Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0476089 (endometrial cancer)
 11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The menopause is centered on the ovary and its in-built obsolescence. The events of the menopause start when the active ovary begins to fail and end when the ovary lapses into inactivity. The duration of these events is variable. Stimulated by the pituitary, 1 follicle develops each month as a hormone-producing organ. The life span of the follicle is then 28 days. Follicles continue to develop unt il none respond to the stimulus of the pituitary. The 32-week fetus has about 7 million primordial follicles. At birth, the number has dropped to 2 million. By puberty only 300,000 3008000 remain. During adult life about 400 follicles will have provided the ova and the hormones. The last few capable of funtion may have poor endocrine function. Ovarian activity is controlled by a "biological clock" in the hypothalamus. This controls the pituitary by a gonadotropin-releasing h ormone. In response the pituitary secretes follicle stimulating hormone (FSH) and luteinizing hormone (LH). The creation of the corpus luteum follows in the ovary and secretes progesterone while estrogen secretion continues. A cyclic drop in pituitary gonadotropin secretions causes the corpus luteum to degenerate. The ovary makes estrogen from cholesterol, converting it to pregnenolone, then to progesterone which is androstenedione to andnostenedione and on to estradiol. Estradiol is the estrogen secreted by the ovary, but it can be changed in the liver t o estrone and estriol. The pathways of the steroid hormone synthesis are the same in the adrenal cortex. When estrogen deficiency occurs in the menopause LH levels increase. Later the FSH is raised and remains high for the rest of life. This raised FSH and low estrogen levels appear to cause the characteristic hot flashes. Abrupt deprivation of estrogen causes more symptoms than a slow decline of function. Estrogen therapy may relieve these symptoms. Prevalence of coronary thrombosis rises sharply in the postmenopausal years. Estrogen-containing pills increase the incidence of venous thrombosis. Estrogen therapy reverses the atrophy of the genital tract. Cycles of treatment imitate the normal action of the functioning ovary but usually are not large enough to promote menstruation. Endometrial cancer appears to be increased by estrogen therapy. It may be that the addition of progesterone would protect against this from of cancer. The adjustment of tissues to an altered hormonal environment and the unrelated changes of aging make complicated problem.
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PMID:The menopause: the events of the menopause. 95 89

Of eight young women, seven had a diagnosis of well-differentiated endometrial adenocarcinoma and one had atypical endometrial hyperplasia. The average age was 40.1 years, with 6.04 years of dimethisterone-ethinyl estradiol (Oracon) sequential contraceptive use. The patients were not typical of those in whom endometrial carcinoma develops. Although these cases do not prove that long-term administration of dimethisterone-ethinyl estradiol causes endometrial adenocarcinoma or atypia, they indicate that it may do so.
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PMID:Severe atypical endometrial changes and sequential contraceptive use. 98 89

In our previous paper, it was reported that in human endometrium the step of formation of nuclear receptor-estradiol complex was not temperature-dependent but in rat uteri it was temperature-dependent. In order to clarify whether this temperature dependency in rat uteri means an energy requirement for this step or not, experiments with 2,4-dinitrophenol as an energy uncoupler were done. Even when rat uteri or endometrium of women were incubated with 10 mcc of tritiated-estradiol and 10 (-4) M of 2,4-dinitrophenol, 8S estrogen receptor-estradiol-17beta (E2) complex in cytosol and 5S estrogen receptor-E2 complex in nuclear extract were recognized in both rat and woman. Namely, no evidence was recognized for this step to require activation energy in rat uterus as well as in human endometrium. The cytosol fraction was prepared after human endometrium had been incubated with tritiated-E2 at 2 degrees C. Cytosol was analyzed on sucrose density gradient after heat treatment (at 10 degrees C, 31 degrees C, or 37 degrees C). At 31 degrees C and 37 degrees C treatment, the 8S receptor peak was difficulty recognized. Namely, the 8S receptor-E2 complex was heat labile in cell free condition. This appears to be 1 of the reasons why 8S cytosol receptor was not visible in human endometrium incubated with teritiated-E2 at 37 degrees C. When the cytosol fraction from the human endometrium was analyzed on 3-20% linear sucrose gradient containing .4 M KC1, the peak 8S diminished and about 4S peak appeared. This was considered to mean that 8S receptor in human endometrium was also split to a 4S binding unit at high salt condition and the 8S receptor in humans had also a subunit structure. 8S receptor in cytosol and 5S receptor in nuclear fraction were recognized in 1 case of human endometrial carcinoma, but in another case both receptors were not recognized. Estrogen binding protein in human serum was sedimented at 6S fraction by sucrose gradient.
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PMID:[Estrogen receptor in human endometrium--energy requirement, stability and subunit structure-- (author's transl)]. 103 70

