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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From the first day of dimethylbenzanthracene administration, daily treatment with 8 or 24 mug of the new antiestrogen 11alpha-methoxy ethinyl estradiol (RU 16117) completely prevented the appearance of mammary tumors in all animals up to the last time interval studied (130 days after dimethyl benzanthracene administration). At daily doses of 0.5 and 2.0 mug RU 16117, the tumor incidence was reduced to 78.6 and 40%, respectively. Not only was the number of animals developing tumors reduced after injection of low doses of RU 16117, but the number of tumors per rat and the size of tumors were also markedly reduced. The levels of receptors for estradiol, progesterone, and prolactin in tumor tissue were reduced after treatment with 2.0 mug RU 16117, while the binding of growth hormone and insulin was not affected. Whereas plasma luteinizing hormone levels decreased after treatment with 8 or 24 mug RU 16117, plasma prolactin levels slightly increased in animals receiving the highest dose of the antiestrogen. It is thus likely that the potent inhibitory effect of RU 16117 on the development of dimethylbenzanthracene-induced mammary tumors results from actions at both the hypothalamic-pituitary and the tumor (mammary gland) levels, the action at the peripheral level possibly being secondary to a reduced sensitivity of the tissue to circulating hormones through lowering of hormone receptor concentrations.
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PMID:High inhibitory activity of a new antiestrogen, RU 16117 (11alpha-methoxy ethinyl estradiol), on the development of dimethylbenz(a)anthracene-induced mammary tumors. 18 38

Newborn female mice of three strains--BALB/cfC3H [mammary tumor virus (MuMTV)-infected], BALB/c, and C57BL (both virus-free)--were given injections of 17beta-estradiol or testosterone, alone or in combination with ovine prolactin, for the first 5 days of life. Half of each group of mice were ovariectomized at 40 days of age, and all mice were killed between 6 and 16 months of age. Mammary glands of BALB/cfC3H mice receiving steroid hormones were better developed than those of mice not receiving steroids. Androgen induced a higher incidence of grossly dilated ducts and secretion-filled alveoli. Mammary nodule and tumor incidences were higher in steroid-treated mice than in controls; androgen resulted in higher incidences than did estrogen. The age of onset of mammary tumors was also earlier after neonatal steroid treatment. In BALB/c mice, neonatal injections of estrogen induced some alveolar development of the mammary gland; neonatal injections of ovine prolactin had a greater effect. The mammary glands of C57BL mice did not show any evidence of stimulation by neonatal hormone treatment, which indicated the probability of strain differences. However, no nodules or tumors occurred in these MuMTV-free strains. Therefore, MuMTV was essential for neoplastic mammary responses to neonatal hormone treatment. Ovariectomy prevented alveolar development and abnormal changes in the mammary glands of all groups, thus indicating that ovary-independent alterations in the mammary gland were not induced by neonatal steroid treatment. We concluded that neonatal steroid exposure resulted in increased mammary tumor risk in mice, but only in the presence of both MuMTV and ovaries.
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PMID:Long-term effects of neonatal steroid exposure on mammary gland development and tumorigenesis in mice. 18 88

Specific iodine-125-labeled prolactin binding was measured in membrane particles prepared from R3230AC mammary carcinoma and liver of tumor-bearing Fischer rats after either prolactin, estrogen, or lergotrile mesylate treatment, or after the induction of diabetes by streptozotocin. Hormone binding to tumors was decreased by treatment with prolactin (.5 or 1 mg/day) or estradiol valerate (7.5 mg/kg/week). In contrast, prolactin treatment was without affect on prolactin binding to liver membrane particles, but estradiol valerate treatment resulted in a 4-fold increase in prolactin binding to this tissue. Lergotrile mesylate, which lowers plasma prolactin levels, had no affect on tumor growth or prolactin binding to either tumor or liver. Prolactin binding to both tumor and liver was significantly reduced in diabetic rats, suggesting that insulin may play an important role in controlling tissue sensitivity to prolactin. Specific binding of iodine-labeled prolactin to enzymatically dissociated cells from R3230AC tumors was demonstrated in vitro. The binding capacity of the cells was found to be of the same order of magnitude as the binding capacity in membrane preparations when appropriate corrections were applied for yields of cells and membranes. R3230AC tumor, which is responsive to prolactin, appears therefore to be a useful model system for further study aimed at elucidation of growth and metabolic response to the hormone prolactin in breast cancer.
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PMID:Prolactin binding to R3230AC mammary carcinoma and liver in hormone-treated and diabetic rats. 18 51

