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

Forty-three women underwent transsphenoidal hypophysectomy for metastatic breast cancer. Endocrine tests (luteinizing hormone, follicle-stimulating hormone, thyrotropin, prolactin and growth hormone) were done in 28 patients to evaluate the completeness of the procedure. Response of the metastatic breast cancer and duration of survival after hypophysectomy were determined and statistically compared with the posthypophysectomy hormone levels. Only one patient had an endocrinologically complete hypophysectomy, but the objective remission rate (32 percent) is comparable to the 30 to 40 percent objective remission rate reported in other studies that claim to have achieved complete hypophysectomy. No statistically significant associations were found between the levels of the hormones measured and the type of response (objective, subjective or none) to hypophysectomy. However, objective responders survived longer than nonresponders (p = 0.01). When analyzing the associations of the various hormone levels with the duration of survival after hypophysectomy, a positive correlation (p less than 0.05) of peak thyrotropin levels with duration of survival was found. Our data indicate that the clinical benefit advanced breast cancer patients received from an endocrinologically incomplete hypophysectomy is probably as great as that received from an endocrinologically complete hypophysectomy. It appears that a nonspecific disturbance of the hormonal milieu may adversely affect the growth of breast cancer. More studies are needed to elucidate the nature of the endocrine disturbance produced by hypophysectomy and its effects on hormone-sensitive tumors.
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PMID:Role of endocrine function tests in the evaluation of transsphenoidal hypophysectomy for advanced breast cancer. 617 33

Following a review of studies on the presence of hormonal receptors in breast carcinoma, reference is made to personal experience with hormone treatment of 96 patients with breast cancer. On the basis of data obtained in clinical practice, it is concluded that in order to apply target hormone treatment, it is essential to carry out a full study of hormone receptors, not just as regards oestradiol, progesterone and prolactin but the others too (testosterone, glycocorticoids, insulin, thyroid and growth hormone).
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PMID:[Hormone receptors in breast cancer]. 626 54

Prolactin-binding sites were determined in 759 human breast tumor biopsy specimens. Ovine prolactin (oPRL) was used in the binding assay of 569 tumors with 13% of the tumors showing a positive content with more than 1% specific binding. Human prolactin (hPRL) was utilized for 343 tumors with 36% of the tumors binding 1% or greater of the added radioactivity. When human growth hormone (hGH) was used as the labeled ligand in 95 tumors, only 2% of the tumors specifically bound more than 1% of the hGH. A total of 153 tumors were assayed simultaneously with the use of labeled hPRL and oPRL. Whereas 10.4% of the tumors showed the presence of prolactin-binding sites (greater than 1% specific binding) when oPRL was used, an approximately threefold increase (29.4%) in tumors possessing prolactin receptors was revealed when hPRL was used as the labeled ligand. Therefore, hPRL is the preferred ligand for the assessment of prolactin receptor levels in human breast cancer biopsy specimens.
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PMID:Prolactin receptors in human breast tumors. 627 92

The presence of receptors for lactogenic hormones in human breast cancer tissue has been documented previously, but the relationship between the expression of these receptors and estrogen receptor (ER) status has not been adequately studied. In this report, the specificity of 125I-human growth hormone (HGH) binding in both cultured human breast cancer cell lines and tumor biopsies was studied to establish that HGH was a suitable ligand for investigating lactogenic receptor concentration in these tissues. In addition, the relationship between specific binding of 125I-HGH and ER concentration in human breast cancer was investigated. Specific 125I-HGH binding to 14 breast cancer cell lines in long term culture and to membrane preparations (microsomal and plasma membrane fractions) from 31 breast cancer biopsy specimens was examined. Human prolactin and HGH were approximately equipotent in inhibiting binding of 125I-HGH to both cultured breast cancer cell lines and to membrane preparations from breast cancer biopsy specimens. Competitive inhibition experiments using lactogenic and somatogenic hormones established that the specificity of 125I-HGH binding to breast cancer biopsy material was similar to that of cultured breast cancer cell lines and similar to that reported for subprimate lactogenic receptors. Saturable, high-affinity (Ka = 0.53 to 2.33 nM-1), low-capacity (330 to 6560 sites/cell) growth hormone binding sites were found on each of the ER-positive cell lines, whereas no specific 125I-HGH binding to ER-negative cell monolayers was detected. When all cell lines were considered, a significant linear correlation (r = 0.745, p less than 0.001) between ER and lactogenic receptor concentrations was found. Significant specific 125I-HGH binding, greater than 1% of the total radioactivity added, was detected in 20 of 31 (65%) breast tumor biopsy specimens. The mean affinity and capacity of the lactogenic receptor as measured in 8 separate membrane preparations were Ka = 0.52 +/- 0.09 (S.E.) nM-1 and 255 +/- 85 fmol/mg protein. Membrane preparations from ER-negative tumors (less than 3 fmol ER/mg cytosol protein) bound significantly less 125I-HGH than did membrane preparations from ER-positive tumor biopsies (1.22 +/- 0.44 versus 3.21 +/- 0.56%, p less than 0.05). A significant linear correlation between specifically bound 125I-HGH and ER concentration (r = 0.412, p less than 0.02) was demonstrated in the 31 breast cancer biopsy specimens studied.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Correlation of lactogenic receptor concentration in human breast cancer with estrogen receptor concentration. 632 92

