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

Estrogen receptor-negative, 7, 12-dimethylbenz(a)anthracene (DMBA)-induced rat mammary carcinoma (TF1357) grew equally well in ovariectomized females, ovariectomized females with thyroidectomy and ovariectomized females given injections of Tamoxifen (0.1 mg/day), Medroxyprogesterone acetate (8 mg/day) or CB-154 (1 mg/day). However, the growth of TF1357 was inhibited markedly by injections of a very large amount of 17 beta-estradiol (1 mg/2 days) and also by hypophysectomy. The growth of estrogen receptor-positive, DMBA-induced rat mammary carcinoma (8K2401) was also almost completely inhibited by hypophysectomy and injections of high doses of 17 beta-estradiol, while 8K2401 grew well in castrated males. Secretory changes characterized by vacuolation in cytoplasm were observed in 8K2401 cells in castrated males with injections of high doses of estrogen but these changes were not found in 8K2401 cells in castrated males with hypophysectomy or in TF1357 cells in ovariectomized females which had had hypophysectomy or injections of high doses of estrogen. These observations suggest that hypophysectomy and/or injections of high doses of estrogen may be effective treatment for breast cancer unresponsive to ovariectomy or injections of antiestrogen drugs.
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PMID:Hypophysectomy and injections of high doses of estrogens inhibit the growth of ovary-independent rat mammary carcinomas. 196 85

Between 1977 and 1983 100 elderly women (median 76.3 years) with breast cancer were treated with tamoxifen as primary therapy. The median follow-up is 59 months. Sixty-eight responded (40 CR and 28 PR) with median response durations of 47 months and 26 months respectively. Twenty-two patients had disease stabilization for a median of 15.5 months and 10 had progressive disease. The median time to best response was 13.5 weeks for patients achieving CR and 14 weeks for those with PR. Oestrogen receptor values were obtained in 37 patients of which two patients had no ER detectable. Sixty-seven per cent of ER-unknown patients responded compared with 74% of ER-rich. Likelihood of response did not appear to depend upon T-stage or age. Survival was better than that of an unmatched historical group treated with surgery/radiotherapy and compares favourably with recent reports. Although 35% have died of breast cancer, 25% died of other causes and 22% remained free of recurrence at the time of reporting or at death. Only 11% underwent subsequent mastectomy/lumpectomy and the most frequent subsequent treatments were radiotherapy to the breast (32%) and further hormonal therapies (40%). Tamoxifen is a practical primary therapy of breast cancer in elderly and frail women obviating the need for surgery in a high proportion of cases.
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PMID:A 10-year experience of tamoxifen as primary treatment of breast cancer in 100 elderly and frail patients. 199 54

The pharmacology of the antiestrogen tamoxifen is reviewed. The drug is currently used extensively in the treatment of all stages of breast cancer and is being considered as a preventive agent for women at high risk for breast cancer. Extensive laboratory studies demonstrate that tamoxifen is a tumoristatic agent in models of mammary carcinogenesis. Any clinical applications must therefore consider long-term (5-10 years) treatment strategies. Tamoxifen prevents rat mammary carcinogenesis. However, the timing of the carcinogenic insult is unknown among women. Tamoxifen must be considered to be a chemosuppressive agent to prevent the appearance of the primary tumor rather than to prevent the initial carcinogenic insult.
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PMID:Chemosuppression of breast cancer with long-term tamoxifen therapy. 200 27

One hundred and thirteen women aged 70 years or more with locoregional breast cancer were treated with tamoxifen alone as primary treatment. They were followed for a minimum of 5 years. Complete response occurred in 38 women, partial response in 17, no change in 34 and progressive disease in 24. Where progressive disease occurred, or where patients relapsed after an initial response, the most suitable conventional therapy was given. The actuarial 5-year survival rate was 49.4 per cent for all patients and was much higher (92 per cent) in those showing an initial complete response. Seventy patients (61.9 per cent) were not controlled by tamoxifen alone to death or most recent follow-up. Tamoxifen provides an alternative treatment for operable breast cancer in older women in the short term and may be particularly suitable for those with concurrent disease or who are unwilling to undergo surgery. The low morbidity rate from tamoxifen must be balanced against the need to maintain close follow-up. In the medium to long term, sole primary treatment by tamoxifen delays more definitive therapy.
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PMID:Long-term follow-up of elderly patients with locoregional breast cancer treated with tamoxifen only. 201 78

