Uterine cancer
Screening and Etiology
Cancer of the uterine corpus is the most common gynecologic malignancy. Approximately 36,000 women per year develop uterine cancer in the United States, making it the fourth most common cancer in women. Unopposed estrogen use results in a fourfold increase in adenocarcinoma of the endometrium. Fortunately, the use of progestins has decreased this risk by approximately 50%.
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The incidence of endometrial cancer in the United States is approximately 0.7 per 1,000 women. Screening and autopsy studies suggest that there may be many occult, undiagnosed endometrial cancers because they are asymptomatic.
Endometrial adenocarcinoma occurs during both the reproductive and the menopausal years. The median age of onset is 61 years; the largest number of affected patients are between the ages of 50 and 59 years. Almost one fourth of all adenocarcinomas of the endometrium are diagnosed before menopause.
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Multiple factors have been associated with adenocarcinoma of the endometrium. The use of combination oral contraceptives decreases the risk of endometrial cancer. Women who use oral contraceptives have a 0.5 risk ratio (relative risk) of developing endometrial cancer compared with those who have never used oral contraceptives. This protection occurs with as little as 12 months of use, and protection continues for at least 10 years. The use of oral contraceptives is believed to prevent about 2,000 cases of endometrial cancer each year.
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Two distinct phenotypes are associated with the onset of endometrial cancer. The first is women with late-onset menopause who are obese and nulliparous. If all three factors are present, the risk for developing endometrial cancer is increased by about fivefold. Such patients tend to have well-differentiated, superficially invasive cancer for which simple hysterectomy and bilateral salpingo-oophorectomy are therapeutic, with a long-term survival rate of 95% or greater. Several studies have suggested that of these women who develop endometrial cancer, those who were taking estrogen therapy have just as good, if not longer, survival rates as those who were not taking estrogen therapy.
A second phenotype is characterized as nonestrogenic. These women tend to be multiparous, thin, and African American, and they usually have histologically poorly differentiated, deeply invasive lesions that may have an extrauterine extent. The prognosis of these women is considerably worse and may account for decreased survival rates in African-American women compared with the rates for white women.
There is growing concern that the increased use of tamoxifen for therapeutic and prophylactic indications in breast cancer may lead to an increased number of endometrial cancers. Tamoxifen is an antiestrogen that competes with estrogen at the receptor site. Other modes of action such as growth factors could be just as important or more so than its competitive action at the receptor site. It appears that specific end organs in the genital tract may respond to tamoxifen in an entirely different manner than do the breasts. In the premenopausal patient, serum estradiol levels can be much higher than estradiol’s peak level during the menstrual cycle, yet atrophic changes in the vagina and uterus are present. In postmenopausal women, it appears that tamoxifen produces a stimulatory effect on the uterus, yet atrophic changes in the vagina are noted and significant vasomotor symptoms are present.
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All of the prospective, randomized studies that identified endometrial cancers in breast cancer patients receiving tamoxifen therapy were designed to evaluate the efficacy of the drug in breast cancer, but did not examine the safety issues of the drug. Patients taking tamoxifen therapy develop uterine bleeding and have other gynecologic symptoms to a greater degree than those not taking tamoxifen. Prospective, randomized studies comparing the number of endometrial cancers in the tamoxifen group with the number in the no-tamoxifen group suggest, but do not positively identify, a relationship between tamoxifen and this cancer. To date, 15 studies have compared tamoxifen either with placebo or no drug in varying doses for different time intervals with nonuniform median follow-up times. Of these studies, 12 noted no difference in the number of endometrial cancers between the tamoxifen and the no-tamoxifen groups, one noted a significantly decreased incidence of endometrial cancer in the tamoxifen group, and two noted an increased number of corpus cancers in the tamoxifen group.
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