancer is staged clinically. The stage of the cancer dictates treatment, which typically consists of either surgery or chemoradiation for early stages, and chemoradiation or systemic chemotherapy for advanced stages. Early detection of cervical dysplasia and vaccination against HPV are effective in preventing cervical cancer.

Statement of the Problem

In the United States, about 13,000 new cases are diagnosed per year and about 4,000 women will die from the disease [1]. The death rate from cervical cancer decreased by 70 percent since the implementation of the Papanicolaou test (Pap test) in the mid-1940s; because preinvasive lesions are detected, cervical cancers can be diagnosed at an early stage.

Multiple factors have been associated with the development of cervical cancer. This malignancy most commonly develops at the squamocolumnar junction on the cervix where the cells are most actively undergoing metaplastic change from columnar to squamous epithelium. Infection with HPV is detected in more than 99 percent of cervical cancers. Typically the progression from dysplasia to invasive cancer requires several years, although wide variations exist. Although more than 70 different subtypes of HPV have been identified, women infected with high-risk subtypes have an increased risk of developing dysplasia and a subsequent malignancy. The most common high-risk subtypes are HPV-16 and HPV-18. These account for 70 percent of cervical cancers in the United States [2]. The E6 protein product of these high-risk HPVs binds to the tumor suppressor protein p53, which is thought to disrupt the p53-dependent control of the cell cycle [3]. The E7 protein causes an inactivation of the tumor suppressor retinoblastoma gene (Rb) via its interaction with the Rb protein, whose normal function is seen with the negative control of cell growth [4].

Risk factors associated with HPV infection include multiple sexual partners, history of other sexually transmitted infections, high parity, immunosuppression, and cigarette smoking [5].