Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Estradiol and progesterone receptors were studied in 44 patients with meningiomas and correlated to the clinicopathological features and amount of preoperative corticosteroid therapy. Thirty-four (77%) of the meningiomas contained high titers of specific high-affinity cytosol [3H]promegestone (R 5020) binding sites (mean 2,902 fmol/g tumor; range 0-9,598 fmol/g tumor) whereas only miniscule amounts of a nonspecific cytoplasmic [3H]estradiol binding component (mean 48 fmol/g tumor; range 0-201 fmol/g tumor) were detectable. No nuclear binding activity for [3H]estradiol was demonstrable. There was no convincing correlation between high PR activity and the age, sex, or menopausal status of the patients. The correlation study between the amount of preoperative corticosteroid therapy with the amount of [3H]promegestone binding revealed no dose relationship. Correlating [3H]promegestone content with the histologic type, we found 96% of meningothelial, 71% of transitional, and 40% of fibroplastic meningiomas to contain progesterone receptors. The necessity of in vitro studies is stressed to assess the biosynthesis and biological activity of the progesterone receptor in meningiomas, which is apparently not estrogen regulated, as is the case in other estrogen target tissues.
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PMID:Estrogen and progestin receptors in meningiomas: clinicopathological correlations. 650 49

Brain tumors from 64 patients were studied for the presence of hormone binding. Estradiol binding was detected in 34 patients: 13 of 21 meningiomas, 4 of 8 schwannomas, 1 oligodendroglioma, 1 of 5 benign gliomas, 4 of 5 malignant gliomas, 5 of 11 metastatic tumors, and 6 of 11 pediatric tumors: 1 medulloblastoma, 2 malignant ependymomas, 1 benign astrocytoma, 1 malignant sarcoma, and 1 malignant teratoma. Eleven patients were studied for progesterone binding, which was measurable in 7: 1 schwannoma, 3 meningiomas, 1 malignant sarcoma (pediatric group), 1 astrocytoma--gemistocytic (pediatric group), and 1 metastatic adenocarcinoma. There were 41 females and 23 males in the study. Fifteen females were premenopausal, 18 were postmenopausal, and 8 were in the pediatric group. Of the 34 tumors with measurable estradiol binding, 23 occurred in females. In the progesterone group, 4 of the 7 tumors with measurable binding activity were from female patients. In the pediatric group, estradiol binding was detected in 1 medulloblastoma, 2 malignant ependymomas, 1 malignant teratoma, 1 malignant sarcoma, and 1 astrocytoma. Five of the 6 pediatric tumors with estradiol binding were malignant, and both pediatric tumors with progesterone binding were also malignant. Of the 10 gliomas studied, 4 of the 5 malignant tumors had estradiol binding, whereas only 1 of the 5 benign tumors showed binding. Our studies with the pediatric tumors and the gliomas suggest that a relationship exists between the malignancy of the tumor and the presence of hormone binding. The ubiquitous nature of the presence of hormone binding is discussed, as is the possible correlation between age, sex, histological grade, and significance of hormone binding in brain tumors.
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PMID:Hormone binding in brain tumors. 664 77

Estradiol and progesterone receptors were measured in tumor cytosols from 3 intact and 4 neutered female cats with spontaneously occurring mammary adenocarcinomas. Serum from 2 of the intact cats which had been in estrus 4 and 4 to 6 weeks before tumor excision contained progesterone concentrations of 16.2 and 2.2 ng/ml, respectively; serum progesterone in the other cats was less than 2 ng/ml. Estradiol receptors were not detected in any cytosols. Progesterone receptors were detected in all of the cytosols, in concentrations ranging from 4.0 to 11.7 (mean = 7.2) fmol/mg of protein. Scatchard plot analysis of tumor cytosol from an 8th cat with mammary adenocarcinoma revealed presence of high affinity progesterone binding with a dissociation constant (Kd) of 3.47 nM. Tumor receptor content could not be correlated with stage of the estrous cycle nor with whether the cat was intact or neutered.
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PMID:Progesterone receptors in feline mammary adenocarcinomas. 671 65

