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

The metabolic mechanism for increased circulating free fatty acids in post-menopausal women with metastatic breast cancer was investigated. Hormone and metabolic response to glucose and growth hormone were compared to cancer patients and control subjects; thyroid, adrenal and pituitary function were evaluated. The results of these studies indicated that breast cancer patients had glucose intolerance and delayed and prolonged insulin secretion, increased basal growth hormone levels and insensitivity of adipose tissue to growth hormone. Cortisol and protein-bound iodine levels were normal and there was no lipolytic factor in the sera of breast cancer patients. The changes observed in breast cancer patients were not attributable to age, obesity, inanition or stress. These metabolic abnormalities may characterize host susceptibility to breast cancer or be effects of tumor.
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PMID:Metabolic parameters in women with metastatic breast cancer. 4 95

Hormone deprivation may cause remission in women with advanced breast cancer. Occasionally this remission may last for 15 years. However, only 30% of women respond in this way. An essential 1st step in the response of hormone-sensitive tissues is binding of the hormone to a receptor protein in or on the target cell. For steroids, receptors have been found in the cytoplasm, while for polypeptide hormones, receptors seem to be on the surface of cell membranes. Between 40-85% of human breast cancers contain estrogen receptors. If estrogen receptors are present, 43-60% of patients have responded to endocrine therapy, whereas only 8% have responded if estrogen receptors were not present. Treatment with antiestrogens has achieved 16% response rates in patients in whom estrogen receptors were not present. Progesterone receptors have been detected in 57% of breast cancers, together with estrogen receptors in 49%. The significance of this finding is not apparent. The main peptide hormone implicated in promoting growth of breast cancers is thought to be prolactin. Growth hormone and human lactogen have also been implicated in promoting breast cancer. Receptors may be detected in human breast, prostate, endometrial, and other cancers and these preferentially bind estrogen, androgen, progesterone analogue, prolactin, growth hormone, or placental lactogen. The heterogeneity of human cancers is thus shown. Most remissions are short-lived and after relapse there is less chance for antihormonal therapy. To choose the best treatment at a given time the most hopeful prospect is that investigations may determine criteria for the study of the particular cancer in each patient.
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PMID:Editorial: Hormone receptors and breast cancer. 17 60

Prolactin receptors have been identified for the first time in a number of human breast cancer cell lines and a normal human breast cell line maintained in long-term tissue culture. Optimal conditions for determining the binding of 125I-labeled human prolactin to these cells were established. Five different tumor cell lines have different content of prolactin receptors ranging from 2,300 to 26,000 sites/cell. All tumor cell lines contained more prolactin receptors than does one normal breast cell line (1700 sites/cell). The prolactin receptors in these human mammary tumor cells not only bind human prolactin but also recognize other lactogenic hormones such as human growth hormone, human placental lactogen, and sheep prolactin, but not animal growth hormone, which are not lactogenic. The affinity (Ka) of binding of human prolactin to these cells is 4 x 10(9) M-1 (Kd = 2.5 x 10(-10)M). The hormone specificity and affinity for hormone of these human mammary tumor cells are very similar to that found for the rabbit mammary gland. These human mammary tumor cell lines in long-term culture should prove very useful to study the biology of prolactin receptors in living human cells and the role of prolactin in the tumorigenesis of the human breast.
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PMID:Prolactin receptors in human breast cancer cells in long-term tissue culture. 22 85