Epidermal growth factor (EGF) may be important in regulating the growth of some breast cancer cells in vivo because of its mitogenic action on some breast cancer cell lines in vitro. Epidermal growth factor receptors (EGF-R) were measured in a series of breast tumors to determine what percentage of breast tumors express EGF-R and whether EGF-R was independent of expression of estrogen receptor and progestin receptor. Specific binding of 125I-EGF to membranes from pooled homogenates of breast tumors reached equilibrium after 45 min at 25 degrees and remained constant. Scatchard analysis of 125I-EGF binding indicated a single class of receptors with an apparent Kd of 2 nM and a binding capacity of 28 fmol/mg of membrane protein, and the binding of 125I-EGF was not effectively competed for by insulin, fibroblast growth factor, growth hormone, or prolactin. Specific binding of 125I-EGF of 1 fmol or greater/mg of membrane protein and 15% or greater specific binding was detected in 48% of 137 unselected primary and metastatic breast tumors. The frequency distribution of EGF binding values was unimodal, with a progressive decrease in the proportion of patients with high EGF binding values. The values of EGF binding ranged from 1 to 121 fmol/mg of protein, with an arithmetic mean of 8.4 fmol/mg of protein and a geometric mean of 3.2 fmol/mg of protein. Forty-two % of 24 metastatic breast tumors were positive for EGF binding, with an arithmetic mean of 6.3 fmol/mg of protein and a geometric mean of 4.1 fmol/mg of protein. The magnitude of EGF binding in individual tumors was independent of either estrogen receptor or progestin receptor levels, although the highest quantities of EGF binding were expressed by tumors lacking steroid receptors. Approximately 20% of the tumors in the study were EGF-R-positive and ER-negative, suggesting that the growth of these tumors may be regulated predominantly by a peptide hormone (EGF) rather than a steroid hormone (estrogen). EGF binding did not correlate significantly with age of the patients. Correlation analysis between EGF binding and the percentage of malignant and nonmalignant cell types present in sections of tumor adjacent to the area assayed for EGF binding indicated that the percentage of malignant cells is an important factor in determining the amount of EGF binding in tumor homogenates. The recent discovery of transforming growth factors which interact with the EGF-receptor system suggests additional roles for EGF receptors in breast cancer.
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PMID:Epidermal growth factor binding by breast tumor biopsies and relationship to estrogen receptor and progestin receptor levels. 633 48

We examined the cytosolic estrogen receptor (ER) level in tumor tissue from 77 patients: 36 meningiomas, 20 gliomas (12 glioblastomas, 2 cerebellar astrocytomas, 2 ependymomas, and 4 medulloblastomas), 8 neurinomas, 7 pituitary adenomas (2 prolactin-producing adenomas, 1 growth hormone-producing adenoma, and 4 nonfunctioning adenomas), and 6 metastatic brain tumors (1 from breast cancer, 4 from lung cancers, and 1 from colon cancer). Nuclear ER levels were assayed in 11 meningiomas and 2 glioblastomas. ER was determined by the dextran-coated charcoal method and calculated by Scatchard analysis. Cytosolic ER was detected in 100% of the pituitary adenomas, 50% of the meningiomas, 50% of the metastatic brain tumors, 25% of the neurinomas, and 15% of the gliomas. In gliomas, only medulloblastomas had ER activity. Nuclear ER was found in three premenopausal women with meningioma. The dissociation constant of the ER complex was, in each case, less than 10(-9) M. These observations suggest that some brain tumors may be responsive to estrogen via the cellular ER.
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PMID:Estrogen receptors in brain tumors. 650 47

