How diet, nutrition and physical activity affect ovarian cancer risk.
The ovaries are the sites of ovum (egg) production in women. They are also the main source of the hormones oestrogen and progesterone in premenopausal women.
There are three types of ovarian tissue that can produce cancers: epithelial cells, which cover the ovary; stromal cells, which produce hormones; and germ cells, which become ova (eggs). About 85–90% of ovarian cancers are epithelial carcinomas.
In addition to the findings on diet, nutrition and physical activity outlined above, other established causes of ovarian cancer include:
The risk of ovarian cancer is affected by the number of menstrual cycles during a woman’s lifetime. Not bearing children, early menarche (before the age of 12) and late natural menopause (after the age of 55) all increase the risk of ovarian cancer. The reverse also applies: bearing children, late menarche and early menopause all reduce the risk of ovarian cancer. Tubal ligation (sterilisation) also decreases the risk of ovarian cancer.
Oral contraceptives protect against ovarian cancer. Use of hormone replacement therapy has been shown to increase risk.
Smoking tobacco increases the risk of mucinous ovarian cancer. It is estimated that 17% of mucinous ovarian cancer cases are due to smoking tobacco.
Most ovarian cancers occur spontaneously, although 5–10% of cases develop due to a genetic predisposition. The latter, involving dysfunctional BRCA1 or BRCA2 genes, produces high-grade carcinomas, with poorer prognosis.
Pathogenesis: how does ovarian cancer develop?
The pathogenesis of ovarian cancer is not well characterised, although various mechanisms have been suggested. Over many cycles of ovulation, the ovarian surface epithelium undergoes repeated disruption and repair. The epithelial cells are stimulated to proliferate, which increases the probability of spontaneous mutations.
Alternatively, following ovulation, these cells may become trapped within the connective tissue surrounding the ovary, which can lead to the formation of inclusion cysts. If this happens, the epithelial cells are subjected to a unique pro-inflammatory microenvironment, which may increase the rate of DNA damage, thus affecting cancer risk.
Most ovarian cancers occur spontaneously, although 5–10% of cases develop due to a genetic predisposition. The latter, involving dysfunctional BRCA1 or BRCA2 genes, produces high-grade carcinomas, with a poorer prognosis.
Full references and a summary of the mechanisms underpinning all the findings can be found in the ovarian cancer report.
In 2018, World Cancer Research Fund International published Diet, Nutrition, Physical Activity and Cancer: a Global Perspective on behalf of AICR, WCRF and WKOF. This was the third in our series of major reports looking at the many ways in which our diets, and how active we are, affect our cancer risk. You can find out much more about ovarian cancer by downloading a pdf of the relevant chapter in the 2018 report. Please note, however, that this webpage may have been updated since the report was published.
Published findings in peer-reviewed journals
Selected findings from this report have been published in peer-reviewed journals. Details of the papers and links to the abstract in PubMed are below:
Anthropometric factors and ovarian cancer risk: A systematic review and non-linear dose-response meta-analysis of prospective studies. Aune D, Navarro Rosenblatt DA, Chan DS, Abar L, Vingeliene S, Vieira AR, Greenwood DC, & Norat T. Int J Cancer 2015; 136(8): 1888-98. Abstract