Existing data indicate that high levels of endogenous estrogens, in particular estrone, predispose to endometrial cancer. Estrogen preparations came into use in the 1930s, and evidence has been accumulating to incriminate them also in cases of endometrial cancer. A recent rise in the incidence of endometrial cancer has followed wider use of these hormones. The risk among postmenopausal estrogen users has been estimated to be 4-8 times the 1/1000/year of postmenopausal nonusers. If estrogens are prescribed to menopausal and postmenopausal patients, such patients should be monitored for the development of endometrial carcinoma. Whether they should be given estrogens at all is still controversial.
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PMID:Editorial: Risks and benefits of estrogen use. 118 93

Research and development in contraception has only limited interest in women over 35 years old, so we know little about safety, side effects, and effectiveness of contraceptives in this age group. In addition, clinical trials use healthy women which further limits our knowledge about contraceptives in women who have cardiovascular problems, diabetes, and liver conditions. Research does indicate, however, that women with high blood pressure should not take oral contraceptives (OCs) after the age of 35. It also shows that healthy and nonobese women over 35 who do not smoke and have no family history of cardiovascular disease before age 45 can take OCs with 30 mcg of ethinyl estradiol. Practitioners should provide these women with balanced and up-to-date information on the link between OCs and breast cancer and their apparent protective effect against endometrial cancer. The pregnancy rate for 35-39 year old married women using the diaphragm for at least 5 months stands at 1.1/100 women years. Contrary to popular belief, barrier methods can be harmful, e.g., urinary tract infections are more frequent in women who use the diaphragm than in those who do not. Women older than 35 should consider the condom because of its ability to reduce the risk of acquiring HIV or sexually transmitted diseases. Considerable research exists on women over 35 who use copper releasing IUDs. These IUDs are safe in women who do not have heavy menstrual bleeding. The levonorgestrel releasing IUDs are well tolerated in women over 35 since they reduce the amount and duration of menstrual bleeding. Besides users of these IUDs are less likely to have pelvic inflammatory disease and endometritis than those using copper releasing IUDs. Older women in developing countries often undergo hysterectomy for contraceptive purposes and because of heavy bleeding. Tubal ligation is a significant family planning method for older women in developing countries.
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PMID:Contraception after thirty-five. 131 37

Sexual activity is quite common among women aged 14 to 20 in developed countries, averaging perhaps 10% at age 15 to about 70% at 19. Thus, the need for contraception may begin quite early in life and will continue for as long as 30 years. One of the best candidates for long-term contraception for young sexually active females is the oral contraceptive (OC), which provides health benefits besides contraception. Long-term benefits include lowered rates of ovarian and endometrial cancer, as well as of benign breast disease and ovarian cysts. Another benefit is protection against upper-tract sequelae of sexually transmitted diseases. Short-term benefits are correction of menstrual irregularity, reduction in menstrual flow, and diminished premenstrual syndrome and dysmenorrhea. Recent OC formulations contain only one-third the estrogenic potency of older OCs and therefore are associated with dramatic decreases in what were always the major side effects of OCs: heart attack, stroke, and pulmonary embolism. Other side effects of OCs have been most closely associated with the progestogenic component, and are related to the androgenic effects of progestins, particularly some synthetic progestins. However, some new synthetic progestins have been found to have minimal androgen receptor activity in preclinical testing and to cause minimal or no androgen-related side effects in clinical trials. One of these new progestins having a favorable androgenic profile is norgestimate. Its efficacy and safety in combination with low doses of ethinyl estradiol have been documented in the European and the American literature.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The androgenicity of oral contraceptives: the young patient's concerns. 136 88

