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

Although both prolactin and growth hormone are believed to play roles in the development and growth of rodent mammary cancer, the role of these hormones in human breast cancer is uncertain. Under carefully specified conditions, serum levels of these hormones were determined by radioimmunoassay (RIA) and prolactin was determined by bioassay in 18 premenopausal women with breast cancer, 23 healthy women with a strong family history of breast cancer, and 39 healthy women with no significant family history of breast cancer. Parity was associated strongly with decreased prolactin levels, and increasing age was associated strongly with decreased growth hormone levels. After controlling for these variables, no differences in prolactin or growth hormone levels were found among the three groups of women. These data do not support roles for these RIA-measured hormones or bioassay-measured prolactin in premenopausal or familial breast cancer in omnivorous white women.
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PMID:Prolactin and growth hormone levels in premenopausal women with breast cancer and healthy women with a strong family history of breast cancer. 187 92

It has been suggested that both the menstrual cycle phase and postoperative changes in prolactin (PRL) secretion at the time of surgery may influence the prognosis of breast cancer. The present study was carried out to evaluate the relation between menstrual cycle period and surgery-induced PRL variations. We evaluated 32 premenopausal women with operable breast carcinoma; 17 were in perimenstrual phase (days 1-6 and 21-28) and 15 were in the mid-cycle (days 7-20) period at the time of surgery. To investigate serum levels of PRL, venous blood samples were collected before and 7 days after surgery. Postoperative hyperprolactinemia occurred in 17/32 patients and it was statistically more frequent in patients surgically treated during the perimenstrual phase than in the mid-cycle phase (12/17 vs 5/15; p less than 0.05), while no other parameter (including axillary node and estrogen receptor status) showed a significant influence on hyperprolactinemia rate. The results suggest that in premenopausal breast cancer patients surgery-induced hyperprolactinemia may be influenced by the menstrual cycle phase at the time of surgery.
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PMID:Relation between surgery-induced prolactin increase and the menstrual cycle phase at time of surgery in premenopausal breast cancer. 189 Mar 13

The aromatase inhibitor, 'pyridoglutethimide' (PyG), has been shown previously to suppress serum oestrogen levels in postmenopausal breast cancer patients and to achieve clinical responses at a dose of 500 mg twice daily (b.d.). This report gives the results of a detailed pharmacokinetic and endocrine study of PyG in ten patients. Four doses were tested at intervals of 2 weeks in the following order: 200 mg b.d., 400 mg b.d., 800 mg b.d., 1200 mg b.d. Concentration-time profiles of serum levels of PyG were curvilinear in all patients probably reflecting a saturation of metabolic enzymes. During repeat-dosing metabolism was enhanced approximately 2-fold. Plasma levels of oestradiol were significantly suppressed by the lowest dose of PyG. Although higher doses appeared to achieve greater suppression this was not statistically significant in this small group of patients. There were no significant effects at any dose on the serum levels of cortisol, aldosterone, luteinising hormone, follicle stimulating hormone, prolactin, sex hormone binding globulin or thyroid stimulating hormone. There was a dose-related increase in 17 alpha-hydroxyprogesterone levels and a dose-related decrease in levels of dehydroepiandrosterone sulphate (DHAS). The androgens DHA, testosterone and androstenedione also were significantly suppressed with at least one of the doses of PyG. Synacthen tests did not support these changes being a result of inhibition of 17,20 lyase. It is possible that they are due to enhanced clearance of DHAS. Two patients experienced no toxicity throughout the study, whilst a total of four patients were withdrawn because of side-effects: one at 400 mg b.d., two at 800 mg b.d., and one at 1200 mg b.d. The most frequent side-effects were nausea and lethargy. One patient showed an objective response to treatment.
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PMID:Endocrine, pharmacokinetic and clinical studies of the aromatase inhibitor 3-ethyl-3-(4-pyridyl)piperidine-2,6-dione ('pyridoglutethimide') in postmenopausal breast cancer patients. 193 11

