TY - JOUR
T1 - The epidemiology of endometrial cancer
AU - Parazzini, Fabio
AU - La Vecchia, Carlo
AU - Bocciolone, Luca
AU - Franceschi, Silvia
PY - 1991
Y1 - 1991
N2 - The descriptive and analytical epidemiology of endometrial cancer is reviewed. Over the last few decades, age-standardized incidence rates have been rising in several countries. The rise has been even greater in terms of absolute numbers of cases, and hence public health implications, due to the aging of the population. Although endometrial cancer rates were found to be higher in richer countries and urban populations, there is now evidence of some changes in the socioeconomic determinants of the disease in developed countries. In etiological terms, any factor that increases exposure to unopposed estrogens (such as menopausal replacement treatment, obesity, and irregular menstrual cycles) tends to increase the risk of the disease, while factors that decrease exposure to estrogens or increase progesterone levels (such as oral contraceptives or smoking) tend to be protective. Less well defined, or more difficult to explain in biological terms, is the role of other factors, such as births, miscarriages, or diabetes and hypertension, and only suggestive evidence is available on diet from analytical epidemiology. The data reviewed herein are discussed in terms of models of carcinogenesis, as well as attributable risks and public health implications.
AB - The descriptive and analytical epidemiology of endometrial cancer is reviewed. Over the last few decades, age-standardized incidence rates have been rising in several countries. The rise has been even greater in terms of absolute numbers of cases, and hence public health implications, due to the aging of the population. Although endometrial cancer rates were found to be higher in richer countries and urban populations, there is now evidence of some changes in the socioeconomic determinants of the disease in developed countries. In etiological terms, any factor that increases exposure to unopposed estrogens (such as menopausal replacement treatment, obesity, and irregular menstrual cycles) tends to increase the risk of the disease, while factors that decrease exposure to estrogens or increase progesterone levels (such as oral contraceptives or smoking) tend to be protective. Less well defined, or more difficult to explain in biological terms, is the role of other factors, such as births, miscarriages, or diabetes and hypertension, and only suggestive evidence is available on diet from analytical epidemiology. The data reviewed herein are discussed in terms of models of carcinogenesis, as well as attributable risks and public health implications.
UR - http://www.scopus.com/inward/record.url?scp=0025728287&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0025728287&partnerID=8YFLogxK
U2 - 10.1016/0090-8258(91)90246-2
DO - 10.1016/0090-8258(91)90246-2
M3 - Article
C2 - 2026352
AN - SCOPUS:0025728287
VL - 41
SP - 1
EP - 16
JO - Gynecologic Oncology
JF - Gynecologic Oncology
SN - 0090-8258
IS - 1
ER -