Epidemiology and risk factors for ovarian cancer

Abstract

Ovarian cancer is a complex disease, mostly observed in postmenopausal women, and is associated with poor survival rates. It is the sixth most common cancer and the fifth most common cause of death due to cancer among women in developed countries. Thus, despite representing less than one third of all gynaecologic cancers, deaths due to ovarian cancer account for more than two thirds of deaths due to gynaecologic cancers. Its prevalence is higher in Western Europe and Northern America than Asia and Africa. In sub-Saharan Africa, there is a considerably lower prevalence of ovarian cancer than other parts of Africa. Ovarian cancer is multifaceted, involving many factors, complex biological processes and unpredictable consequences. Unlike other female cancers that have early warning symptoms, ovarian cancer's symptoms are non-specific. As a result, ovarian cancers are normally undetected until advanced stages (III or IV). The major risk factors for ovarian cancer include older age, genetics, family history, hormone replacement therapy, nulliparity, and dietary fat. Controversial factors include obesity, infertility, talc powder, radiation exposure, fertility medications and in vitro fertilization. The current review discusses the aetiology, epidemiology and risk factors for ovarian cancer. Nevertheless, identification of the main risk factors for ovarian cancer may increase the awareness among women of the general population. This should help to decrease the incidence rate of ovarian cancer and increase the five-year survival rate.

Keywords: aetiology; epidemiology; family history; genetics; older age; ovarian cancer.

Fig. 1

The most accepted hypotheses explaining the development of ovarian cancer and their supporting evidence [3]

Fig. 2

BRCA1 mutation carriers display a higher risk towards the development of ovarian cancer across all age groups

Fig. 3

Pathway analysis demonstrating drug resistance in patients with KRAS mutation. KRAS mutation contributes to the resistance through constitutive activation of epidermal growth factor receptor (EGFR) downstream signalling cascades regardless of EGFR blockade. In normal EGFR, the use of anti-EGFR drugs blocks KRAS and stops cancer cells’ division and metastasis, while in mutant EGFR, anti-EGFR drugs are not effective