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Query: UMLS:C0006142 (breast cancer)
 160,383 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Estrogen replacement in menopause should be used for specific symptoms such as ovarian failure, hot flushes, vaginal atrophy, atrophy of the vulva, and atrophic urethritis. The dose should be as low as possible to be effective and perscribed for as short as time as possible, since there are possible risks of uterine cancer, breast cancer, increased blood pressure, gallstones, deep vein thrombosis, and thromboembolism. Estrogens should be administered to provide the maximum benefit with the minimum risk involved. Estrogens should not be given to patients with known contraindications such as: suspected breast or uterine cancer; undiagnosed genital bleeding; Dubin-Johnson syndrome; acute hepatic disease; previous or present thromboembolism; or severe thrombophlebitis. Careful evaluation should be made before administering estrogen to women with uterine myomata, hyperlipidemia, hypercholesterolemia, sevare varicose veins, chronic hepatic dysfunction, diabetes mellitus, porphyria, or severe hypertension.
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PMID:Estrogen replacement in the menopause. 39 Apr 56

This lengthy discussion of possible associations between both endogenous and exogenous estrogens and progestins to occurrence of human cancers begins by discussing endogenous metabolism of the 2 sex steroid types. For example, the endogenous production of estrogen is associated with anovulation and endometrial cancer, although clearly other risk factors are associated with these diseases, and breast cancer, which account for some or all of the sex hormones apparent carcinogenic effect. Also discussed are the modulating effects of estriol on response of the breast and endometrium to estradiol and estrogens, and the modulating effects of androgens on development of breast cancer. The bulk of the monograph concerns summaries of data on the correlations of exogenous sex hormones and human cancers. Attention is also paid to the use of exogenous sex hormones for treatments of human cancers. Estrogens have been used to treat endometrial cancer, breast cancer, and benign breast disease. Side effects of hormonal contraception discussed include gross and microscopic changes in the breast, benign breast disease, and breast cancer; in the uterus, exogenous hormonal contraception is associated with neoplastic changes in the cervix, cervical neoplasia, endometrial cancer, trophoblastic tumors, and uterine fibroids. Ovarian effects include nonneoplastic and benign lesions and ovarian cancers. Oral contraception may also correlate with incidences of pituitary and melanoma malignancies. Liver effects include both benign neoplasms and malignant tumors.
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PMID:Oestrogens and progestins in relation to human cancer. 39 83

The most important short-term uses of estrogen are in the control of vasomotor disturbances, often called hot flashes, and in the therapy of athrophic vaginitis. Dosage should be as low as possible and on a cyclic basis. Estrogens can be employed cyclically but for an unpredictable term in the case of hypogonadism, female castration, and especially in the treatment of osteoporosis. The synthetic estrogen diethylstilbestrol (DES) is used as a contraceptive after coitus, in a large dose and within 72 hours, since it inhibits implantation of the fertilized ovum in the uterus. The use of estrogens in controlling some of the emotional conditions prior to menopause is not advisable, but they can be helpful in controlling acne and to arrest uterine bleeding. Conversely, estrogens have been shown to be associated with vaginal adenosis, and with clear cell carcinoma in girls whose mothers had been given DES during pregnancy; also with endometrial carcinoma in postmenopausal women who had taken the drug for years. The association between estrogens and breast cancer is still not clear, since the drug produces different results in different patients. Since estrogens increase blood coagulability their use is associated with an increased risk of thromboembolism and cardiovascular accidents. In prescribing estrogens physicians must evaluate each patient carefully, and require regular visits at six month intervals.
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PMID:Estrogens: their function, uses and hazards. Part 2. 62 3

