Cancer uterine

Central to epidemiology is the use of rates to express the health experience of populations. Rates arc important because epidemiology is inherently a comparative discipline. An epidemiologist is constantly attempting to compare the disease experience of a study population with that of a comparison population, A rate is nothing more than a specialized proportion in which the counts of people with a particular disease are placed over a denominator that is composed of people who are at risk, i,e, who have a chance of dcr cloping the disease. Men, for example, would not be included in the denominator used to calculate the prevalence or incidence of uterine cancer,... 

EM-800 (SCH-57050) and its active metabolite EM-652 (acolbifene, SCH-57068), are highly potent antiestrogens in human breast and uterine cancer cells in vitro as well as in vivo in nude mice and are currently undergoing clinical trials in the treatment of hormone-dependent breast cancer and endometrial cancer (Labrie et al 1999). Acolbifene shows a higher capacity of binding to... 

Because estrogen monotherapy increases the risk of uterine cancer, a gestagen needs to be given concurrently (except after hysterectomy), as e.g in an oral contraceptive preparation (p. 256). 

Secondary amenorrhea/abnormal uterine bleeding - For secondary amenorrhea and for abnormal uterine bleeding due to hormonal imbalance in the absence of organic pathology, such as fibroids or uterine cancer. 

Antiprogestins, such as RU-486 (lift-hydroxy-11/3 (4 dimethylamino phenyl-1 )-17ry-(prop-l-ynyl)-estra-4.9-diene-3-one) (33) and ZK98299 1 l/J-(4-dimethylaminophenyl)-17a-hydroxy-17/j-(3-hydroxypropyl-13a-methyl-4,9-gonadien-3-one) represent a new class of drags for fertility regulation. Also, these drugs have potential applications in the treatment of uterine cancer. 

Ferguson SE, Olshen AB, Viale A, Awtrey CS, Barakat RR, Boyd J. Gene expression profiling of tamoxifen-associated uterine cancers evidence for two molecular classes of endometrial carcinoma. Gynecol Oncol 2004 92 719-25. 

Sexton E, Van Themsche C, LeBlanc K, Parent S, Lemoine P, Asselin E. 2006. Resveratrol interferes with AKT activity and triggers apoptosis in human uterine cancer cells. Mol Cancer 5 45-58. 

Carcinoma. Estrogen has been used to treat metastatic breast cancer in men and postmenopausal women. Advanced prostate cancer in men may also respond to estrogen treatment. Progesterone is helpful in treating uterine cancer and several other types of metastases, such as breast, renal, and endometrial carcinoma. 

As indicated, raloxifene may also reduce the incidence of breast and uterine cancers.20,57 This drug may cause several bothersome side effects, including hot flashes, joint or muscle pain, depression, insomnia, and gastrointestinal disturbances. More serious problems with raloxifene may be indicated by symptoms... 

Estrogen receptor blockers (fulvestrant, tamoxifen) can likewise help prevent and treat breast and uterine cancers that are stimulated by estrogen.37 Fulvestrant (Faslodex) is classified as a pure antiestrogen... 

Human menopausal gonadotropin, uFSH or rFSH should be administered only by a physician experienced in treating infertility. Before treatment of women, a thorough gynecologic evaluation must be performed to rule out uterine, tubal, or ovarian diseases as well as pregnancy. In cases of irregular bleeding, uterine cancer should be ruled out. 

Rhenium tricarbonyl complexes containing substituted cyclopentadi-enyl and bis diphenylphosphine ligands also were investigated as anticancer agents. The antiproliferative effects on breast cancer of complex A shown in Fig. 23 were examined relative to the known active metabolite, 4-hydroxy tamoxifen, and found to have a similar effect [107]. The cytotoxicity of five rhenium tricarbonyl bis-diphenylphosphine complexes B shown in Fig. 23 was examined for 18 different human cancer cell lines. The tests showed that all the complexes were active against specific tumor cell lines, especially a line of breast and uterine cancer [108]. 

Although estrogen replacement therapy at menopause can prevent bone loss and cardiovascular disease, there is evidence that estrogens are associated with an increased risk of breast cancer as well as endometrial cancer(Gambrell, 1994), which thus seriously limits the use of estrogen replacement therapy. The ideal compound for women s health should be one able to decrease the risk of the most important causes of morbidity and mortality in women, namely breast cancer, uterine cancer, osteoporosis, bone fractures, and cardiovascular disease. Heart disease is, in fact, the leading cause of death in postmenopausal women (Lerner and Kannel, 1986). This ideal compound should also have an excellent safety profile to ensure compliance over 20 to 40 years of a woman s life. 

Despite the well-known beneficial effects of estrogen therapy on menopausal symptoms (Grady et al., 1992 Greendale and Judd, 1993 Lomax and Schonbaum, 1993) and their role in reducing bone loss and coronary heart disease (Barrett-Connor and Bush, 1991 Field et al., 1993 Harris et al., 1991 Lindsay, 1993 Lobo, 1991 Stampfer et al., 1991), compliance is low. Women decide not to take estrogens or stop treatment early because of the fear of breast and uterine cancer (Grady et al., 1992) and of symptoms associated with their therapy, namely, uterine bleeding, breast tenderness, and fluid retention. 

When the reporter gene was controlled by an AP-1 instead of an ERE element, E2, DES (diethylstilbestrol), tamoxifen, and raloxifene as well as ICI 164,384 all stimulated transcription with ERa. When ER(3 was transfected instead of ERa, E2 and DES had an inhibitory effect, whereas the three antiestrogens exerted a stimulatory effect (Fig. 6). Most interestingly, E2 could reverse the stimulatory effect of raloxifene mediated by ER(3 and the AP-1 element in a dose-dependent manner. Although these experiments were performed in HeLa cells, it is relevant to mention that in human breast cancer MCF-7 and uterine cancer Ishikawa cells (Paech et al., 1997), ER 3 acting at an AP-1 element led to the same observations, namely stimulation by antiestrogens and inhibi-... 

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