The epidemiology of female genital tract cancers

Abstract

Endometrial, ovarian and cervical cancer are among the leading causes of death in women. The role of unopposed estrogens in endometrial carcinogenesis is well established. Any factor that increases the exposure of the endometrium to unopposed estrogen, such as menopausal replacement treatment, obesity, or irregular menstrual cycles tends to raise the risk of the disease, while factors that lower exposure to estrogens or increase progesterone levels, such as oral contraceptives (OC) or smoking, decrease the risk. These well-established risk factors can have different effects at different ages, particularly in pre- and postmenopausal women: more generally, the interaction between various factors is still not totally defined. With reference to ovarian cancer, OC and parity, late menopause and lifelong regular menstrual periods increase the risk of the disease. In terms of biologic mechanisms, these factors are thought to act on ovarian cancer risk by affecting lifetime number of ovulations. Along this line, 'incessant ovulation' could be the relevant exposure that defines the incidence of the neoplasm. Among the factors other than reproductive or hormonal, diet is likely to be the most relevant, but it is still however, poorly quantified. There is now consistent evidence that Human Papillomavirus (HPV) has a causal role in the ethiology of cervical cancer and that sexual habits and reproductive/hormonal factors are associated with the risk of invasive cervical cancer. Less clear is the role of smoking and dietary habits, but recent studies have shown a direct relationship between smoking and the risk of invasive cervical cancer and an inverse one between selected vitamin intake and risk of the disease. In this paper we review and discuss these evidences.