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Query: UMLS:C0476089 (endometrial cancer)
 11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Many studies show that the risk of a coronary event is reduced by about 50% in postmenopausal women using unopposed oral estrogen compared to women not taking oral estrogens. This protection is biologically plausible, and the magnitude of the benefit would be large if selection factors could be excluded. Studies also show an approximate 50% reduction in hip fracture after three or more years of hormone replacement. An increased risk of endometrial cancer approximately equals the number of years of unopposed estrogen use and continues after estrogen has been discontinued. Use of estrogen for more than five years may increase the risk of breast cancer by 50%, but more data are needed to exclude the effects of selection and diagnostic detection bias. Until clinical trial data are available on estrogen-progestin use, no universal recommendation for hormone replacement or type and duration of treatment can be made.
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PMID:Risks and benefits of replacement estrogen. 158 May 88

Tamoxifen is a nonsteroidal antiestrogen that has found successful applications for each stage of breast cancer in the treatment of selected patients. Tamoxifen was originally introduced for the treatment of advanced disease in postmenopausal women; however, the drug is now also available for the palliative treatment of premenopausal women with estrogen receptor (ER) positive disease. The proven efficacy of tamoxifen and the low incidence of side effects made the drug an ideal agent to test as an adjuvant therapy for women with node-positive breast cancer. Laboratory studies indicate that long-term treatment schedules may provide maximal benefit in preventing recurrence, and recent analysis of clinical trials demonstrates that between 2 and 5 years of adjuvant tamoxifen therapy provides a survival advantage for postmenopausal women with node-positive disease. Similarly, adjuvant studies in node-negative breast cancer have demonstrated an increase in the disease-free survival of both pre- and postmenopausal patients with ER-positive tumors. However, the extended use of tamoxifen has raised questions about the long-term safety of antiestrogen therapy. Of special concern is the impact of tamoxifen on ovarian function in premenopausal women and the potential risks to the fetus if pregnancy occurs. Fortunately, there are no reports about the teratogenicity of tamoxifen in the human, but it is important that physicians counsel women about the risk of pregnancy. Tamoxifen should not be used if a patient is pregnant. Initial concerns that the long-term administration of an antiestrogen would increase bone loss and increase the risks of coronary heart disease appear to be unwarranted. Tamoxifen has some estrogen-like activities in postmenopausal women and causes a preservation of bone in the lumbar spine and a decrease in circulating cholesterol. Indeed, a reduction in fatal myocardial infarction (MI) has been noted during 5 years of tamoxifen therapy, possibly the direct result of a prolonged reduction in circulating cholesterol. However, the estrogen-like qualities of tamoxifen that could be valuable as a hormone replacement therapy for all postmenopausal women following a diagnosis of breast cancer may also increase the risk for developing endometrial carcinoma. To date, there are only a few reports of endometrial carcinoma being diagnosed during adjuvant therapy with tamoxifen; however, any instances of uterine bleeding or spotting should be followed up with an endometrial biopsy. There are some concerns about large doses of tamoxifen promoting liver cancer in rats. These results are of particular concern if tamoxifen is to be used as a preventive in normal women.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The role of tamoxifen in the treatment and prevention of breast cancer. 158 40

Studies show that OCs have several benefits besides prevention of pregnancy. They protect against ovarian and endometrial cancer, pelvic inflammatory disease, and ectopic pregnancy. OCs also prevent iron deficiency anemia, primary dysmenorrhea, functional ovarian cysts, and benign breast disease. They may even protect against some benign uterine tumors, osteoporosis, toxic shock syndrome, and rheumatoid arthritis. Despite many concerns, some large studies have not identified an overall effect of OCs on breast cancer, but subgroup analyses showed increased risk in 30-34 year old women and in women with 1 child. A reanalysis of a large US study indicated an increase risk of breast cancer in nulliparous women with increasing use of OCs by young women. Cervical cancer is the leading cancer of women in developing countries which emphasizes the need to examine the link between OC use and cervical cancer. Several studies show an increased risk of cervical cancer. Several studies show an increased risk of cervical cancer in long term OC users. In 1 study, long term use meant 5 years. Yet these studies did not adequately address confounding factors such as smoking and sexual behavior. 3 case control studies in the US and the UK found an increased risk of liver cancer among OC users, yet a large case control study in developing countries did not find a link between OC use and liver cancer. Studies of high dose OCs found considerable increased risks of cardiovascular disease in OC users, but they did not take into account cigarette smoking which indeed increases the risk. Further health practitioners today do a more thorough job of identifying underlying medical problems before prescribing OCs. Moreover estrogen doses have fallen 10 fold since the original OCs. Finally, despite a transient delay, women who take OCs experience a return to fertility at the same rate as those who use other contraceptives.
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PMID:The safety of oral contraceptives: epidemiologic insights from the first 30 years. 160 84