The effect of prolactin in supporting the growth of 7, 12-dimethylbenz(a)anthracene-induced mammary tumor in adult female Sprague-Dawley rats was investigated when estrogen receptors were blocked by the nonsteroidal antiestrogen, Tamoxifen, ICI 46,474. Following an oophorectomy-induced remission, perphenazine, which stimulates endogenous prolactin release, was able to restore tumor growth whether or not Tamoxifen was added. A second course of perphenazine treatment, instituted after the tumors were allowed to shrink, was again effective in stimulating tumor growth. After a regression in tumor size induced by oophorectomy and daily administration of Tamoxifen, perphenazine was able to restore original tumor size despite continued treatment with Tamoxifen. In intact rats, after regression was obtained by daily administration of Tamoxifen and the prolactin inhibitor, lergotrile mesylate, perphenazine induced tumor growth when the latter was discontinued, even though Tamoxifen was continued for 50 days. Estrogen receptors measured at the time of maximum stimulation by perphenazine were undetectable. On the other hand, estradiol did not stimulate tumor growth when serum prolactin was depressed to undetectable levels by lergotrile. These results indicate that prolactin supports the growth of 7, 12-dimethylbenz(a)anthracene-induced rat mammary tumor and that estrogen receptors are not required under these conditions.
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PMID:Predominant role of prolactin in stimulating the growth of 7, 12-dimethylbenz(a)anthracene-induced rat mammary tumor. 19 Nov 82

It is unequivocal that prolactin is an influential hormone in murine mammary tumorigenesis. The Berenblum hypothesis (7), a well-known theoretical model of tumorigenesis that depicts this oncogenic process as a two-step mechanism, i.e., initiation and promotion, is a conceptual scheme in which the action of prolactin in mammary tumorigenesis may be understood. According to this conceptual model, prolactin would participate in both the initiation and promotion steps of mammary tumorigenesis, In the initiation phase, variations in prolactin secretion appear to influence the metabolism of the mammary epithelium, so that the epithelium would be either more receptive to or refractory to an initiating agent (e.g., chemical carcinogen, physical carcinogens, oncogenic viruses, ets.) i.e., a permissive action. In the promotion phase, prolactin may act as either a promoter or an antipromoter of the "transformed" mammary epithelium. In promotion, the hormone may either directly or indirectly (via the ovary) stimulate mitotic activity of the "transformed" epithelium. In antipromotion the hormone, in the presence of requisite hormones (e.g., glucocorticoids), may synergistically induce differentiation (e.g., lactation) in the "transformed" epithelium. A tumor would result in the former (promotion) but not in the latter (antipromotion) case. Whether or not prolactin is significantly influential in human breast tumorigenesis remains to be determined. This is an extremely important area of research which is justifiably receiving increased attention. For if prolactin can be shown to influence human breast epithelium in a manner similar to its effect on rodent mammary tissue, then prophylactic and/of chemotherapeutic control of human breast tumorigenesis may be feasible by appropriate drug-mediated prolactin suppression.
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PMID:Prolactin and murine mammary tumorigenesis: a review. 19 Nov 83

In this investigation, prolactin receptor sites were localized by autoradiography in 7,12-dimethylbenz(a)anthracene (DMBA)-induced mammary tumors from rats. Tumors were removed when they reached the size of 2 X 4 cm and sliced to a thickness of .5 mm. Sections cut from the slices were incubated for 3 hours in medium 199 (1% bovine serum albumin, 5 mM CaC12, 5mM HEPES buffer) at pH 7.4 and 400,000 counts/minute of iodine-125-ovine prolactin in the presence or absence of 1 mcg of unlabeled prolactin. After further preparation and storage for 4 months in a light-tight box slides were developed, fixed and stained and then photographed. All tumors were labeled by iodine-125-ovine prolactin. Prolactin receptors were associated with only half the total cells. Specific prolactin binding was confined to tumor cells and nonspecific binding was present in alveolar spaces and connective tissue. In some tumors prolactin recepotrs were found in all tummor cells, whereas in other tumors half of the cells did not contain any receptors, or very few. Reproductions of autoradiographs illustrate findings. Results suggest that variations in receptor content of the tumors may be caused by 2 distinct populations of cells. 1 type contains many receptors and the other very fewreceptor sites, or none at all.
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PMID:Autoradiographic localization of prolactin receptors in 7,12-dimethylbnez[a]anthracene-induced rat mammary carcinoma. 19 27