Tamoxifen (ICI 46474), an antiestrogen, was given to 89 selected patients with stage IV breast cancer at a dose of 20 mg orally every 12 hours. Forty-seven percent of the patients had objective tumor regression averaging 11+ months with 25 of 42 women still in remission. In the first 39 patients where the minimum follow-up period is 16 months the average duration of remission is more than 15 months with 8 of 19 patients still in remission. These results are approaching those of surgical hypophysectomy, where, in our experience the average remission lasts about 18 months. Thus, Tamoxifen is a highly effective antitumor agent and is probably the initial treatment of choice for women with hormone responsive breast cancer. Antiestrogen induced objective remissions in 5 of 19 patients who had previously responded to surgical hypophysectomy, and 5 additional patients showed no progression of disease lasting 15+ months. Estradiol and estrone were detectable in the serum of these patients whereas, prolactin and growth hormone were not detectable. Thus, antiestrogen can induce remissions in some patients in the absence of the pituitary gland, and this constitutes additional palliation and provides evidence that estrogens can directly stimulate tumor growth. Four of 7 patients who obtained remissions from Tamoxifen obtained further improvement from hypophysectomy, and 1 of 8 patients who failed to benefit from antiestrogen improved after hypophysectomy. These results suggest that prolactin and growth hormone may also play a role in stimulating tumor growth in some patients.
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PMID:Treatment of breast cancer with antiestrogen: approach to medical hypophysectomy? 61 66

To assess endocrinologic completeness of transethmoidal trans-sphenoidal hypophysectomy and the relation between postoperative pituitary hormone levels and relief of bone pain, we tested pituitary reserve by measuring base-line values of follicle-stimulating hormone and luteinizing hormone, thyrotropin-relasing-factor-stimulated thyrotropin and prolactin, and levodopa-stimulated growth hormone after hypophysectomy in 15 menopausal women with metastatic breast cancer. In all 15 bone pain diminished or disappeared within 24 hours of operation. Pituitary-function testing identified only one patient as having had an endocrinologically complete hypophysectomy. Base-line gonadotropin levels and thyrotropin-releasing-factor-stimulated prolactin were the most reliable measures of residual pituitary function. We conclude that transethmoidal trans-sphenoidal hypophysectomy may not totally ablate pituitary endocrine function; effective relief of bone pain in patients with metastic breast cancer can follow this procedure despite residual pituitary function and the lack of objective tumor remission.
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PMID:Endocrinologically incomplete transethmoidal trans-sphenoidal hypophysectomy with relief of bone pain in breast cancer. 65 92

1 Low doses of carbidopa/levodopa (12.5 mg 1-alpha-methyl-dopahydrazine, 125 mg levodopa) were administered orally to 29 patients with tumours of the breast (16 with breast cancer, 13 with benign breast disease). 2 Plasma dopa response curves were similar in all the patients studied. 3 Prolactin and growth hormone showed similar responses to carbidopa/levodopa irrespective of age or diagnosis. 4 Prolactin showed an unusual reponse in four patients which has not previously been recorded.
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PMID:The effect of low dose carbidopa/levodopa on prolactin and growth hormone concentrations in patients with breast cancer and in benign breast tumours. 65 81

Fragments of pituitary tissue obtained from a total of 37 patients with either breast cancer, diabetic retinopathy, galactorrhea, or acromegaly were dissociated into single cell suspensions prior to cell culture. Release of human growth hormone (hGH) and human prolactin (hPRL) into the culture medium was measured by radioimmunoassay. During a 3-week culture period, prolactin cells released 9--13 times the intracellular levels of hPRL at the time of seeding, whereas hGH release from growth hormone cells was only 1--2 times that of their initial intracellular level during this same time. Both growth hormone and prolactin cells retained distinctive ultrastructural features during culture. The prolactin cells responded to TRH stimulation by elevated release of PRL into the medium. No evidence for mitotic division of prolactin cells in vitro was found.
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PMID:Culture of human pituitary prolactin and growth hormone cells. 68 60