The effects of treatment with a somatostatin analog (Sandostatin, SMS201-995) were investigated in female rats with dimethylbenzanthracene (DMBA)-induced rat mammary tumors. A 3-week treatment was performed using sandostatin, the LHRH-agonist buserelin alone, or buserelin in combination with sandostatin. Twice daily sandostatin treatment was performed with dosages of 0.05 microgram, 0.2 microgram, 1 microgram, 5 micrograms, and 20 micrograms. Buserelin was used in a 2 x 5 micrograms/day dosage. The combined results from six different experiments show that the various dosages of sandostatin caused no tumor growth inhibition. Somatostatin receptors could not be demonstrated in these mammary tumors. Sandostatin treatment by daily injections did not suppress levels of growth hormone, prolactin, or epidermal growth factor-like activities. Estrogen (ER) and progesterone (PgR) receptor contents of the mammary tumors were not changed. In contrast, buserelin treatment caused highly significant tumor remission. The combined treatment with sandostatin and buserelin did not alter the treatment results obtained after treatment with buserelin alone. In conclusion, sandostatin treatment in this tumor model had no direct growth inhibitory effect and did not cause an endocrine inhibition of mammary tumor growth. However, these results do not exclude antitumor effects in human breast cancer in view of the presence of somatostatin receptors in approximately 20-45% of human tumors, besides possible different endocrine effects.
Breast Cancer Res Treat 1990 Nov
PMID:The somatostatin analog Sandostatin (SMS201-995) in treatment of DMBA-induced rat mammary tumors. 196 5

The present experiments were designed to evaluate the polyamine involvement in hormonal actions on proliferation and receptor content of neoplastic tissue (hormone-responsive breast cancer) as well as on growth of normal endocrine target tissue (uterus) in the same animals. Administration of estradiol and perphenazine (to stimulate endogenous prolactin release) stimulated N-nitrosomethyl-urea (NMU)-induced rat mammary tumor growth following ovariectomy-induced tumor regression. Such hormonal activation of breast cancer growth was completely abolished by treatment with alpha-difluoromethyl-ornithine (DFMO), a specific irreversible inhibitor of ornithine decarboxylase, which lowered tumor content of polyamines. The growth inhibitory effect of DFMO was partially reversible by exogenous putrescine administration. In contrast, the rise in cytosolic content of progesterone receptors induced by hormonal treatment was not affected by suppression of tumor polyamine levels by DFMO. Similarly, DFMO administration failed to influence the hormone-induced increase in uterine weight in the same animals. Thus, our data suggest selectivity of polyamine involvement in hormone actions, which, in our experimental system, seems to be restricted to the endocrine control of neoplastic cell proliferation.
Breast Cancer Res Treat
PMID:Selectivity of polyamine involvement in hormone action on normal and neoplastic target tissues of the rat. 203 41

The biological role of transforming growth factor-alpha (TGF-alpha) in basal and hormone-stimulated proliferation of primary human and rat mammary tumor cells was studied using antibodies against TGF-alpha and its receptor. A monoclonal antibody, MAb-425 against human EGF receptor was added to in vitro soft agar, clonogenic cultures of human breast carcinoma cells under basal and estradiol(E2)-stimulated conditions. The antibody had an antagonist effect on colony growth in 4 of 10 tumors and an agonist effect in 4 (72 and 153% of control). E2-stimulated colony growth in 5 tumors (167% of control) and the antibody blocked E2-stimulation in 3 of the 5. Inhibition of E2-stimulated growth in 3 and basal growth in 4 other tumors by the EGF receptor antibody suggest that endogenously secreted TGF-alpha has a role as an autocrine/paracrine growth factor in constitutive and E2-stimulated tumor cell proliferation in a majority of human tumors. A polyclonal antibody against TGF-alpha was used to study the role of TGF-alpha in E2-, prolactin(Prl)- and progesterone(Prog)-stimulated proliferation of NMU(nitrosomethylurea)-induced rat mammary tumor cells under similar culture conditions. TGF-alpha, E2, Prl and Prog stimulated colony growth equally to 176, 187, 168 and 181% of control. The antibody produced significant and similar inhibition of TGF-alpha and E2-stimulated growth (95 and 83%). In contrast, inhibition of Prl- and Prog-stimulated growth by the antibody was only 24 and 37%. The TGF-alpha ligand antibody did not have an agonist or antagonist effect when added alone. Thus, TGF-alpha seems to be a major stimulatory growth factor mediating E2-induced tumor cell proliferation in rat mammary tumors. It is less important in Prl- and Prog-induced tumor growth and not essential for basal growth in these tumors. We conclude that TGF-alpha is a biologically important autocrine/paracrine growth factor in primary human breast cancer cell proliferation and in E2-induced rat mammary tumor growth.
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PMID:Role of transforming growth factor-alpha (TGF-alpha) in basal and hormone-stimulated growth by estradiol, prolactin and progesterone in human and rat mammary tumor cells: studies using TGF-alpha and EGF receptor antibodies. 206 83

