Endometrial Cancer

Endometrial cancer (cancer of the uterine lining) was the first cancer to be recognized as being obesity-related. There is convincing and consistent evidence from both case-control and cohort studies that overweight and obesity are associated strongly with endometrial cancer (18,33). A linear increase in the risk of endometrial cancer with increasing weight or BMI has been observed in most studies (3,18,34-36). The increase in risk generally ranges from 2- to 3.5-fold in overweight and/or obese women (Table 3), and might be somewhat higher in studies of mortality than incidence (3,18,37).

The probable mechanism for the increase in risk of endometrial cancer associated with obesity in postmenopausal women is the obesity-related increase in circulating estrogens (38). In premenopausal women, endometrial cancer risk is also increased among women with polycystic ovary syndrome, which is characterized by chronic hyperinsulinemia and progesterone deficiency (39). Thus, in both pre- and postmenopausal women, endo-metrial cancer is increased by the mitogenic effects of estrogens on the endometrium when these effects are not counterbalanced by sufficient levels of progesterone. Many studies have shown large increases in endometrial cancer risk among postmenopausal women who take unopposed estrogen replacement therapy (i.e., estrogen in the absence of progesterone) (40), as well as increases in risk among women with higher circulating levels of total and bioavailable estrogens (18).

Studies on BMI and prognosis among women with endometrial cancer suggest that heavier women may have a better prognostic profile, as indicated by more favorable pathological features, and longer survival (41-44). This finding lends additional support to the mechanistic hypothesis of unopposed estrogens, as it mirrors the better prognostic profile seen in women whose endometrial cancer was induced by estrogen replacement therapy (45,46).

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