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

The relatively restricted use of hormone replacement therapy in the United Kingdom has frequently been noted. It is possible that low prescribing rates may, in part, be due to the difficulty in interpreting the wealth of research evidence relating to the risks and benefits of hormone replacement therapy. Conflicting conclusions from research can cause considerable uncertainty and confusion. This paper reviews the evidence relating to hormone replacement therapy and the risks of breast cancer, endometrial cancer and cardiovascular disease and discusses the issues which require critical assessment. This should add to the information base available to general practitioners and thus assist in decision-making in the context of uncertainty.
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PMID:Hormone replacement therapy and breast cancer, endometrial cancer and cardiovascular disease: risks and benefits. 149 29

RU-486 or mifepristone is best known as an antiprogestin and an abortifacient, but it has broad medical applicability. The drug is also a potent blocker of corticosteroid receptors, and it has shown promise in the treatment of breast cancer, inoperable meningioma, and cushing's disease. Cushing's is a model for the symptomatology of aging which may involve enhanced response to corticosteroid. RU-486 has reversed the osteoporosis, thinning of skin, muscle atrophy, obesity, adult onset diabetes, depression, hypertension, and immunosuppression associated with this disease. RU-486 may be of value in aiding cervical dilation, lactation, and the treatment of endometriosis. In addition, breast, bowel, kidney tumors, hepatomas, endometrial cancer, and fibrosarcomas can show corticosteroid dependency, suggesting that RU-486 may have clinical value against inoperable tumors. In a preliminary 1987 phase I study, in estrogen-positive, chemotherapy-refractory breast cancer patients in Montpelier, France, Ru-486 produced objective tumor regression (6 of 22) that was prolonged (3 months) in 4 patients. Clinical relief of bone pain was observed in 7 of 23 patients with a decline in carcinoembryonic antigen (CEA) tumor makers in 8 patients. Growing in vitro data also show that RU-486 can directly inhibit breast cancer cell proliferation. RU-486 has application for HIV infection, based on data that there is a serum factor in AIDS patients that enhances corticosteroid lympholysis. IN addition, the immune restorative action of RU-486 suggests that it could counteract the immunosuppression seen in aging, in cancer, or in viral or stress-related disease, which has recently focused clinical attention on its potential in the treatment of senile dementia and depression. Scientific conferences and workshops are needed to alert scientists, physicians, and the public to the potential medical benefits of this drug.
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PMID:RU 486: how abortion politics have impacted on a potentially useful drug of broad medical application. 150 96

The use of estrogens is the single therapy that has been found consistently to prevent bone loss and fractures in postmenopausal women. Traditional osteoporotic risk factors should be used to select women for bone densitometry. The numeric result provided by densitometry, combined with age-based comparisons, is extremely useful in convincing reluctant women to be treated. The few studies that have been done in geriatric women show that estrogen therapy continues to be effective in reducing bone loss, but the absolute benefit is less than in perimenopausal women. The effects of estrogen therapy extend beyond osteoporosis. A consensus of epidemiologic reports has shown that women who comply with postmenopausal estrogen therapy have a 30% to 50% reduction in the risk of coronary artery disease. Given the frequency of these two conditions, widespread use of estrogen as a national health care policy would be appropriate if it were not for the evidence that estrogens may increase the risk of breast cancer and endometrial cancer. Given these lingering cancer fears, recent calls for a randomized national women's health study of postmenopausal estrogen therapy should be heeded.
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PMID:Estrogen therapy for geriatric osteoporosis: just one ball in a complex juggling act. 150 6

Marked changes in both growth factor and proto-oncogene expression occur due to treatment of hormonally-responsive human cancers with progestins and antiestrogens. In human endometrial cancer cell lines the antiproliferative effects of progestins and antiestrogens in a particular cell line appear to be associated with similar effects on growth factor and/or proto-oncogene expression. This suggests that although these compounds initially interact with different steroid hormone receptors, the molecular mechanisms of their growth inhibition may be essentially similar. In the case of human breast cancer cell lines, however, the effects of progestins and antiestrogens on gene regulation are often different, suggesting that the molecular mechanisms of progestin and antiestrogen growth inhibition may be essentially dissimilar.
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PMID:Mechanisms of growth inhibition by antiestrogens and progestins in human breast and endometrial cancer cells. 152 52

