Does hormone replacement therapy prevent epithelial ovarian cancer?

Area of Science:

• Gynecology
• Oncology
• Reproductive Endocrinology

Background:

• Two primary hypotheses for epithelial ovarian cancer (EOC) aetiology involve incessant ovulation and gonadotrophin stimulation.
• Risk factors for EOC include ovulation frequency, while protective factors include pregnancies, oral contraceptive (OC) use, and breastfeeding duration.

Purpose of the Study:

• To investigate the roles of ovulation and gonadotrophins in epithelial ovarian cancer (EOC) aetiology.
• To explore the differential effects of oral contraceptives (OC) and hormone replacement therapy (HRT) on EOC risk.
• To review the relationship between hormones, particularly estrogen, and post-menopausal EOC.

Main Methods:

• Literature review and analysis of epidemiological data correlating reproductive factors with EOC risk.
• Examination of studies on gonadotrophin roles in EOC, including receptor presence in ovarian tissues.
• Analysis of hormonal influences, including OC and HRT effects, on EOC development.

Main Results:

• A significant inverse correlation exists between EOC risk and factors like pregnancies, OC use, and breastfeeding.
• Ovulation in younger age groups (20-29 years) increases EOC risk, whereas late childbirth (>35 years) confers maximum protection.
• While hormone replacement therapy (HRT) lowers gonadotrophin levels, it does not reduce EOC risk, unlike oral contraceptives (OC).

Conclusions:

• Reproductive history significantly modulates EOC risk, with ovulation suppression via OC use being protective.
• The mechanisms by which OC reduce EOC risk, compared to HRT, remain unclear.
• Further research is needed to understand the precise role of gonadotrophins and hormonal balance in EOC aetiology and prevention.