Adjuvant therapy in operable breast cancer (stage I and II) can significantly reduce the risk of recurrences and improve survival. In stage I disease, 20-30% of patients will eventually recur. Several prognostic factors may help in identifying poor prognostic subgroups of stage I patients, including ER and PR status, flow cytometry data, nuclear grade, neu oncogene expression, and perhaps haptoglobin-related protein, Cathepsin-D, and Ki-67 expression. Single-agent chemotherapy and oophorectomy have not resulted in prolongation of survival. Combination chemotherapy regimens are superior to single agents, and doxorubicin-containing regimens may be superior to non-doxorubicin-containing regimens. Tamoxifen is effective in improving survival in patients who are ER positive, particularly those women older than 50 years. It appears that six cycles of an effective regimen is as effective as more prolonged administration of the same drugs, and drugs should be given at the optimal dose rate. Preliminary results of alternating non-cross-resistant chemotherapy regimens show promise, but additional data are needed to determine its impact on survival.
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PMID:Current status of adjuvant therapy of early breast cancer. 202 18

The antiestrogen tamoxifen is the most widely used hormonal therapy for breast cancer. The drug exerts its antiproliferative effects primarily through estrogen receptor (ER)-mediated mechanisms, although other cellular actions may augment tumor inhibition. Clinically, tamoxifen has been less well studied in premenopausal than in postmenopausal patients. The drug has complex endocrine effects that are dependent on the treatment duration and dose, menopausal status, and target organ. In postmenopausal women receiving tamoxifen, serum estrogen levels remain low, and the normally elevated gonadotropin levels decrease. In contrast, serum estrogen levels are strikingly elevated in many premenopausal women, and gonadotropin concentrations are either unchanged or slightly increased. Large systematic trials in metastatic breast cancer have established tamoxifen as the recommended hormonal therapy for postmenopausal women with ER-positive tumors. Tamoxifen is also an active agent for premenopausal metastatic disease, and response rates are comparable to those reported for oophorectomy. Clinical experience with tamoxifen in this younger age group, however, is more limited. Few premenopausal women (less than 400) have been included in phase II and phase III trials. Two randomized trials (total of 160 patients) comparing oophorectomy with tamoxifen do not definitively establish therapeutic equivalence, and a survival advantage for either treatment cannot be excluded. Many questions remain concerning the appropriate role for tamoxifen in premenopausal patients. Still, tamoxifen has an attractive toxicity profile, and it offers a favorable therapeutic alternative for premenopausal women with ER-positive metastatic breast cancer who wish to avoid surgical or radiation castration.
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PMID:Tamoxifen in premenopausal patients with metastatic breast cancer: a review. 204 68

In 1980, there were 570,000 cases of breast cancer in the world. In Norway, there are an average of 2000 new cases per year, and incidence had increased 50% from 1955 to 1984. About 40% of those afflicted die of the disease. Environmental, age, and reproductive factors seem to be implicated in its genesis. The rate increased almost fivefold in the course of a generation among Polish people who migrated to California from low incidence areas. It doubled among Chinese and Japanese who moved to California. The rate increases sharply up to age 50, then it levels off, thus early menopause is protective. Ovarial hormones (estrogen and progesterone) play a role in the development of preclinical tumors. Younger age at first delivery offers protection, but women who give birth to their first child after age 35 face a higher risk than nulliparas. Women with early menarche, which can be delayed by a lower caloric intake and vigorous physical activity, also face a heightened risk. Before menopause, overweight women are relatively protected, but the reverse is true after age 60. The consumption of animal fat is another risk factor, although a US study that involved 90,000 nurses did not bear this out. The Japanese increased their intake of animal fat from 10-25% from 1955-1975 without a corresponding increase in the rate of breast cancer. A vegetarian diet is nonprotective. Even the moderate consumption of alcohol increases the risk by 40% for women aged 15-30. Long-term use of oral contraceptives before birth of the first child up to age 35 increases the risk. Tamoxifen has protected women with a familial history of breast cancer who face a 3-5 fold higher risk. After menopause, its estrogenic properties promote the risk. Tamoxifen has an antitumor effect that can treat tumors clinically which are not manifested; it also lowers LDL (low density lipoprotein) and increases HDL (high density lipoprotein) cholesterol.
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PMID:[Can breast cancer be prevented?]. 206 86

