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

Receptors for steroid hormones are necessary for hormonal action. All tissues which are targets for hormonal action contain receptors. Estrogens seem to be required to induce progesterone receptor. Progesterone, in turn, has been shown to lower the level of estradiol receptors in the endometria of normal women. This would be likely to prevent the development of endometrial hyperplasia, a known precursor of endometrial cancer. Progesterones are, thus, related to endometrial cancer as both antagonists of estrogens and as therapeutic agents.
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PMID:Sex steroid receptors in endometrial hyperplasia and neoplasia [proceedings]. 693 74

Various experimental and clinical studies have been made to evaluate possible relationships between estrogen and endometrial cancer. Estrogens do not induce endometrial carcinoma in most species of laboratory animals. In contrast to the limited species effect of estrogen, known carcinogens such as 2-naphthylamine, nitrosamines or aflatoxin B1 produce tumor incidence in a variety of species. Some case-control studies provide the hypothesis that estrogens in menopausal or postmenopausal women may be associated with increased risk of endometrial carcinoma. These studies provide only for association, and the theory of direct relationship must be confirmed or denied by more direct measurements. Other data on estrogens do not show a relationship between estrogens and endometrial cancer. Cases of endometrial cancer have been observed in women using sequential oral contraceptives, particularly dimethisterone with ethinylestradiol, but a cause-and-effect relationship has not been established. Progestins may arrest the progress or cause regression of endometrial carcinoma, but the indications are that the progestin is not protective against the carcinoma in the dosage employed. No data indicates that combination oral contraceptives cause endometrial cancer. The progestin in combination oral contraceptives may offer some protection against endometrial neoplastic changes.
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PMID:Relationship of estrogens and oral contraceptives to endometrial cancer in animals and women. 698 99

After reviewing the pathophysiology of the menopause, attention is directed to a review of the benefits of estrogen progestogen replacement therapy (vasomotor symptoms, urogenital atrophy, psychosomatic complaints, osteoporosis, cardiovascular disease, lipid metabolism); the risks of estrogen progestogen replacement therapy (endometrial cancer, endometrial hyperlasia, breast cancer, coagulation factors, gallbladder disease); and evaluation for estrogen therapy (nonoral estrogen administration). This author regards the menopause to be a hormonal deficiency state, and, like all endocrinopathies, should be managed as vigorously as need be, and without a necessary limitation of time. A wide variety of physical changes and symptoms have been associated with the climacteric. Some patients may only experience cessation of menses; others experience severe reactions that are occasionally disabling. Several factors may influence development of symptoms during the postmenopausal years, and the most important factor is probably the degree of estrogen depletion and the rate at which estrogen levels decrease. Additional factors may be an inherited or acquired propensity to withstand or succumb to the aging process and the psychologic impact of aging and the woman's ability to accept or deny the emotional changes of the menopause. The proven and almost universally accepted benefits of estrogen replacement therapy include relief of vasomotor symptoms, prevention of atrophic vaginitis, and prevention of osteoporosis. Estrogens may also help alleviate some of the psychogenic manifestations that menopause aggravates. Decreasing the risk of cardiovascular disease, particularly in oophorectomized young women may be another benefit by estrogen increased HDL cholesterol. 10 days of cyclic progestogen reduces the risk of endometrial cancer by preventing or treating estrogen induced endometrial hyperplasia. The risk of breast cancer has not been shown to be increased with estrogen therapy, and progestogens may provide additional protection for this tumor. The prognosis for breast carcinoma developing in hormone users is improved, most likely because of an earlier detection. Estrogens prevent demineralization of bone, and the addition of progestogen apparently promotes new bone formation. An increased risk of gallbladder disease may be associated with estrogen therapy, but this risk is minimal and has not been observed in all studies. There is no evidence that either estrogens or progestogens, in the small doses needed for menopause, increase the risk of thromboembolic disease. Newer routes of estrogen administration may further reduce the risks and increase the benefits.
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PMID:The menopause: benefits and risks of estrogen-progestogen replacement therapy. 704 Jan 16

