Epidemiology of endometrial cancer.

Abstract

This review of endometrial cancer summarizes the demographic characteristics of patients with the disease, their hormonal risk factors related to endogenous and exogenous estrogens and medical history, and other risk factors. Endometrial cancer increased in incidence in the US in the early 1970s, but then declined again in the last 2 decades. Possible reasons are classification including estrogen- induced hyperplasia, but also increased use of exogenous estrogens primarily in post-menopausal women, who are the predominant victims. Postmenopausal estrogen usage decreased at the same time. The highest incidence occurs in Polynesian women, although US Caucasians have more endometrial cancer then Blacks or European women. Endometrial cancer is common in women with estrogen-secreting ovarian cancer. Women with polycystic ovaries, where the steroid androstenedione is secreted and converted to estrone in peripheral tissues, but progesterone is lacking, are higher risk for endometrial hyperplasia and cancer. Obese women are also at risk (estimated 20-fold), as they have low sex binding globulin and higher estrogen levels. Any exogenous estrogen, by any route, even if stopped for a week per month confers higher risk for endometrial cancer, as shown by virtually all case control studies. Very little data exists on the actual effect of taking progestins with postmenopausal estrogens. These tumors are less invasive, more differentiated, and often detected earlier than non-estrogen dependent endometrial cancers. Other putative risk factors, e.g., diabetes, hypertension, gall bladder disease, radiation exposure, and family history of breast cancer have no solid evidence for association. Smoking, however, is associated with a lower risk of endometrial cancer.