Cervical, Vulvar, and Vaginal Cancer

Abstract

In the year 2001, the American Cancer Society estimated that 12,900 women would be diagnosed with invasive cervical cancer and 4400 women would die as a result of this disease [1]. The median age at diagnosis is 47 years, with nearly half of all patients diagnosed before the age of 35. However, those patients over the age of 55, many of whom have not had a Pap smear within the previous 3 years, contribute significantly to the numbers of patients diagnosed with advanced-stage disease [2]. The primary etiologic agent in the development of cervical cancer is the human papillomavirus (HPV). HPV types 16, 18, 31, 35, 39, 45, 51, 52, 56, and 58 have been associated with malignant transformation [3]. More than 90% of squamous cervical cancers have been found to contain human papillomavirus DNA, which is acquired primarily through sexual activity [4–6]. HPV 16 and 18 have two transcriptional units, E6 and E7, that encode for proteins critical for viral replication. The E6 oncoprotein exerts its effect by binding to and inactivating the tumor suppressor gene p53, which disrupts an inherent cell cycle checkpoint [7–9]. The E7 oncoprotein binds to and inactivates products of the retinoblastoma gene, pRb, which ultimately allows for unchecked cell cycle progression in those cells infected with HPV 16 and 18 [10,11].