The effectiveness of monophasic and multiphasic oral contraceptives (OCs) depends on their ability to suppress ovulation, change endometrial growth and ovum receptivity, and reduce cervical mucus receptivity to sperm. They are all more than 99% effective, but, depending on the type and dose of hormone components, they have different side effects. The estrogen component (ethinyl estradiol) of most new OCs is between 30 and 35 mcg, which reduces the risk of estrogen side effects, especially thromboembolism and hypertension. The Food and Drug Administration does not recommend use of an OC with an estrogen component for lactating mothers, while the American College of Obstetrics and Gynecology and the American Academy of Pediatrics believe it is fine. Estrogen may protect against coronary artery disease, yet the estrogen component of today's OCs is so low that the progestin component may cancels this beneficial effect. It also prevents breakthrough bleeding. The most frequently used progestins in OCs are norethindrone and norgestrel. They prevent ovum implantation, sperm penetration through the cervical mucus, and ovulation. Progestins, especially norgestrel, increase the risk of coronary artery disease. Other side effects include acne and weight gain. Progestin benefits are reduced menstrual blood loss, pain during menstruation, premenstrual tension, and endometrial cancer risk. The ideal estrogen-progestin balance depends on the individual, but the estrogen component should be between 30 and 35 mcg, and the progestin component should be the lowest possible dose to reduce metabolic side effects. If an OC user with a well stabilized cycle who takes another recently prescribed drug experiences unexpected breakthrough bleeding or spotting, this change may indicate a drug interaction. Absolute and/or possible contraindications of OC use are smoking after age 35, history of breast or endometrial cancer, liver disease or impaired liver function, cardiovascular risk factors, and diabetes mellitus.
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PMID:Benefits and risks of oral contraceptive use. 143 13

Uterine papillary serous carcinoma (UPSC) is an aggressive malignancy that accounts for a disproportionate number of intraabdominal failures among endometrial carcinoma patients. The histologic appearance and tendency toward intraabdominal spread resemble those of papillary serous adenocarcinoma of the ovary. Because approximately 70% of untreated ovarian carcinoma patients respond to platinum-based chemotherapy, it has been suggested that UPSC patients might respond to similar treatment regimens. Twenty patients with UPSC were treated with cisplatin, doxorubicin (Adriamycin), cyclophosphamide (PAC) chemotherapy between January 1982 and December 1989. They included 9 patients with advanced primary disease, 5 with recurrence, and 6 who received PAC as adjuvant therapy. Patients received a mean of five cycles of PAC. Only 2 of 11 patients with measurable disease greater than 2 cm achieved complete clinical responses of 12 and 31 months duration; there were no partial responses. Actuarial 5-year survival for all patients was 23%. The mean progression-free interval was 9 months. Patients with clinical stages I or II disease had a higher survival rate than those with stage III or IV disease (P = 0.003). Survival did not correlate with depth of myometrial invasion (P = 0.81) or size of residual tumor following initial surgery (P = 0.16). Estrogen or progesterone receptors were detected in 10 of 11 tumors tested. Seven of 9 patients tested had elevated serum levels of CA-125 (greater than 35 U/ml). Correlation between CA-125 value and clinical course was demonstrated in 3 of 5 patients who had serial measurements. Of all patients, 3 are currently alive; 1 has documented disease. Moderate to severe toxicity was seen in 14 patients (70%). There was one possible treatment-related death from cardiomyopathy. UPSC, despite its histologic and clinical similarities to ovarian carcinoma, was relatively resistant to PAC chemotherapy in this mixed group of patients.
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PMID:Uterine papillary serous carcinoma (UPSC) treated with cisplatin, doxorubicin, and cyclophosphamide (PAC). 152 8

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

To prevent hyperplasia and carcinoma of the endometrium during Estrogen Replacement Therapy (ERT), addition of progestogens once a month is considered mandatory. There is, however, no good scientific basis for this assumption. Since the addition of progestogens has several disadvantages, it is important to minimise the frequency of progestogen addition. Vaginosonography is a rather new technique, which has not yet been used for monitoring ERT. This study uses the growth of the endometrium, as it was measured by vaginosonography, as a parameter for stimulation of the endometrium by estrogens. ERT with Estraderm 50 twice a week was started in postmenopausal women. The endometrial thickness at the beginning was less than 3 millimeters. During estrogen treatment the endometrial thickness was determined every 6 to 10 weeks. As long as there was little or no increase during the estrogen treatment, no progestogen was added. Where there was a considerable growth, progestogen was added. With the use of vaginosonography, it is possible, to distinguish "fast growers" (women whose endometrium responded fast) from "slow growers".
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PMID:[Endometrial growth in continuous, estrogen substitution monotherapy with Estraderm TTS (0.05 mg/die) in 31 postmenopausal females]. 163 98


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