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

Paraffin-embedded tissue sections from 29 patients with primary liver carcinomas were retrospectively studied for the presence of estradiol and testosterone using the peroxidase-antiperoxidase (PAP) technique. Twenty-seven hepatomas and two cholangiomas were treated with antiestradiol and antitestosterone primary serum. Estradiol was detected in 17 cases and testosterone in 11 cases of hepatomas. The two cases of cholangiocarcinoma were positive for estradiol and negative for testosterone. The immunohistochemical reaction in the tumor cells was mainly cytoplasmic and in a few cases both cytoplasmic and intranuclear. The positivity of the reaction in the tumour cells was compared with that of the adjacent non-neoplastic liver tissue and bile duct cells. Our findings were also analyzed in relation to tumor differentiation and the age and sex of the patients.
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PMID:Immunohistochemical study of sex steroid hormones in primary liver cancer. 307 82

A malignant hamster melanoma cell line HM-1 derived from the heterogenous malignant hamster melanoma MM1 contains a specific, high affinity binding protein for estrogens. Partial purification of the binding protein with ammonium sulfate (40% saturation) increased mean binding content (3.1 +/- 1.2 (SD) fmol/mg protein) 15-fold without any change in affinity (10(10) M-1). The binding protein sedimented at 8-9S on 10-30% low salt sucrose gradients and 9-10S in the presence of 20 mM molybdate ion. Addition of 0.4 M KCl shifted the 8S peak to 4S. Binding was specific, saturable, and indicative of a single class of high affinity sites over a concentration range of 0.01-10.0 nM [3H]estradiol. Estradiol produced a dose related inhibition of HM-1 growth in vitro without altering the growth of an additional line (HM-2) which did not bind estrogen. The antiestrogen tamoxifen (10(-7) M) also significantly inhibited HM-1 melanoma growth in vitro, which was reversed by the addition of estradiol (10(-9) M). HM-1 xenografts grew faster in female BALB/c-nu/nu mice than male mice while there was no sex difference in HM-2 growth. Pharmacological doses of estradiol and the antiestrogen nafoxidine significantly inhibited HM-1 growth without altering tumor incidence or latency. Our observations suggest that HM-1 cell lines bind estrogens specifically and with high affinity and that hamster melanoma cells positive for this binding protein respond to estrogen.
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PMID:Inhibition of hamster melanoma growth by estrogen. 309 10

The effects of the synthetic antiprogestin mifepristone (RU486) on growth of dimethylbenzanthracene (DMBA)-induced mammary tumors in female rats were investigated. Prophylactic treatment with mifepristone (10 mg/kg/day) for 3 weeks starting from the day of first DMBA injection resulted in a doubling of the average tumor latency period (81 +/- 16 days, n = 17 treated, versus 39 +/- 5 days, n = 75 controls; P less than 0.005) and was accompanied by a significant growth retardation as shown by lower body weight increments. A 3-week therapeutic treatment of rats bearing mammary tumors was performed by administration of different dosages of mifepristone (2.5, 10, or 40 mg/kg/day) or megestrol acetate (2.5 or 10 mg/kg/day), with the luteinizing hormone-releasing hormone agonist buserelin (40 micrograms/kg/day), buserelin plus mifepristone (10 mg/kg/day), or by ovariectomy. The effects of treatment on tumor load, pituitary, adrenal and reproductive organ weights, steroid receptor contents of mammary tumors, and blood plasma hormone concentrations were investigated. Mifepristone and megestrol acetate treatment gave rise to inhibition of mammary tumor growth with all dosages studied, in which mifepristone was more potent than megestrol acetate (80%-90% vs 40% inhibition, P less than 0.01). In contrast, buserelin treatment and ovariectomy resulted not only in inhibition, but in tumor remission by about 50%. Combined treatment with buserelin and mifepristone gave the same tumor remission as resulted from ovariectomy or single treatment with buserelin. Estradiol-stimulated growth of the human mammary cancer MCF-7 cells in culture was fully abolished by mifepristone (3.6 X 10(-8) M) or tamoxifen (4 X 10(-8) M), whereas growth of MCF-7 cells under control incubation was not affected by either agent. Therefore, a direct inhibition of the growth of rat mammary tumor cells by mifepristone appears likely. Based on the effects of mifepristone on plasma hormone levels (increased: luteinizing hormone, estradiol, progesterone; unchanged: follicle-stimulating hormone, adrenocorticotropic hormone, corticosterone), organ weights (increased: pituitary, ovaries, uterus; unchanged: adrenals) and steroid receptor contents of mammary tumors (decreased: estrogen receptor and progesterone receptor contents), the main mechanism of action is probably a direct antiprogestational effect at the level of the mammary tumor cells through occupancy of the progesterone receptor.
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PMID:Comparison of the actions of the antiprogestin mifepristone (RU486), the progestin megestrol acetate, the LHRH analog buserelin, and ovariectomy in treatment of rat mammary tumors. 311 99

