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

An understanding of the basic mechanisms of hormone action is becoming an important part of a clinician's training. With the advent of radioreceptor assays and their comparison with radioimmunoassays, we are becoming increasingly aware that the normal physiological function of a hormone is not necessarily dependent on "normal" levels of hormone being present in the plasma. Even if plasma levels are normal, if a particular target cell lacks the receptor for the particular hormone the target tissue will not respond to the hormone. It has been shown, for example, by many workers that steroid hormones act on their cells via a receptor located in the cytoplasm of the target cells (1-4). Since the presence or absence of such receptors are becoming increasingly important in terms of unexplained infertility, endometrial carcinoma and breast cancer, it is necessary that the practicing clinician be familiar with the concept of receptors and have some understanding of their mode of action. In this brief presentation, I will explain certain terminology and summarize the state of the art so that you can critically read the literature concerning new developments in the area of hormone action which is to become increasingly important in the next few years. I will discuss some of the aspects of the mechanism of peptide hormones such as LH and FSH but will devote most of my attention discussing the details of steroid hormone action since our knowledge in this area is much more complete. I will also explain the terms frequently discussed in the literature concerned with hormone-receptor interactions.
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PMID:Hormone-receptor interactions--basic mechanisms. 1 18

A proportion of cancers in endocrine target tissues can show the presence of specific receptors for either steroid or polypetide hormones. Manipulation of the controlling hormones does not guarantee regression. A third of cancers in endocrine target organs (breast, uterine endometrium, and prostate) show a 50% reduction in size of lesions after hormonal therapy. If regression resulting from an aggressive form of therapy lasts a short while and the tumor reactivates by the time the unpleasant effects of the therapy wear off, the treatment is not palliative. Endocrine therapy in prostatic cancer is palliative but there is no evidence that is increases survival. 11 different progestational agents in endometrial cancer therapy in the past 25 years resulted in a 30-35% response. Response must be maintained by continual treatment and may last from 12 months to 7-8 years. In breast cancer, tumors with a significant level of estrogen receptor (ER+) have about a 60% chance of regression vs. tumors without estrogen receptors (ER-), 10%. Advanced cancers of the thyroid of the papillary or follicular type regress when the patient is treated by thyroxine, .3 mg daily. Leukemia and lymphoma are frequently treated, with varying degrees of success with corticosteroid therapy, which may also predispose the patient to intercurrent infection. Renal cancer has been often treated by medroxyprogesterone acetate or testosterone propionate, with little success.
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PMID:Endocrine therapy in cancer. 8 86

A relationship between exposure to exogenous estrogens and endometrial carcinoma has been reported in numerous studies. The incidence among those so exposed has been estimated to have been increased from 7.5 to 8 times that of those not exposed. Long-term therapy with estrogens for menopausal symptoms has been the usual history. Breast cancer patients treated with estrogens and young women taking sequential oral contraceptives have had increased risks. In this study, the records of Olmsted County, Minnesota, residents with endometrial uterine cancer diagnosed between 1945-1974 at the Mayo Clinic or at other medical facilities were reviewed. There were 122 adenocarcinomas and 23 adenoacanthomas. In 3 instances, adenocarcinomas contained zones of uterine sarcoma. For each of the 146 patients there were 4 age-matched controls. Estrogen use for 6 months or more was recorded for 39 (27%) of the 145 cases and for 163 (28%) of the 580 controls. The controls had more frequent histories of short-term estrogen therapy. Cancer patients had relatively more estrogen use for menopausal symptoms. The relative risk of endometrial cancer tended to increase with the duration of exposure to conjugated estrogens from 2.0 with any exposure to 4.9 (p less than .01) after 6 months or more and to 7.9 after 3 years or more. The risk increased with larger doses (1.25 mg or more) and with continuous administration of conjugated estrogen. Myometrial invasion was superficial in 77 cases and deep in 44 cases. Long-term use of conjugated estrogen was frequently associated with low-stage low-grade superficially invasive endometrial malignancy. The 5-year survival rate of the 145 patients was 85%. Patients with Stage 1 had a 95% relative 5-year survival rate. Those with Stages 2, 3, or 4 had 50% survival rates. Of other risk factors, obesity and nulliparity were noted. Patients had more frequent records of benign cystic adenoma and of adenomatous hyperplasia than controls. The corrected age-specific rate for endometiral cancer increased to a maximum of about 90/100,000 population per year in the group aged 55-64 and then diminished with age. An increase in endometrial cancer among those at risk may have been nullified by an increase in those who have had a hysterectomy. In this study the incidence of endometrial carcinoma in Olmsted County does not show an increase in the last 3 decades. It is noted that the long-term use of conjugated estrogens in this area has been relatively low.
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PMID:Exogenous estrogen and endometrial carcinoma: case-control and incidence study. 19 Aug 87

Three patients with metastatic breast cancer responded to diethylstilbestrol (DES) therapy, but later they developed endometrial carcinoma. Evidence is presented to support the hypothesis that endometrial carcinoma can occur in breast cancer patients receiving diethylstilbestrol therapy.
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PMID:Endometrial carcinoma following estrogen therapy for breast cancer. Report of three cases. 20 83

