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Endometrial and ovarian malignancies: epidemiology, etiology and prognostic factors

Endometrial and ovarian cancer share many similarities in their epidemiology and etiology (1). The geographical patterns of distribution are similar for both cancers, with highest incidence rates reported in white females in Western Europe and North America ( 2 ) . In the Nordic countries, the highest incidence rates for both cancers are observed near Copenhagen and Stockholm, and in Southern Sweden ( 2 ) . The Scandinavian countries, especially Sweden, have the highest cumulative incidence rates of ovarian cancer worldwide (2, 3 ) . The high incidence of ovarian and corpus cancer in the industrialized countries have stimulated the hypothesis that environmental agents may be important etiologic factors. This hypothesis has also been supported by migrant studies which showed that genetic differences are of less significance as etiologic factors than environmental ones (4, 5). This has been manifested in the early studies of Haenszel and Kurihara (4) who observed an increase in the incidence of ovarian and endometrial cancer among Japanese migrants to the U.S.A (who moved from a country with very low risk for both cancers to one with a very high risk). More recent data (5) based on incidence rates in Hawaii (1973-1977) showed that ovarian cancer incidence among first and second generation Japanese migrants was 7 per 100,000 compared to 3.4 per 100,000 in Japan and 9.4 per 100,000 among Hawaii whites. A similar pattern of increase in the incidence of endometrial cancer among first and second generations of Japanese migrants (15.5 and 20.3 per 100,000 respectively) was observed. The corresponding figures for endometrial cancer were 2 per 100,000 (in Japan) and 34.8 per 100,000 (in Hawaii whites). Among environmental factors suspected to play a r61e in the pathogenesis of ovarian and endometrial malignancies, great importance is attached to fat consumption, obesity and patterns of fat distribution (6-8). A strong relationship between a high Quetelet index (defined as weight (kg) divided by height (m) squared) and risk for ovarian and endometrial cancer has been reported by many authors (6-8). Farrow et al. (6) found that a high Quetelet index significantly increased the risk for ovarian cancer, especially those of serous and endometroid histologic types. Austin et al. (8) also found a statistically significant excess risk for endometrial cancer with central obesity and this excess risk could not be explained by increased estrogen levels. The r61e of pregnancy, breast feeding and hormonal therapy on the pathogenesis of ovarian and endometrial cancers has been widely discussed in the literature (9-15). Regarding ovarian cancer, the most consistent finding among case control studies has been a relative deficit of pregnancies among cases. Several case-control studies have found a decrease in risk of the epithelial ovarian cancer associated with pregnancy, breast feeding and use of oral contraceptives (00) (9-14). This prompted the hypothesis of incessant ovulation which holds that factors which suppress ovulation may reduce the risk of developing ovarian cancer (9-14). Gwin et al. (11) showed in a multicenter population-based, case-control study, that the estimated relative risks of epithelial ovarian cancer were 0.6 (95% confidence interval 0.5-0.8) for women who have ever been pregnant, 0.6 (95% confidence interval 0.5-0.8) for women who have ever breast fed, and 0.5 (95% confidence interval 0.5-0.7) for women who have ever used oral contraceptives. The risk of ovarian cancer seemed to de-