The generally accepted classification of pituitary adenomas into eosinophilic, basophilic, mixed, and chromophobe types has not been very useful since no clear correlation exists between the staining character of the tumor cells and the clinical syndrome produced. The ultrastructural examination of different adenoma types with clinically manifest endocrine activity (acromegaly, amenorrhea-galactorrhea-syndrome, Cushing's disease) shows that the type of hormone secreted can only be determined in few cases. The ultrastructure is more representative of the activity of the secretory process than of the type of the product. Histoimmunological methods achieve the specific identification of the various types of adenomas with endocrine symptomatology. The so-called "chromophobe" adenomas, which only manifest signs of a space occupying lesion with pituitary insufficiency of varying degree and compression of the visual pathways, represent a mixed group. The majority of the cases (about 60%) shows increased prolactin secretion with amenorrhea or loss of potency, but without galactorrhea or gynecomastia. A small group of cases may either produce normal hormones (growth hormone or prolactin) at a very low rate, or secrete hormone fragments or abnormal, as yet undeterminable substances. The oncocytomas, which stain with eosin in light microscopy, seem to suffer from a defective metabolism and therefore may have lost the ability of hormone production.
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PMID:[Functional histopathology of pituitary neoplasms (author's transl)]. 19 40

The specific binding of labeled porcine insulin, human prolactin, and human growth hormone was studied in 63 human breast tumors and 15 nonmalignant breast tissues. Most (90%) of the tumors demonstrated significant binding of insulin, as did 80% of nonmalignant tissues. Autoradiographic studies indicated that insulin bound dominantly to tumor cells, rather than to fat and fibrous tissue contained within tumors. Specific binding of prolactin and growth hormone of greater than 1% was seen in 20 and 12% of tumors, respectively, and one tumor studied in detail showed a small amount of saturable, high-affinity prolactin binding. The affinity of binding of insulin and prolactin to tumor was similar to that seen in target tissues in subprimate species (Kd = 4 X 10(-10) M), but the prolactin-binding capacity in the one tumor studied in detail was very low (10 fmoles/mg membrane protein), compared with prolactin-responsive experimental mammary carcinoma.
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PMID:Hormone binding by human mammary carcinoma. 19 30

A 37-year-old woman had symptoms of Cushing's disease for two years. Galactorrhea was present. The diagnosis was confirmed by finding intermittently elevated urinary 17-hydroxysteroids, absent circadian rhythm, and elevated plasma ACTH. Plasma prolactin was slightly elevated. Films of the sella turcica were normal. A 9 mm basophilic microadenoma was removed by the transphenoidal approach. Immunocytochemical and electron-microscopic studies showed that the tumor was composed exclusively of ACTH secreting cells. Endocrine re-evaluation one year later revealed normal adrenal function. Serum prolactin had returned to normal. This case provides further evidence that Cushing's disease can be caused by a pituitary microadenoma insufficient in size to deform the sella.
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PMID:Cure of Cushing's disease by transsphenoidal removal of a microadenoma from a pituitary gland despite a radiographically normal sella turcica. 20 60

Prolactin receptors have been identified in estrone-progesterone induced mammary tumors from GR mice. 125I-labeled ovine prolactin binding to tumor homogenates reached a steady state in 12 hours at 22 degrees and was specific for prolactin. Prolactin receptors were highest (16 fmoles/mg protein) in primary, hormone-dependent tumors and declined progressively in transplanted hormone-dependent and transplanted hormone-responsive tumors. In autonomous tumors, binding was approximately 5% of that found in primary tumors. Scatchard analysis of binding to selected tumors indicated that the observed decrease in bound hormone was due to a loss in the number of receptor sites; binding affinity was unaltered (kd approximately 1 X 10(-10) M). Since receptors for estrogen and progesterone as well as those for prolactin decline in a concerted manner with the transition to autonomy, autonomous growth may result from a loss of receptors or an increase in the relative proportion of autonomous cells present in the tumor.
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PMID:Prolactin receptors in mammary tumors of GR mice. 20 73


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