Numerous investigators have alluded to an association of cancer of the endometrium and breast. There is no available information relating the histologic forms of cancer of the endometrium to breast cancer. We found ten cases of adenosquamous carcinoma of the endometrium in one tumor registry in a ten year period, 1967-1977. Five of these cases also had breast carcinoma. In three of these cases the breast carcinoma was discovered two to three years after hysterectomy; in one case both tumors were discovered at the same time, and in one case the breast carcinoma antedated the diagnosis of endometrial malignancy by approximately one year. These observations, although from a small number of cases, warrant an expansion of this study in order to determine whether patients with adenosquamous carcinoma of the uterus have a higher risk of developing breast cancer.
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PMID:Association of carcinoma of the breast with adenosquamous carcinoma of endometrium. 20 53

The effects of long-term estrogen replacement therapy upon neoplastic diseases were studied in 301 treated patients and 309 untreated patients. 207 women of each group had uteri in situ. Incidence figures for neoplasia were compared between the 2 groups and with the Third National Cancer Survey, yielding a risk ratio for the development of adenocarcinoma of the endometrium among estrogen-treated women of 3.8 (p .05) and 9.3, respectively. The addition of synthetic progestin to estrogen therapy provided significant (p .001) protection against the likelihood of developing endometrial cancer and did not reduce previously reported metabolic benefits of estrogen treatment. The data did not show an increased incidence of breast cancer among estrogen treated women, even with higher dosages or long-term therapy. It is recommended that estrogen therapy should be instituted whenever appropriate indications are present and no major contraindications exist; estrogen should be administered in the lowest dosage and duration that can adequately treat the indication for its use. Estrogens should probably be administered in cyclic fashion, especially if the uterus is in place, with sequentially added progestin.
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PMID:Effects of long-term estrogen replacement therapy. II. Neoplasia. 22 Aug 75

An overview of the sex hormones is presented. Testosterone is a natural androgen produced in the testes, adrenal glands, and ovaries. It has anabolic as well as androgenic effects. Testosterone is used to treat inoperable breast cancer and osteoporosis, and to stimulate erythropoesis. Androgens are absolutely counterindicated in cases of prostate cancer. Estrone, estradiol, and estriol are natural estrogens produced in the ovaries, placenta, testes, and adrenal glands. These hormones also influence the production of gonadotropins by the pituitary gland. Estrogens are used to treat menopausal disorders, ovarial insufficiency, estrogen-independent breast cancer, prostate cancer, and in some cases pregnancy disorders. Estrogens and progestagens are 2 components used in oral contraceptives. Progesterone, a natural progestagen, is produced by the corpus luteum. It promotes the proliferation phase of the endometrium, fertilization, and nidation, and it works to maintain pregnancy. Progesterone is used to treat spontaneous abortion, corpus luteum insufficiency, and endometrial cancer.
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PMID:[Sex hormones]. 24 26

Estrogens and progesterone seem to have at times antagonistic, at times synergetic action on breast and uterine tissues. While estrogens stimulate cell proliferation, progestrerone favors secretion. While estrogens favor myometrial and endometrial hyperplasia, progesterone seems to dominish congestive phenomena caused by estrogens, especially on breast tissues. Women who experience menopause at 55 have a twice as high risk of breast cancer than women who menopause at 45. Breast and endometrial cancer are often associated with a history of menstrual disorders, and it is very possible that endometrial hyperplasia and cystic mastosis are connected. While treatment with estrogens helps to avoid vaginal atrophy and to arrest osteoporosis, it is doubtful whether the treatment should be systematic over 45. Breast examination and a thorough gynecological examination are essential once a year.
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PMID:[Menopause, estrogens and genital cancer]. 24 20

Despite many years of extensive investigation, there has been neither a clear-cut pattern of hormonal production nor milieu found in women with breast cancer. Estrogen replacement therapy for menopause does not significantly increase the risk of breast cancer and one study indicated that estrogen users have a lower incidence of breast cancer than that observed in untreated women. Some studies have shown that the mortality rate from breast cancer is lower in estrogen-treated postmenopausal women. Only one investigator has found any significantly increased risk of breast cancer in oral contraceptive users. In that report, increased duration of birth control pill use decreased the risk of breast carcinoma. Several studies were unable to find an increased risk of breast cancer from oral contraceptives while one investigation observed a lower incidence in birth control pill users than that expected. The mortality from carcinoma of the breast in oral contraceptive users was lower than in non-users, most likely due to earlier detection. Although some retrospective studies have indicated that estrogen use increases the risk of endometrial cancer, a prospective investigation found only an insignificant increase. Progestogens afford some protection from cancer in estrogen-treated postmenopausal women. The incidence of endometrial adenocarcinoma is lower than that observed in untreated postmenopausal women. Combination oral contraceptives are protective against developing adenocarcinoma of the endometrium but sequential birth control pills may afford less protection.
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PMID:The role of hormones in the etiology of breast and endometrial cancer. 29 15

The factors that increase the risk of development of endometrial cancer are reviewed. Many of these conditions are frequently associated with an elevated production of estrone in peripheral (nonendocrine) tissues from circulating androstenedione. Elevated estrone production may occur in young, anovulatory or postmenopausal women whose ovaries secrete higher than normal amounts of androstenedione. Alternatively, conditions such as obesity and liver disease are associated with higher than normal rates of conversion of androstenedione to estrone, resulting in high estrone levels. Neither the exact tissue site(s) of conversion nor the normal function of this process has yet been established. Much less information concerning steroid hormone receptor measurements in endometrial cancer than in breast cancer is available. However, it seems certain that measurement of progesterone receptors will provide a useful guide in the selection of progestational therapy.
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PMID:Steroid hormones and endometrial cancer. 35 36


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