Physiochemical properties of an estrogen binding protein were characterized in three human melanoma cell lines, UISO-MEL-1, UISO-MEL-2, and UISO-MEL-4. Estrogen binding to melanoma cytosol was saturable, specific for estrogens, and represented by a single class of high-affinity, limited-capacity binding sites (Kd 5.5 x 10(-10) M, 2.7 +/- 0.5 fmol/mg of cytosol protein, UISO-MEL-2; 2.2 x 10(-10) M, 7.8 +/- 3.3, UISO-MEL-4) (SEM). UISO-MEL-1 cytosols did not bind estradiol. The binding protein in UISO-MEL-2 and -4 sedimented at 8.5S and 9.2S, respectively, in the presence of 10 mM sodium molybdate. Solid-phase radioimmunoassay with a monoclonal antibody specific for human estrogen receptor (H222 sp lambda) showed good correlation (r = 0.84) with a hydroxyapatite biochemical assay of identical melanoma cytosols. Exposure of UISO-MEL-2 to estradiol produced a time- and temperature-dependent increase in total nuclear receptor for estrogen in vitro. Estradiol treatment of athymic mice also significantly increased cytosol progesterone receptor content in UISO-MEL-2 and UISO-MEL-4 xenografts. Estradiol had no effect on the plating efficiency or growth of any melanoma cell line or normal melanocytes in vitro. Tamoxifen also had no effect on melanoma growth in vitro. In contrast, chronic exposure of athymic mice carrying estrogen receptor-positive UISO-MEL-2 to estradiol resulted in a sex-dependent increase in tumor latency and overall inhibition of tumor growth. Taken together, these observations suggest that a subset of human melanomas contains limited amounts of an estrogen binding protein similar to that observed in other estrogen-responsive tissues. The lack of effect of estradiol on melanocyte and melanoma growth in vitro, coupled with a decrease in tumor growth in athymic mice, suggests that, while inhibition may be receptor mediated, possible indirect actions of estradiol must also be considered.
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PMID:Effect of 17 beta-estradiol on the growth of estrogen receptor-positive human melanoma in vitro and in athymic mice. 319 86

The role of estrogens in the development of skin cancer is controversial. Sex steroids have a profound effect on the epidermis and epidermal appendages. Estradiol in pharmacologic doses has been reported to stimulate basal cell carcinoma in an animal model. Sex hormones act by means of a specific protein receptor. In this study we used a specific, highly sensitive monoclonal antibody to evaluate sex steroid receptors in human basal cell carcinoma. No estrogen or progesterone receptor protein was detected in the basal cell tumor, despite clear positive control tissues. We conclude that these sex steroid receptors are not present in significant amounts to mediate a direct effect in basal carcinoma.
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PMID:Determination of sex steroid receptor in human basal cell carcinoma. 329 Feb 80

