Introduction

There are significant similarities between the pathophysiology of cervical and vaginal cancers as the majority are squamous cell carcinomas caused by persistent infection with high-risk human papillomavirus (HPV). The introduction of the HPV vaccination programme aims to reduce the number of cancers caused by HPV including cervical, vagina, vulva, penile, anal and laryngeal cancers.

Both cervical and vaginal cancers are treated by a multidisciplinary team (MDT) that includes gynaecological oncologists, medical oncologists, clinical oncologists, pathologists, radiologists and clinical nurse specialists. Both tumours are staged clinically by an examination under anaesthesia. Although lymphnode involvement is of paramount importance in determining appropriate treatment approaches, and outcome, it does not form part of the International Federation of Gynecology and Obstetrics (FIGO) staging system.

Human Papilloma Virus

HPV is a DNA virus and is the most common sexually transmitted infection globally. The virus is ubiquitous, and consequently most individuals get infected at some stage of their lives. However, the vast majority of infections resolve spontaneously without ever developing symptoms, as HPV is eliminated by their immune system. Individuals with HIV infection or other immune deficiency states (such as transplant recipient on immunosuppression, drug usage) and smoking act as cofactors that prevent the elimination of HPV by the immune system. Persistent HPV infection with high-risk oncogenic subtypes causes precancerous lesions such as cervical intraepithelial neoplasia (CIN), vulval intraepithelial neoplasia (VIN), anal intraepithelial neoplasia (AIN) and vaginal intraepithelial neoplasia (VaIN). These lesions may either progress into invasive cancer or can regress spontaneously if HPV is subsequently eliminated. The longer an oncogenic HPV subtype is present and the greater the viral load, the higher the chance of developing a precancerous lesion.

HPV is detected in 99% of cervical tumours and 75% of vaginal tumours. HPV subtypes 16 and 18 account for 70% of all cervical tumours. Other oncogenic subtypes of HPV include 31, 33, 35, 39, 45, 51, 52, 53, 56, 58, 59, 66, 68, 73 and 82.

Cervical cancer is more common than other HPVderived cancers (vagina, vulva, penile, anal and laryngeal) due to the presence of the transformation zone on the cervix. The transformation zone is the area of exposed columnar tissue present on the surface of the cervix that undergoes the process of squamous metaplasia, and transforms into squamous tissue. This area is particularly susceptible to the effects of oncogenic HPV infection.