Hypothalamic threshold of sensitivity to homeostatic inhibition was studied by means of the dexamethasone test of inhibiting excretion of steroid hormones in 47 patients with the primary breast cancer of different age groups. Before the dexamethasone test and after it, blood specimens were taken for the following tests: daily variation of blood sugar or sensitivity to insulin action, cholesterol, lipoproteins, phospholipids, uric acid, growth hormone and insuline levels, and level of corticosteroids. On the base of the results obtained all the patients could be divided into two groups: 1. patients with signs of elevated threshold of hypothalamic sensitivity to inhibition and 2. patients without such signs. The breast cancer developing against the background of endocrine metabolic disturbances characteristic of advanced age is on the whole prognostically more favorable than tumors in women who have no disturbances of that kind. However, metabolic shifts characteristic of ageing obviously play an important role in creating a background that promotes higher incidence of mammary cancer in elderly subjects.
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PMID:Endocrine-metabolic criteria for distinguishing two pathogenetic types of breast cancer. 86 49

Mean 24-hr growth hormone, luteinizing hormone, follicle-stimulating hormone, estradiol, and progesterone concentrations determined preoperatively in 16 women with benign breast masses and 17 patients with breast cancer were similar to those levels found in 25 age- and weight-matched control subjects. Mean 24-hr testosterone levels, however, were significantly elevated in women with breast cancer evaluated in the luteal phase of their cycles and were normal in postmenopausal breast cancer women. In addition, serum thyroid-stimulating hormone, thyroxine, cholesterol, and triglyceride levels were normal in these subjects. Plasma cortisols and urinary 17-hydroxysteroid excretion tended to be higher in both the benign and malignant breast disease group and probably reflected preoperative anxiety. Hence, we have found normal concentrations of a variety of endocrine and other biochemical agents that can stimulate breast tissue growth and/or have been previously reported to be disordered in women with breast cancer.
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PMID:Twenty-four-hour preoperative endocrine profiles in women with benign and malignant breast disease. 92 46

Several somatostatin analogs with recently synthesized acetylated N terminus were assayed in vivo for their effects on sodium pentobarbital-stimulated growth hormone (GH) levels in fed male rats and gastrin-releasing peptide (14-27)-stimulated gastrin levels in fasted male rats. The binding characteristics of these analogs to somatostatin receptors were also examined in various human tumors and normal tissues. The analog RC-101-I, injected at a dose of 0.1 micrograms/100 g body wt, significantly suppressed GH release (P less than 0.01) for at least 2 hr. Analog RC-160-II caused the longest inhibition of GH release, greater than that induced by nonacetylated parent analog RC-160, with GH levels showing significant suppression (P less than 0.01) for more than 3 hr. Analogs RC-160-II and RC-101-I and RC-160, injected at a dose of 1.0 micrograms/100 g body wt, significantly (P less than 0.01) suppressed gastrin-releasing peptide (14-27)-stimulated serum gastrin. Analog RC-101-I was active in this test at a dose of 0.1 micrograms/100 g body wt. RC-160-II showed significant binding to somatostatin-14 receptors in all investigated tissues (human colon, human colon cancer, breast cancer, human pancreas and pancreatic cancer, human prostate and prostate cancer, and rat cerebral cortex), but there were marked variations in binding affinities among various normal and cancerous tissues. The highest affinity was found in membranes of colon cancer (Ka = 18.4 nM-1) and breast cancer (Ka = 12.46 nM-1). The binding affinity of RC-160-II to somatostatin receptors in membranes of the breast cancer was similar to that of RC-160. RC-101-I showed higher binding affinity to somatostatin-14 receptors than RC-160 in human breast, pancreatic, and prostate cancer. With the exception of breast cancer tissue, the binding affinity of RC-101-I was significantly lower than that of RC-160-II in membranes of all investigated tissues. It can be concluded that acetylated somatostatin analogs RC-101-I and RC-160-II possess prolonged and enhanced biological activities in suppressing serum GH and gastrin in rats. Significant variations in binding affinities for these analogs in different tissues and various tumors suggest that differences may exist between somatostatin receptors in normal versus malignant tissues. This raises the possibility that some of these analogs could be used more selectively in the treatment of various neoplasms.
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PMID:Biological activity and receptor binding characteristics to various human tumors of acetylated somatostatin analogs. 134 89


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