Endometrial cancer is the most common gynaecological malignancy. Risk factors include obesity, hypertension, diabetes and hyperoestrogenism – all of which are linked to activation of the renin-angiotensin system (RAS). The endometrium expresses all of the components of the RAS in both glandular and stromal cells, with levels varying though the menstrual cycle.

The endometrial RAS has been implicated in angiogenesis, neovascularisation and cell proliferation, factors which are involved in tumour growth and spread. Overexpression of angiotensin II and its receptor have been found in several malignancies, while a reduction in the relative risk of cancer has been demonstrated in patients using angiotensin-converting enzyme (ACE) inhibitors for hypertension.

Over-activation of the RAS can be attributed to single nucleotide polymorphisms (SNPs) in RAS genes. Pringle et al. measured the prevalence of five polymorphisms in RAS genes in 184 Australian women with endometrial cancer and in healthy controls. They found SNPs in the genes for angiotensin II and the angiotensin II receptor which are predicted to increase RAS activity, and which were associated with a statistically significant increase in the prevalence of endometrial cancer.

Read the full article in Endocrine Connections doi: 10.1530/EC-15-0112 (OA)