Cervical cancer mostly occurs in sexually active women. The risk for developing cervical cancer increases with number of sexual partners. Infection with the human papilloma virus (HPV) has shown to be the primary cause of this type of cancer (1).
Development of cervical cancer takes multiple years and goes through pre-stages varying in severity (cervical intraepithelial neoplasia – CIN 1–3). CIN 1–2 often repairs itself, but this occurs less commonly with CIN 3. Not all CIN 3 develops into cancer, but there is no possibility for predicting progression/regression. All cases of CIN 3 are therefore treated. Treatment for CIN 2 cases is chosen individually.
Human papilloma virus (HPV)
The virus is transmitted by sexual contact, and infection with HPV is usually harmless, asymptomatic and temporarily. There are many types of the HPV virus. Types 6 and 11 cause genital warts (condylomas), while a number of types are considered oncogenes and as a high risk virus (2). Of these, types 16 and 18 are the most common, but also types 31, 33, and 45 have been found in tissue of cervical cancer in Norway (3). Vaccines against HPV have shown promising results by reducing the frequency. Two vaccines are commercially available. One of the vaccines is against virus 6, 11, 16, and 18, and the other against 16 and 18.
Only a small percentage of women infected with HPV develop cervical cancer. It is presumed that most sexually active women are susceptible to HPV infection, but only about 1% develops cervical cancer.
Women with compromised immune systems are at higher risk for developing cervical neoplasias including cervical cancer. This is often found in women receiving immunosupressing treatment or with HIV infection. Smoking appears to increase the risk for developing this type of cancer, probably due to influencing the immune system of the cervix.