In some families breast cancer aggregates as the predominant site-specific neoplasia and in others in association with defined malignancies. In the case of familial adenocarcinomatous (Lynch II-syndrome) it occurs together mainly with colorectal and endometrial carcinoma whereas in the case of the Li-Fraumeni/SBLA-syndrome it belongs to a wider spectrum including sarcoma, brain tumors, lung and laryngeal cancer, leukaemia and adrenocortical carcinoma. The occurrence of these malignancies is reported as they were observed in the families of 600 women suffering from breast cancer.
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PMID:[Tumor diseases in families of 600 breast cancer patients with special reference to familial adenocarcinomatosis and the Li-Fraumeni-/SBLA syndrome]. 152 35

Current epidemiologic data from research on the association between combined oral contraceptives (OCs) and breast cancer show that longterm OC use does not significantly increase the risk of developing breast cancer after age 45, but may indeed protect against postmenopausal breast cancer. Yet, older studies with high dose OCs demonstrate a somewhat increased risk (relative risk = 1.5) for young women who have used OCs early and for at least 4 years. Nevertheless, the lack of association even holds true for women with a family history of breast cancer or for those who have benign breast disease. Studies should continue, however, since the OC user cohort is aging and to increase the statistical power of current studies. Standard hormonal replacement therapy consists of a progestin and estrogen. Addition of progestin prevents the risk of endometrial cancer. Some research indicates that it may also protect against breast cancer. However, research from Uppsala, Sweden, suggests that combined estrogen-progestin treatment slightly, but not significantly, increases the breast cancer risk. Further research and longer duration of hormonal replacement therapy should provide clinicians with more information about the breast cancer risk. Individual physicians should inform their patients about concerns raised by the research about hormones and breast cancer, but should be optimistic since the possible risk has not been proven. Some medical associations have already developed guidelines for physicians and included them into continuing medical education programs.
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PMID:The risk of breast cancer associated with oral contraception and hormone replacement therapy. 153 27

Except for the control of smoking, hormone replacement therapy (HRT) is potentially one of the most useful means of preventing major causes of morbidity and mortality in older women, who are likely to spend more than one-third of their lives in a postmenopausal (estrogen-deficient) stage. A full assessment of the overall long-term effects of noncontraceptive estrogens--with and without cyclically added progestins--therefore is needed urgently. This paper briefly reviews the available epidemiologic findings to date, with emphasis on a prospective study in Uppsala, Sweden. An increase in the risk of endometrial cancer which is substantially dependent on dose and duration of the exposure has been established, whereas a biologically plausible protective effect of progestins has been documented in only a few studies. A moderate, perhaps twofold, increase in the incidence of breast cancer has been found in several recent studies, notably among long-term and/or current users of potent estrogens; there is no evidence that progestins counteract this adverse effect. The risk of osteoporotic hip fractures can be reduced substantially, at least during ongoing, treatment starting early after menopause. A 25 to 50 percent reduction in cardiovascular morbidity and mortality has been shown consistently and might outweigh any conceivable adverse effect of HRT. Notwithstanding these largely encouraging epidemiologic data--including evidence of lower all-cause mortality in users than in nonusers of HRT--it is argued here that randomized control trials are needed to provide the necessary basis for widespread preventive use of HRT.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term consequences of estrogen and estrogen-progestin replacement. 153 19