Estradiol-17 beta was previously shown to stimulate glucose transport (as measured by phosphorylation of 2-deoxyglucose) in rat uterine tissue in vivo (Meier, D.A. and Garner, C.W. (1987) Endocrinology 121, 1366-1374) but attempts to demonstrate this in uterine organ strips in vitro, in uterine tumor cell lines or in uterine cells in primary culture have been unsuccessful. However, aqueous uterine extracts and uterine luminal fluid did stimulate glucose transport in uterine tumor cells and uterine cells in primary culture. Estradiol in vivo and uterine extracts in vitro each increased the initial rate of glucose transport 1.5- to 3-fold. In each case, 2-3 h were required for the stimulation to be fully expressed. The stimulation was not inhibited by cycloheximide suggesting that protein synthesis was not required. Uteri from ovariectomized rats injected daily for 4 days with 10 micrograms estradiol contained 4-fold more activity than uteri from saline-injected control animals. The activity was acid- and heat-stable, inactivated by trypsin treatment but not removed by dextran-coated charcoal treatment, suggesting that the activity is (or is associated with) a protein. The activity eluted in the 6-12 kDa range upon chromatography on Sephadex G-50. Insulin (1-1000 ng/ml) and epidermal growth factor (1-100 ng/ml) stimulated glucose transport, but only less than 50% of the stimulation by extracts. The substance(s) present in the extracts, possibly a known growth factor, may be involved in the estradiol stimulation of glucose transport and other estradiol actions in vivo.
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PMID:Stimulation of glucose transport in cultured uterine cells by rat and rabbit uterine extracts. 329 57

In both primary cultures and transformed tumor cultures of rat pituitary cells, preincubation with T3 or dexamethasone increases GH secretion, mRNA accumulation, and gene transcription. GRF stimulates secretion and transcription in primary rat pituitary cultures. Sex steroids stimulate GH secretion in man, but contradictory findings have been reported in vitro. We studied the hormonal regulation of bovine GH (bGH) in primary monolayer cultures of adult bovine pituitaries. Neither T3 nor dexamethasone changed immunoreactive bGH secretion during a 3-h experimental incubation. After 72-h preincubation with T3 or dexamethasone, bGH secretion remained unchanged. T3 (10(-8) M) or dexamethasone (10(-8) M) did not alter the bGH secretory response to doses of GRF from 10(-12)-10(-8) M. However, T3 (P less than 0.001; r = 0.73) and dexamethasone (P less than 0.001; r = -0.71) decreased bGH mRNA content in dose-dependent fashions, as determined by Northern analysis and RNA dot blots probed with 32P-labeled bGH cDNA. T3 10(-7) M) decreased bGH mRNA content to 70% of the control value, 10(-7) M dexamethasone decreased bGH mRNA content to 77% of the control value, while GRF increased bGH mRNA content to 174% of the control value in a dose-dependent fashion (P less than 0.001; r = 0.72). Preincubation with testosterone or dihydrotestosterone did not change basal or GRF-stimulated GH secretion. Seventy-two-hour preincubation with 10(-8) M estradiol did not alter basal GH secretion, but increased the bGH secretory response to doses of GRF from 10(-11)-10(-8) M (P less than 0.001). Incubation with estradiol did not change bGH mRNA levels. These results demonstrate that, in contrast to rat GH mRNA, bGH mRNA accumulation is inhibited by T3 and dexamethasone. Estradiol augments the response to GRF, but this effect is not mediated by an increase in mRNA content. The hormonal responses of somatotropes vary significantly among mammalian species.
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PMID:Hormonal regulation of growth hormone secretion and messenger ribonucleic acid accumulation in cultured bovine pituitary cells. 334 13