Tamoxifen is a widely used drug in medical oncology, mainly for treatment of breast cancer, but also for second line treatment of endometrial cancer. We recently reported an increased incidence of endometrial cancer associated with long-term adjuvant tamoxifen. This observation, previous reports of stimulatory effects of tamoxifen in the female genital tract, and experimental data are in accordance with a mainly estrogenic effect of tamoxifen in these tissues. An increased incidence of endometrial cancer may limit the usefulness of tamoxifen for benign indications. For adjuvant treatment of early breast cancer, however, the improvement of both recurrence-free survival and overall survival probably outweighs the increased frequency of uterine tumors. However, the possibility of growth stimulation of tumor subclones should be considered when tamoxifen is used in the treatment of endometrial cancer.
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PMID:Effects of tamoxifen on the female genital tract. 206 3

Two hundred fifty evaluable patients with breast cancer entered a protocol combining neoadjuvant and consolidation therapy by vinblastine (V), thiotepa (T), methotrexate (M), and 5-fluorouracil (F) (VTMF), with or without Adriamycin (A) (doxorubicin; Adria Laboratories, Columbus, OH), and radiation therapy as exclusive locoregional treatment. Tamoxifen was given to 195 patients (130 postmenopausal and 65 premenopausal) and was omitted in 55 patients (31 postmenopausal and 24 premenopausal). There were 19 Stage I, 86 Stage IIA, 51 Stage IIB, 36 Stage IIIA, and 58 Stage IIIB patients. Primary chemotherapy induced tumor volume regression of more than 75% in 41% of the patients and complete clinical regression in 30% of the patients. The 5-year disease-free survival (DFS) rates were 100% for Stage I, 82% for Stage IIA, 61% for Stage IIB, 46% for Stage IIIA, and 52% for Stage IIIB patients. Among the 72 primary relapses there were 39 distant metastases. The actuarial rate of locoregional recurrence was 13% for T2, 18% for T3, and 19% for T4. At 5 years the rate of breast preservation was 94%. Cosmetic results were excellent or good for most patients. The 5-year overall survival (OS) rates were 95% for Stage I, 94% for Stage IIA, 80% for Stage IIB, 60% for Stage IIIA, and 58% for Stage IIIB. Most patients with breast cancer should be given the option of breast-preserving treatment.
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PMID:Results of neoadjuvant chemotherapy and radiation therapy in the breast-conserving treatment of 250 patients with all stages of infiltrative breast cancer. 211 76

Breast cancer cell lines (MCF-7, T47D, BT-20 and STT-11) and fresh cells from malignant effusions of eight breast cancer patients were examined for their in vitro sensitivity to 17 beta-estradiol (E2), tamoxifen and toremifene in a miniaturized, improved nucleic acid precursor incorporation assay (MINI assay). Seven of the eight patients received either tamoxifen or toremifene following a MINI assay and the correlation was examined between in vitro sensitivity and clinical responses to the hormonal agents. In cell lines, E2 stimulated thymidine incorporation by estrogen receptor (ER)-rich cells, MCF-7 and T47D, but not by ER-poor cells, BT-20 and STT-11. Tamoxifen induced both ER-mediated and -unmediated effects in ER-rich cells. The latter effect was also observed in ER-poor cells. Toremifene had less ER-unmediated effect in all of the cells tested than tamoxifen did. The ER-mediated effect of toremifene was weaker than that of tamoxifen in cell lines but was equipotent to tamoxifen in fresh cells. E2 affected thymidine incorporation by cells withdrawn from patients who showed a partial response to the anti-estrogens. No clear correlation was demonstrated between in vitro sensitivity to anti-estrogens of fresh cells and clinical response to these agents. The present results suggest that 1) the MINI assay is a useful system to investigate hormonal effects on breast cancer cell lines; 2) clinical responses to anti-estrogens are not predicted by in vitro response to the agents but might be predicted by the in vitro response to E2; and 3) toremifene has a smaller non-specific effect on breast cancer cells than tamoxifen and is equipotent to tamoxifen in the ER-mediated effect in vitro.
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PMID:In vitro sensitivity test of breast cancer cells to hormonal agents in a radionucleotide-incorporation assay. 214 80


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