The authors report the case of a 28 year old patient with a prolactin and somatotropin secreting pituitary adenoma who presented several months later with lobular carcinoma of the breast with lymph node metastases. This case raises the question of the role of prolactin and growth hormone in the pathogenesis and growth of breast cancer. It is noteworthy, in particular, because of the exceptional clinical manifestations.
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PMID:[Association of lobular epithelioma and hypophyseal adenoma in a young woman. A case report]. 653 47

The authors study the nyctohemeral changes of prolactin and growth hormone during the evolution of breast cancer and in fibrocystic mastopathy. Prolactin shows a circadian rhythm with higher amounts during sleep in cancer patients. Changes are not significant for fibrocystic mastopathy, although there is a tendency towards higher concentrations than in the control group. No significant changes were observed for the growth hormone.
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PMID:[Pre- and postoperative differences in the circadian secretion of prolactin in carcinoma of the human breast]. 668 Jul 77

The effect of tamoxifen on serum levels of basal prolactin and basal and stimulated growth hormone was assessed in 10 women with advanced breast cancer prior to and after 1 and 8 weeks of treatment. Tamoxifen had no effect on basal levels of either hormone or on insulin-stimulated growth hormone. Two of 4 patients undergoing arginine provocation testing had a partial response to tamoxifen and both exhibited marked diminution of growth hormone stimulation which was not seen in the non-responders.
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PMID:The effect of tamoxifen on plasma growth hormone and prolactin in postmenopausal women with advanced breast cancer. 668 48

We have demonstrated previously that many human cancer cell lines maintained in tissue culture possess specific cell surface receptors for human prolactin (HPRL) and human growth hormone (HGH). In the present studies, the biological response in vitro of one human breast cancer cell line, T-47D, to the two pituitary hormones was examined. T-47D cells, when grown on tissue culture dishes, display typical epithelioid characteristics; cells are flat and polygonal in shape and are very adhesive to the plastic substratum. Upon the addition of HPRL or HGH (10 to 1000 ng/ml), in the presence of hydrocortisone, insulin, and triiodothyronine, each at 1 microgram/ml, the T-47D cells became round and refractile. In addition, there was a dramatic reduction in the adhesiveness of the cells to the substratum; 80% of the hormone-treated cells were detached by trypsin (25 micrograms/ml) in 30 min at 37 degrees, as compared with 5% for cells not treated with hormones. These prolactin-induced changes could be abolished upon the addition of antiserum to prolactin. Neither HPRL nor the combination of hydrocortisone, insulin, and triiodothyronine alone was active, indicating a synergism between HPRL and hydrocortisone, insulin, and triiodothyronine. It was subsequently found that only hydrocortisone was required for the action of HPRL, and that human luteininzing hormone and ovine growth hormone were inactive, whereas ovine prolactin exerted a very weak effect. In addition, in the presence of hydrocortisone (or hydrocortisone, insulin, and triiodothyronine), HPRL (or HGH) retarded cell proliferation by 30%, whereas HPRL or hydrocortisone by itself had no effect on cell growth. Ultrastructural studies revealed that, accompanying cell rounding and reduced adhesion, HPRL and HGH increased the formation of intracytoplasmic lipid droplets in the T-47D cells. The increase in lipid synthesis was confirmed by the staining of cells with Oil Red O, and by monitoring the incorporation of [14C]acetate into lipid; HPRL stimulated lipid synthesis and accumulation by approximately 2-fold. Thus, receptor-positive human breast cancer cells are biologically responsive in vitro to HPRL and HGH.
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PMID:Alteration of cell shape, adhesion, and lipid accumulation in human breast cancer cells (T-47D) by human prolactin and growth hormone. 669 2


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