While antiestrogens are useful agents in the treatment of breast cancer, the usefulness of these agents in the treatment of endometrial cancer remains controversial. There is some concern that the currently available antiestrogens may have partial agonist activity in uterine tissue. To better understand the mechanisms by which estrogens and antiestrogens modulate growth of endometrial adenocarcinoma cells, we have compared the effects of 17-beta estradiol and three antiestrogens, 4-hydroxytamoxifen (OH-TAM), ICI 164384, and LY 117018 on proliferation and transforming growth factor (TGF) mRNA accumulation in two human endometrial adenocarcinoma cell lines. In HEC-50 cells, neither estradiol nor anti-estrogens had any effect on cell proliferation or TGF mRNA abundance under estrogen-depleted culture conditions [basal medium containing 1% twice charcoal-treated fetal bovine serum (ctFBS)] or in the presence of estrogen (basal medium containing 5% fetal bovine serum). At very high concentrations, both estradiol and OH-TAM caused a small decrease in HEC-50 cell proliferation in medium containing 5% serum. In contrast, the antiestrogens had different effects on Ishikawa cells, depending upon the culture conditions. In medium containing 5% fetal bovine serum, the antiestrogens inhibited cell proliferation and significantly decreased TGF-alpha mRNA abundance and TGF-alpha secretion. OH-TAM was more potent than the other antiestrogens. Under these culture conditions, estradiol had no effect on cell proliferation or TGF-alpha mRNA levels but increased TGF-alpha secretion. In medium supplemented with 1% ctFBS, estradiol increased cell proliferation and TGF-alpha mRNA (2.72-fold, P less than 0.005) and TGF-alpha secretion (700 +/- 156 versus 250 +/- 23 pg/10(6) cells/24 h, P less than 0.05), whereas OH-TAM, which also stimulated cell proliferation, reduced TGF-alpha mRNA abundance (P less than 0.05) but had no significant effect on TGF-alpha secretion. Under these conditions, ICI 164384 and LY 117018 had no effect on either cell proliferation or TGF-alpha expression. Estradiol treatment decreased, whereas OH-TAM increased, epidermal growth factor receptors in Ishikawa cells. Both estradiol and the antiestrogens decreased TGF-beta 1 mRNA abundance when cells were grown in media containing 1% ctFBS. In summary, the response of human endometrial adenocarcinoma cells to estrogen and antiestrogens varied between cell lines and was dependent upon the culture conditions used. In addition, OH-TAM, unlike the other two antiestrogens tested, had growth-stimulating effects on Ishikawa cells.
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PMID:Differential effects of estrogen and antiestrogen on transforming growth factor gene expression in endometrial adenocarcinoma cells. 155 Nov

Researchers applied published data on cancer incidence and age specific mortality to standard life table techniques to estimate the lifetime probability of developing reproductive cancer for women living in countries representative of 3 patters of risk of reproductive cancer and for long term oral contraceptives (OC) users under best case, worst case, and likely case assumptions. The reproductive cancers included breast, ovarian, endometrial, and cervical cancers. The data consisted of urban women from China, Japan, United States (California), England, Wales, Costa Rica, and Colombia. Under the likely case assumption, OCs just barely reduced or increased the lifetime probability of any reproductive cancer in any setting. Further, under the worst case scenario, OCs increased the lifetime probability or reproductive cancer moderately in countries with low cancer rates (Asian countries) and in countries with high rates of breast, ovarian, and endometrial cancer (Western Europe, North America, and Australia). Yet in countries with high cervical rates (South and Central America), OC use significantly affected the lifetime probability of reproductive cancer. The best case scenario revealed that OCs decreased lifetime probability of reproductive cancer in each country, especially those countries where endometrial and ovarian cancer incidences were great. The analysis also showed that OC use has the greatest effect on lifetime probability of reproductive cancer, be it positive or negative, in countries with high underlying rates of reproductive cancer. Further it demonstrated that the effect of OC use will most likely be small in countries with low incidence of reproductive cancers. Overall the researchers felt reassured about OC use and reproductive cancer. Even though long term OC use increases the risk of breast cancer in young ages.
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PMID:Worldwide variations in the lifetime probability of reproductive cancer in women: implications of best-case, worst-case, and likely-case assumptions about the effect of oral contraceptive use. 155 40

The present study investigated comparatively the relation between host age and age-specific incidence rate (ASIR) of breast cancer in the United Kingdom and Japan. Comparison was also made between breast cancer and 5 non-mammary neoplasias as regards the cancer incidence/age profile. The results obtained are as follows: 1) the ASIR profile of breast cancer in the age range of 22.5 years to 47.5 years was characterized by a rapid rise versus age which was common between the United Kingdom and Japan. By use of the log-log plot, the growth of breast cancer risk was found to be quasi-exponential, and the above time range was termed the stage of exponential growth. 2) From 47.5 years of age on, the stage of stagnation ensued: the ASIR for the United Kingdom kept on rising with a much reduced inclination, whereas that for Japan followed the way of gradual decline. In the log-log plot, the junction between the 2 stages was recognized as a distinct break point. 3) A similar two-stage structure was found in the ASIR profiles of cancers of the stomach, lung, cervix uteri, and corpus uteri. The break points for the first 2 neoplasias were located at senescent ages, and those for cervical cancer and endometrial cancer were located at the pre- and peri-menopausal ages respectively (27.5-32.5 and 52.5 years). The profile of lymphoid leukemia gave 2 distinct surges at the ages of infancy and senescence, regardless of the country. The significance of the break point in the ASIR profile of breast cancer was discussed in relation to the two-step carcinogenesis theory.
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PMID:The genesis of breast cancer is a two-step phenomenon. I. Differential effects of aging on the cancer incidence in the United Kingdom and Japan. 156 61


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