One of the major problems being researched and studied by the World Health Organization is the incidence of harmful side effects in users of steroid contraceptives. A literature search indicates that Anglo-Saxon countries report alarming hyperplastic changes, particularly in the liver, blood clots, hyperlipidemia leading to high blood pressure, porphyria, atypical leiomyomas and cervical hyperplasia. Currently attention is being focused on the relationship between steroid contraceptives and breast cancer. Fazala and Paffenbarger in their study of 1770 women found such benign changes as fibroadenoma, mastopathia fibrosa cystica and papilloma intraductale. In women who had used oral contraceptives for 2-4 yrs, malignancies were 1.9% to 2.5% more frequent than in non-users; in 6 yrs of use, 11 times greater than in non-users. Estrogens, particularly mestranol has been recognized as being harmful to the liver. Length of usage is a definite factor. Beginning with 1960, relatively frequent occurrences of hepotoma in young women on the pill were noted. Caught at an early stage, peliosis hepatis can be reversed if the patient discontinues the use of contraceptives. In some cases, even after a long interval of 6 months to 10 yrs, the disease continued to develop. Liver cell adenoma in the U. S. occurs 1/500,00 to 1/1,000,000. After 5 to 7 yrs of using oral contraceptives, the chance of developing liver cell adenoma is 5 times greater; after 10 yrs of use, 35 times greater. Hepatomas rupture in 43.4% of cases when the patient had been on a contraceptive, while in only 22.2% in cases of non-users. The literature which the author investigated did not establish a clear proof that the hyperplastic changes discussed were due exclusively to usage of oral contraceptives.
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PMID:[Hyperplastic changes and oral contraceptives in Anglo-Saxon countries]. 69 6

A continuing education examination of estrogen therapy is discussed. The most common indication of estrogen therapy is for replacement in menopausal women. Estrogens can also be used in the treatment of certain types of cancer such as prostatic cancer. A diagnosis of estrogen deficiency must be established first and then estrogen therapy must be selectively used. Psychoemotional problems must be ruled out. Perimenopausal patients may be treated somewhat differently than postmenopausal patients. 1 of the major controversies surrounding estrogen therapy, other than cancer and osteoporosis, is its implication to coronary heart disease. The evidence indicates that estrogen in some way contributes to endometrial carcinoma. Estrogen administration does not seem to show a correlation to breast cancer. Actual treatment must be individualized, and which estrogen, how much, and how long it should be used is still not clear.
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PMID:Estrogen therapy. 70 1

Estrogens are well known to play a predominant role in human breast cancer. The current endocrine therapy of breast cancer consists in administering an antiestrogen which blocks the action of estrogens at the receptor level. However, the currently available antiestrogens possess mixed estrogenic and antiestrogenic activity, thus limiting their potential therapeutic efficacy. The present data show that a series of new estrogen derivatives demonstrate not only pure antiestrogenic activity in the sensitive in vivo mouse uterus assay, but simultaneously exert potent inhibitory effects on 17 beta-hydroxysteroid dehydrogenase activity, the enzyme responsible for the formation of 17 beta-estradiol from estrone, the last step in estrogen formation. Such compounds having a dual site of inhibitory action, namely on estrogen formation and on the estrogen receptor, could well lead to an improved endocrine therapy of breast and other estrogen-sensitive cancers as well as other nonmalignant estrogen-sensitive diseases.
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PMID:Novel compounds inhibit estrogen formation and action. 131 67

Antiestrogens are widely used in the management of hormonally responsive breast cancer in both adjuvant and palliative settings, and are currently being evaluated as chemopreventive agents. The classical mechanism of action of these drugs involves inhibition of estrogen-stimulated neoplastic cell proliferation by blockade of estrogen receptors present on breast cancer cells. This paper reviews recent clinical and laboratory data that suggest that the commonly used antiestrogen tamoxifen also acts to reduce serum IGF-I levels. Estrogens appear to play a permissive role in growth hormone (GH) release by the pituitary gland and GH is known to stimulate IGF-I expression by hepatocytes. It is therefore possible that blockade of estrogen receptors in the hypothalamic-pituitary axis by tamoxifen interferes with GH release, leading to reduced hepatic IGF-I expression. In view of results suggesting that IGF-I is a more potent mitogen than estradiol for breast cancer cells and data demonstrating a positive correlation between estrogen receptor level and IGF-I receptor level of breast cancer cells, the IGF-I lowering effect of tamoxifen may contribute to the cytostatic activity of the drug. The interrelationships between steroid hormone physiology and IGF-I physiology may have relevance to a variety of commonly used treatments for hormonally responsive cancers.
Breast Cancer Res Treat 1992
PMID:Tamoxifen reduces serum insulin-like growth factor I (IGF-I). 142 27


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