Exogenous hormones, aside from their use as a contraceptive, are prescribed for treatment of menopausal symptoms (estrogens) and endometriosis/endometrial cancer (progestogens). This has enabled investigation of certain structural differentiations which occur during carcinogenesis in the cervix. Estrogens stimulate proliferation of stratified squamous epithelium of the ectocervix, but not that of endocervical columnar epithelium. On the other hand, progestogens stimulate the columnar epithelium and reserve cells beneath it, but not the squamous epithelium. Under estrogenic stimulation, an epithelial defect developing on the external cervical surface becomes reepithelialized mainly by the stratified squamous epithelium and is covered by regenerative epithelium. Under progestogenic stimulation, regeneration of the squamous epithelium is often preceded by proliferation of reserve cell hyperplasis. All these are benign repair processes which account for the largest proportion of the reepithelialization phenomena and healing seen in cervical ectopia. The appearance of the 3rd mucosa is the last stage of the healing process; here, a layer of mature stratified squamous epithelium covers the cervical mucosa. In a small number of cases, reepithelialization is followed by the development of precancerous lesions of various grades, and the beginning of carcinogenesis. It is possible to determine the origin of the cells from the appearance of various forms of intraepithelial neoplasis (e.g., dysplasia and carcinoma in situ of the squamous cell type, mucoid dysplasia and carcinoma in situ of the reserve cell type, microcarcinoma, and adenocarcinoma of the endocervical mucosa). An etiologic link between progrestogen administration and adenocarcinoma has been suspected. The highly potent hormone norgestrel appears to be the factor in many typical hyperplasias and carcinomas.
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PMID:Structural variations of cervical cancer and its precursors under the influence of exogenous hormones. 729 31

A reappraisal of endometrial cancer over the past decade reveals: 1) new concepts in its pathologic nature; 2) increase in incidence; 3) acceptance of the theory of hormonal relation; and 4) acceptance of individualization of treatment. Although endometrial carcinoma is still thought of as a predominantly well-differentiated adenocarcinoma, an increase in more virulent tumors has been seen in recent years. These include: adenosquamous carcinoma; adenoacanthoma; mesodermal sarcomas; and adenometous hyperplasia. Women at high risk for these tumors include those suffering from obesity, infertility, failure of ovulation, dysfunctional uterine bleeding, and those on long-term estrogen therapy. These women can be recognized and monitored by means of endometrial biopsy of the aspiration-curettage type. Adenomatous hyperplasia, the precursor of cancer, requires treatment with progestin or hysterectomy according to patient's age and reproductive status. Estrogens should be used only when indications are clear and in the smallest possible dose for the shortest period of time until the therapeutic goal is achieved. Aggressiveness of treatment should correspond to virulence of tumor. Dilatation and curettage under anesthesia should be used for clinical staging of endometrial cancer. Other means of treating endometrial cancers' include: total hysterectomy; bilateral salpingo-oophorectomy; iliac-aortic lymphadenectomy; pelvic irradiation; radical hysterectomy; chemotherapy, and a drug regimen (including cyclophosphamide, doxorubicin, fluorouracil, megestrol acetate).
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PMID:Current concepts in cancer: The changing nature of endometrial cancer. 735 80

I read with interest Dixit's review article concerning the liver and (OC) oral contraceptives (Can J Surg 23:222, 1980), and I think attention should be drawn to 1 or 2 possibly erroneous generalizations and inaccuracies. The author refers to both OCs and menopausal replacement medications and lists a group of general long-term effects which he describes as being common. In fact their rate of occurrence is quite low. Endometrial carcinoma has been reported to be associated with estrone sulfate therapy but not with combined estrogen-progesterone OCs; however, Silverberg and Makowski reported several cases of endometrial carcinoma associated with the use of the sequential OC Oracon, a product containing dimethisterone. Sequential agents are no longer used and indeed it is possible that combination agents may have a protective effect vis-a-vis endometrial carcinoma. Further, it is confusing to state that estrogen may be causally associated with carcinoma of the cervix; this was not the intent of the quoted article. All currently used OCs contain 19-nortestosterones but substituted progesterones have been used in the past. The progestins that have been used are numerous but should include norithisterone and d-norgestrel, the latter being 1 of the most widely used synthetic progestins. Estrogens are currently used in doses as low as 0.02 mg, and 0.035 mg doses are usual. The plasma coagulation proteins are indeed elevated (page 225) but in addition to those mentioned, factors 5 and 8 should have been included. In the section on changes in pregnancy (page 226), "increased serum fibrinogen" is mentioned. Surely the author means "plasma fibrinogen," as serum is totally devoid of that particular protein. This very comprehensive review emphasizes the effect of these potent agents on hepatic function in general. In view of the elevation of coagulation protein levels produced by OCs (and the consequent tendency to hypercoagulability), it might be interesting to ask general surgeons how frequently they discontinue OC medication before they perform elective surgery.
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PMID:Effects of oral contraceptives on the liver. 744 54