In postmenopausal women estrogens alone are effective in reversing vasomotor symptoms and vaginal atrophy. They also prevent the bone loss associated with osteoporosis and reduce the risk of cardiovascular disease, probably through their beneficial effects on lipid metabolism. Unopposed long-term estrogen therapy, however, increases the risk of developing endometrial hyperplasia, endometrial cancer, and possibly breast cancer as well. The risk of developing endometrial cancer can be reduced by combining a progestin with the estrogen, by controlling obesity, and by rigorous clinical screening and surveillance. The effect of progestins on the risk of developing breast cancer is still controversial. Although some progestins may reverse the cardioprotective effect of estrogens, those with minimal androgenicity appear less likely to do so. Hormone replacement therapy that combines estrogen with a progestin of minimal androgenicity is thus a rational alternative to unopposed estrogen therapy. Current epidemiologic knowledge suggests that the benefits of hormone replacement therapy, with or without any progestins, strongly outweigh the risks.
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PMID:The benefits and risks of hormone replacement therapy: an epidemiologic overview. 160 89

Biomedical researchers have added cardiovascular disease (CVD) to the list of symptoms resulting from lowered estrogen levels and menopause. Thus health providers promote hormone replacement therapy (HRT) to prevent CVD. Yet most women tend to be healthy during the postmenopausal years which constitute at least 33% of their lives. The medical community has taken a natural event, menopause, and labeled it as a disease which causes other diseases. Science is basically patriarchal. Physicians use it to justify their privilege to define illness and treatment. They reduce organic processes into a narrow cause-effect relationship and ignore socioeconomic and political factors. An often ignored problem with the scientific community's view of CVD is that almost all cardiovascular intervention studies included only men as subjects except the prospective Framingham Study. Traditional risk factors of CVD in women are hypertension, cholesterol levels, cigarette smoking, diabetes, excess weight, oral contraceptives, and genetics. Various studies show a reduction in the age adjusted risk of CVD morbidity any mortality in women on estrogen replacement theory (ERT). Specifically, estrogen affects serum lipids in a positive direction. Yet the women in the studies are healthy, lean, and exercise regularly. Some studies reveal an increased risk of breast cancer and endometrial cancer in women on ERT. HRT consists of a combination of estrogen and progestin, but data do not confirm that it is as protective against CVD as ERT. HRT is postmenopausal women is an untested hormonal experiment. In 1986, the US National Institutes of Health wrote a policy to include women as subjects in research studies. It did not happen so in 1991 it established the Office of Women's Health Research. The US Congress has also taken up the issue. Nurse researchers should critique methods used by patriarchal science to study menopause. Nurses can inform postmenopausal women about their choices concerning HRt to prevent CVD.
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PMID:Cardiovascular disease in women and noncontraceptive use of hormones: a feminist analysis. 160 87

Menopause and hormone replacement therapy (HRT) continue to be controversial subjects. The main concern is the potential risk of prolonged HRT and the possible development of endometrial and breast carcinoma. There is no obvious evidence at present to suggest that HRT increases endometrial carcinoma provided the patient receives progestogen for a period of 10 or more days (usual period is 12 days) during each month. However the breast does not seem to enjoy this safety margin and there is some concern about possible increase in the incidence of breast cancer if the treatment period is longer than 5 years. The increase in the risk is higher after 15 years of estrogen use. There is no obvious adverse effect on the ovary or on the cervix following HRT.
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PMID:Sex steroids and cancer in older women. 160 52

Exogenous hormones are widely prescribed in the United States, primarily as oral contraceptives and hormone-replacement therapy. Each of these frequently used categories of drugs has important potential for altering risk of several major human cancers. The efficacy of oral contraceptives in preventing ovarian cancer and endometrial cancer is well established. There remains controversy about the relationship between oral-contraceptive use and breast cancer risk, but most studies show that use in the postmenarcheal and perimenopausal periods is associated with an increased risk of breast cancer in a duration-dependent manner. As with oral contraceptives, the relationship between estrogen-replacement therapy and breast cancer risk is controversial, but several well-designed studies showed a moderate increased risk after long-term use. Estrogen-replacement therapy is a major cause of endometrial cancer. Combination hormone-replacement therapy will probably reduce some of the excess risk of endometrial cancer, but few epidemiological data exist on this relationship. The sparse data suggest that combination therapy may enhance breast cancer risk. As with endometrial and ovarian cancers, hormonal chemoprevention of breast cancer is also feasible. We review two such strategies, ie, gonadotropin-releasing hormone agonists and the antiestrogenic drug tamoxifen.
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PMID:Relationship of hormone use to cancer risk. 161 98

