Abstract
B85
Purpose >Endometrial carcinoma is the most common cancer of the lower female genital tract in the United States. Its incidence is growing in the US and worldwide. Hormonal levels, production and balance have been implicated as risk factors. Little information is available on second primary cancers (SPC) in endometrial cancer patients. The study of SPC may help understanding the role of hormones and other risk factors in the etiology of endometrial cancer. >Design/Methods >Using the National Cancer Institute’s Surveillance, Epidemiology, and End Results data, the risk of second primary cancer in endometrial cancer cases was compared with that of the general population of women and with women with other primary cancers. Data were analyzed according to three age groups roughly corresponding to menopausal status: ≤44 years, 45-54 years, ≥55 years. We included 9585 women who had a first diagnosis of endometrial cancer between 1973 and 2002 and who developed a SPC at least 1 month subsequent to their cancer diagnosis. >Results >The lifetime risk of SPC in endometrial cancer patients was higher in premenopausal women (age < 44 years) than in the general population of women of the same age (standardized incidence ratio SIR =1.19, 95% CI =1.07 - 1.33). The majority of the increase could be attributed to malignancies of the digestive system, including colon, cecum, rectum, and biliary cancers. When compared to the women in the same age groups with other primary cancers, the risk of digestive system cancers was in excess in premenopausal (standardized incidence ratio SIR =11.69, 95% CI =11.66 - 11.73 ) and perimenopausal groups(standardized incidence ratio SIR =5.79, 95% CI =5.7 - 5.8 ), but not in postmenopausal. We evaluated the median age at the diagnosis of the first primary cancers and SPC between women whose primary cancers were endometrial and those whose primaries were not endometrial, and we found no significant differences. >Conclusions >Premenopausal and perimenopausal patients with endometrial cancer develop an excess SPC compared with the general population and in comparison with females with other cancers. Chemo and/or local radiotherapy could be responsible for the excess of digestive tract SPC. Hereditary mutations in non-polyposis colorectal cancer genes, which are implicated in the development of early endometrial and early colorectal cancers, could also play a role in this excess risk. Prevention and early detection of SPC is especially important in younger women who would like to preserve their fertility. More studies are needed to investigate modifiable risk factors for endometrial cancer and determine whether preventive measures for endometrial cancer such as exercise and weight loss can also prevent SPC.
Sixth AACR International Conference on Frontiers in Cancer Prevention Research-- Dec 5-8, 2007; Philadelphia, PA