The use of estrogens in postmenopausal women has been the subject of much controversy regarding hormone formulation, dosage, use in combination with progestins, duration of treatment, and contraindications. Estrogens have been prescribed to relieve menopausal symptoms for more than three decades. The hormones reduce the gynecologic and psychologic changes associated with menopause while inhibiting bone resorption and possibly reducing the risk of cardiovascular disease. Their use however has been complicated by an increased risk of endometrial cancer and possibly breast cancer. The use of estrogens as cardioprotective agents is discussed and the clinical experiences and the possible mechanisms of action are reviewed. The clinical pharmacology of estrogens and the various formulations that are available as monotherapy or in combination with progestins will also be reviewed.
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PMID:Clinical pharmacology of estrogens: cardiovascular actions and cardioprotective benefits of replacement therapy in postmenopausal women. 775 8

The use of estrogens in postmenopausal women has been the subject of much controversy regarding hormone formulation, dosage, use in combination with progestins, duration of treatment, and contraindications. Estrogens have been prescribed to relieve menopausal symptoms for more than three decades. The hormones reduce the gynecologic and psychologic changes associated with menopause while inhibiting bone resorption and possibly reducing the risk of cardiovascular disease. Their use however has been complicated by an increased risk of endometrial cancer and possibly breast cancer. The use of estrogens as cardioprotective agents is discussed and the clinical experiences and the possible mechanisms of action are reviewed. The clinical pharmacology of estrogens and the various formulations that are available as monotherapy or in combination with progestins will also be reviewed.
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PMID:Clinical pharmacology of estrogens: cardiovascular actions and cardioprotective benefits of replacement therapy in postmenopausal women. 760 24

The presence of estrogens alone increases the risk of cancer of the endometrium. The risk increases with dosage and length of administration. Estrogens have a promoting rather than an initiating role since the risk progressively disappears after stopping treatment. Hormone-induced cancers have a better prognosis than spontaneous cancers. The association of progesterone or a progestogen obviates this risk. Prescription of oestrogens after treatment of cancer of the endometrium is non longer strictly contraindicated. Each case should be considered independently.
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PMID:[Estrogens, progestins and cancer of the endometrium]. 814 58

Hormone replacement therapy for postmenopausal patients following primary treatment of gynecologic malignancies has changed considerably during recent years. Estrogens have been found useful to prevent osteoporosis and cardiovascular disease as well as to ameliorate symptoms of estrogen deprivation. Thus, hormone replacement therapy can improve life quality of patients. Estrogen-gestagen replacement therapy after primary treatment of endometrial cancer is no longer contraindicated, at least in stage Ia to Ib disease. For breast cancer patients, the German Society of Senology has published recommendations based on the receptor status and lymph node status of an individual patient. Exogenous estrogens and gestagens are not contraindicated for breast cancer patients with negative receptors and negative lymph nodes. However, tamoxifen is indicated for patients with positive receptors and positive lymph nodes. If symptoms of hormonal deprivation occur, gestagens may be added to tamoxifen in these patients. There are no contraindications for hormone replacement therapy in patients with malignant tumors of the ovary, fallopian tube, cervix, vagina, and vulva.
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PMID:[Hormone substitution in patients after primary treatment of gynecologic malignancies]. 814 98


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