One out of 11 women is destined to develop breast cancer. All women should be "under observation". Does a "normal" breast really exist? A discharge from a single orifice could suggest a papillomatosis, a real borderline lesion, the adenofibroma practically never degenerates, the essential problem is that of the fibrocystic disease, (or mastosis) which was the object of a recent detailed analysis (W. Dupont and D. Page), pre-menstrual mastodynia does not seem to be a risk factor. On the other hand, certain dystrophic lesions constitute a high risk, such as atypical epithelial hyperplasia, especially if it is associated with a direct family history of breast cancer. Recent studies on mammary cysts insist on their hormone and electrolyte content, the presence of EGF, as well as that of certain proteins (GCDFP 15). They also insist on the local tissue enzymatic activities, the importance of myoepithelial cells and of fibroblasts. On a practical level, the attention is drawn on: cysts whose diameter exceeds 5 mm, certain histological lesions found during the biopsies. The value of mammography and thermography in the assessment of the high risk is discussed. Finally, the present well-established notions are recalled: the family history, late pregnancies, the diet, the weight, certain pathological associations, the endogenous hormonal balance bearing on E2/P and the blood prolactin level, the exogenous hormone intake.
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PMID:[What is mastopathy at risk? Epidemiologic and clinical basis]. 206 85

Gonadal and hypophyseal hormones were investigated in 15 males with breast cancer and 15 tumour referents, on average 1 month postoperatively. Plasma prolactin was found to be significantly more often elevated in men with breast cancer compared with referents (p less than 0.005). Another group of men with breast cancer disclosed a tendency for lower S-FSH levels compared with the referents (p less than 0.01). No significant difference was seen between cases and referents regarding S-LH, p-estradiol or p-testosterone. The size of the primary breast tumour was correlated with a higher prolactin level. The findings lend support to a theory implicating prolactin and possibly prolactinomas as a risk factor for the disease in males.
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PMID:Increased plasma prolactin levels in a group of men with breast cancer--a preliminary study. 211 Apr 33

In the present paper we have studied the quantitative variations in estrogen (ER) and progesterone receptor (PR) content of breast cancer induced by tamoxifen. In addition to receptors, hormonal levels of estradiol, progesterone, prolactin, FSH, LH and testosterone were also measured. The cases included in our study were consecutively selected among those breast cancers in which an aliquot of the tissue sample sent for analysis of the steroid receptors was positive for cancer and also found to have at least one of the steroid receptors positive, not only in the biopsy but also in the surgical specimen. Following this criterion, we finally collected 14 cases of breast cancer treated daily with 30 mg of tamoxifen during an interval of 3 weeks from the initial biopsy to the final surgery. From our results we can conclude that tamoxifen reduced significantly the ER concentration while no changes were observed in PR values. Concerning hormones, while in premenopausal patients tamoxifen induced a rise in plasma estradiol, in postmenopausal women the only modification observed was a decrease in plasma FSH. The variation in steroid receptor content under tamoxifen therapy may also contribute to the evaluation of the hormone dependency of gynecologic malignancies.
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PMID:Variation of estrogen and progesterone receptor status in breast cancer after tamoxifen therapy. 212 23

Hormone concentrations in blood and total 12 h urine values were compared between 40 post-menopausal women with breast cancer and 40 control women in a study which carefully controlled for the possible confounding effects of age, weight and pregnancy history by individually matching cases and controls on these factors. Breast cancer cases had received only surgical treatment for their localised disease, which was diagnosed from 1 to 9 years before hormonal evaluation. Cases had 15% higher serum oestradiol levels (P = 0.02), 40% more urinary oestradiol (P = 0.03) and 44% more urinary oestriol (P = 0.04) than control women. Cases also had higher levels of serum and urinary oestrone, but these differences were not statistically significant. The percentages of serum oestradiol not bound to albumin or sex-hormone binding globulin did not differ between cases and controls, nor were there statistically significant differences in the serum levels of prolactin, sex-hormone binding globulin or dehydroepiandrosterone sulphate. These results provide further support for the hypothesis that breast cancer risk is determined in part by post-menopausal serum oestrogen concentration.
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PMID:Hormone levels in older women: a study of post-menopausal breast cancer patients and healthy population controls. 213 30


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