Sixteen steroids with different endocrine activities were administered to female rats for 6 or 7 days, in a broad range of doses. Liver growth was recorded by measuring weight and DNA contents and monooxygenase activity by assaying the turnover of five different substrates. According to their effects on these parameters steroids were assigned into one of the following three groups: (a) Estrogens estradiol and ethinylestradiol, as well as the progestins norethynodrel and norethisterone (norethindrone) which have estrogenic activity in rats. These agents induced pronounced liver growth and excessive DNA increase which was not associated with major monooxygenase induction. (b) A different type of response consisted of liver growth and DNA increase associated with a pronounced induction of monooxygenase(s) in a characteristic pattern. This response was elicited by pregnenolone-16 alpha-carbonitril, by progestins progesterone, cyproterone acetate, and medroxyprogesterone (but not gestoden and levonorgestrel), by the antimineralocorticoid spironolactone and by the glucocorticoids cortisol and dexamethasone. Apparently, this response pattern was not related to any specific endocrine action but to certain structural features, in particular to the presence of a saturated, at least two-membered alkyl substituent at C17 of the steroid ring system. (c) No or small effects were observed after gestoden, levonorgestrel and the androgens testosterone and methyltestosterone. Dose-response stuides revealed that estrogens estradiol and EE2 induced hepatic effects more potently by four orders of magnitude than progestins. The response patterns observed may be relevant to the tumor-promoting activity of some of the steroids tested.
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PMID:Quantitative structure-activity studies on effects of sixteen different steroids on growth and monooxygenases of rat liver. 335 10

We have examined the estrogen responsiveness and estrogen receptor in medullary thyroid carcinoma using a model of an established human cell line, TT. TT cells bind [3H]estradiol with high affinity. Scatchard analysis reveals a single class of binding site with a concentration of 173 fmol/10(6) cells and a dissociation constant of 2.1 x 10(-9) M, values which are comparable to those of a well established model cell line for estrogen responsiveness, MCF-7 human breast cancer cell line. Estradiol in physiological concentrations moderately stimulated TT cell proliferation, whereas in pharmacological concentrations it markedly inhibited cell growth. [3H]Thymidine incorporation into acid-insoluble material was also stimulated following a 5-day treatment with 5 x 10(-9) M estradiol. Tamoxifen at a concentration of 1 microM reduced cell proliferation by 43-48% after 5-7 days of treatment. The growth suppression induced by tamoxifen was reversed by addition of 10 nM estradiol. This is the first report of estrogen growth stimulation and tamoxifen growth inhibition of a tumor cell line derived from human medullary thyroid carcinoma.
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PMID:Estrogen receptor and hormone responsiveness of medullary thyroid carcinoma cells in continuous culture. 335 36

The agonist high- and low-affinity states of the dopamine (DA) receptor were investigated with apomorphine competition for [3H]spiperone binding to DA receptors in 7315a tumors grown in intact female rats, while the antagonist site was investigated with saturation of [3H]spiperone binding. Such as for the intact pituitary, the antagonist binding site density in 7315a tumors was not affected by NaCl and/or Gpp(NH)p, and its binding affinity was increased in the presence of NaCl. The DA receptor in 7315a tumors existed in high- and low-affinity agonist states, and the two apomorphine sites had similar affinities in tumoral and intact tissue. However, the proportion of the high affinity state was slightly lower in the 7315a tumor compared to intact tissue. Tumor (7315a) growth in ovariectomized rats was slower than in intact animal; chronic 17 beta-estradiol treatment inhibited growth of these tumors. Prolactin (PRL) concentration and density of DA receptors were higher in tumors grown in ovariectomized than in intact female rats, whereas both decreased after 23 days of 17 beta-estradiol treatment. Estradiol treatment decreased the affinity of the high- and the low-apomorphine binding sites, whereas their proportions remained unchanged. Thus, changes of DA receptors and 7315a tumor growth seem to be related; however, their relationship is complex.
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PMID:Estradiol and guanine nucleotide modulation of dopamine receptor agonist and antagonist binding sites in 7315a pituitary tumors. 339 Feb 4


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