Chronological trend of urinary steroid excretions in Japanese women was investigated during the period of June 1972 to August 1986 using healthy women of urban and rural origins, patients with breast cancer and patients with either cervical cancer or endometrial cancer. The excretions of 14 neutral steroids were estimated by gas liquid chromatography, and the obtained data were tentatively correlated with the epidemiological backgrounds. In the course of the chronological transition from the 1st stage (1972-1974) to the 2nd stage (1975-79), the urinary steroid pattern of Japanese women with and without cancer experienced a common change to produce specific deviations that were in agreement with the hormonal characteristics of a pill user or of an endometrial cancer patient. At the 3rd stage (1980-86), patients with either cervical cancer or endometrial cancer were distinguished from 1st stage controls by non-specific depression of all androgens, progestins and corticosteroids in urine. Throughout the whole period, both the risk for cervical cancer and the reproductive activity (birth rate) were found to decrease continuously in Japanese women. Evidence was presented to suggest that the above deterioration of the hormonal environment in Japanese women could be related to the stress of modern life rather than to defects in the diet. On the basis of the above findings, the 1st, 2nd and 3rd stages of our investigation were tentatively termed the pro-cervical cancer age, the pro-endometrial cancer age and the pro-hypogonadism age. The relation between the chronological change of urinary steroids and that of the epidemiological background was analyzed from the view point of population ecology.
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PMID:Interrelation between Western type cancers and non-Western type cancers as regards their risk variation in time and space. IV. Hormonal transition of Japanese women from the pro-cervical cancer age through the pro-endometrial cancer age to the pro-hypogonadism age. 162 26

Epidemiologic studies of breast, ovarian, and endometrial cancer and physiologic studies of epithelial tissues from which these cancers originate indicate that medical researchers can develop interventions to reduce women's risk of these 3 cancers. They already know that use of combined oral contraceptives considerably reduced the risk of endometrial and ovarian cancer. The key etiologic factors for endometrial and breast cancer are ovarian steroid hormones. Specifically, any estrogen not checked by progestogen stimulate cell division in the epithelial tissue of the endometrium thus increasing the risk of cancer. Yet estrogen and progestogen induces significantly more cell division in the epithelial tissue of the terminal duct lobular unit (from which many breast cancers originate) than does just estrogen. Ovulation damages the ovarian surface making it the leading etiologic factor for ovarian cancer. Medical researchers at the University of Southern California (USC) have designed a prototype contraceptive regimen which should prevent all 3 cancers. They re presently testing it in a clinical trial at USC. The prototype regimen consists of administration of the gonadotropin releasing hormone agonist (GnRHA) leuprolide acetate depot on day 1 of each 28-day cycle, 0.625 mg of oral conjugated equine estrogens (CEE) on Monday-Saturday (24 days) per each 28-day cycle, and 10 mg of oral medroxyprogesterone acetate (MCA) for 13 days every 4th cycle. The GnRHA reduces the risk of all 3 cancers. CEE prevents bone mineral loss, possible increase in cardiovascular disease risk, menopausal symptoms, and urogenital atrophy. MCA reverses endometrial hyperplasia and prevents increased risk of endometrial cancer. The predicted relative reduction in lifetime breast cancer risks over 5,10, and 15 years for the prototype regimen are 31%, 53%, and 70%, respectively. For endometrial cancer, they are 18%, 33%, and 45%, respectively. For ovarian cancer, they are 41%, 67%, and 84%. This regimen should also reduce the incidence or severity of hormonally mediated benign gynecologic disorders. Further research on such a regimen is needed.
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PMID:The prevention of breast cancer through reduced ovarian steroid exposure. 162 31

The occurrence of new primary tumours among postmenopausal patients with primary breast cancer subsequent to adjuvant treatment in Denmark was assessed by linkage to the cancer registry. Following primary surgery, patients in low risk of recurrence (n = 1,828) received no further treatment while patients in high risk randomly received either adjuvant radiotherapy alone (n = 846) or radiotherapy + tamoxifen 30 mg daily for 48 weeks (n = 864). With a median follow-up of 8 years, the incidence of tumours in the contralateral breast was similar among tamoxifen-treated, and non-treated high-risk patients even after adjusting for tumours arising within the first year. The standardized incidence ratio for endometrial cancer was 1.9 (95% confidence interval 0.8-3.9) among tamoxifen treated, the cumulative incidence 1% compared to 0.3% among non-treated patients (p = 0.11). The cumulative risk of non-lymphocytic leukaemia was 0.9% and 0.1% among irradiated and non-irradiated patients respectively (p = 0.4). Prolonged follow-up of tamoxifen-treated patients with regard to new tumours is recommended.
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PMID:Carcinogenic effects of adjuvant tamoxifen treatment and radiotherapy for early breast cancer. 162 43


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