Experiments were performed to observe the role of estrogen receptor in the proliferation of androgen-dependent mouse tumor, Shionogi carcinoma 115. Estradiol and diethylstilbestrol inhibited tumor growth as well as the weight gain of seminal vesicles and prostate glands in intact male mice. Tamoxifen decreased the tumor weight in intact males. Both nitromifene given to intact mice and tamoxifen given to castrated androgenized mice decreased the weight of seminal vesicles, but increased tumor weight. Estradiol was bound to the androgen receptor of the tumor cytosol with relatively high affinity, whereas diethylstilbestrol, tamoxifen and nitromifene were not. These were effective competitors in the estrogen receptor present in the tumor cytosol. These results suggest that the estrogen receptor system in Shionogi carcinoma 115 inhibits the proliferation of tumor cells.
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PMID:Effects of estrogens and antiestrogens on androgen-dependent growth of Shionogi carcinoma 115: role of estrogen receptor. 674 83

A previously demonstrated synergistic interaction between diethylstilbestrol (DES) and radiation on rat mammary carcinogenesis was extended to another estrogen, 17-ethinylestradiol (EE2). These newly reported results with EE2 demonstrated that the previously reported synergistic interaction between DES and radiation is not confined to just DES. Instead, these new results implied that the synergistic interaction is a synergistic interaction between the estrogenic activity of DES and radiation on rat mammary carcinogenesis. Female inbred ACI rats were used. By the end of the experiment, no neoplasia was detected in rats bearing cholesterol pellets, with and without X-ray exposure. No significant tumor data were obtained from rats treated with 0.1 me EE2, with and without X-rays. Approximately 50% of the rats treated with DES and approximately 90% of the rats treated with 1 mg EE2 had 1 or more mammary adenocarcinomas (MAC). X-rays synergistically increased the number of MAC per rat in the groups implanted with DES or 1 mg EE2. X-rays also increased the trend toward earlier increased incidence of rats with MAC as compared to rats treated with estrogens only. All rats treated with DES and 1 mg EE2 had pituitary tumors. The mean weight of the pituitary tumors in the groups treated with 1 mg EE2 was approximately 1.5 times that of the groups treated with DES. Mean terminal plasma prolactin levels for rats treated with 1 mg EE2 or DES were, respectively, 17.5 and 9.5 times control values.
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PMID:Synergism of estrogens and X-rays in mammary carcinogenesis in female ACI rats. 694 82

Biopsy specimens from 52 consecutive cases of primary human breast cancer were collected over a period of seven months and included in a study for histochemical localization of estrogen binding sites (EBS), using a fluorescein labelled Estradiol conjugate. Cryostat frozen sections from each tumor were examined to determine the localization of the tracer and to evaluate the percentage of positive cells in a given tumor. Results are correlated with the values of the biochemical assay for the estrogen receptor (ER) protein done on the same tumor. The localization of EBS by a tracer is a simple technique that can be done and interpreted in any surgical pathology laboratory. It was concluded that this method could be a valuable supplementary technique to the biochemical assay; allowing more accurate selection of patients and prediction of their response to endocrine therapy. Clinical follow-ups are extremely necessary to evaluate the suitability and the accuracy of the technique in choosing breast cancer patients for endocrine manipulation.
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PMID:Cellular localization of estrogen binding sites in human breast cancer. 707 49

The present studies examined the biochemical characteristics which were carried on from parent cells during fusion of human skin fibroblasts (HSF) with spleen cells of BALB/c mice preimmunized with hormone-responsive and nonresponsive human malignant melanoma cells (HMMC-ShA and HMMC-SR). The melanoma cells used as immunogens were either unmodified or preincubated with vibrio cholera neuraminidase (VCN), with estradiol (E), or with progesterone (P). Responsiveness was monitored by (3H) thymidine and (35S) methionine incorporation. Responsiveness to estradiol, concanavalin A (Con A) and to phytoheamagglutinin (PHA) were carried out, whereas malignancy was suppressed extensively in the cloned hybrids. On the immunizing tumor cells, VCN treatment enhanced (3H) thymidine but reduced (35S)-methionine incorporation and malignancy of the estradiol responsive melanoma cells (HMMC-ShA). VCN treatment enhanced (3H)-thymidine incorporation, but had no effect on (35S)-methionine incorporation and malignancy of the estradiol nonresponsive HMMC-SR cells. Estradiol treatment enhanced plasminogen activator (PA) activity and malignancy, whereas progesterone treatment reduced (inhibited) plasminogen activator activity and suppressed malignancy of the immunizing tumor cells. The PA from estradiol-responsive and from nonresponsive melanoma cells differed in their electrophoretic mobility on polyacrylamide gel electrophoresis.
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PMID:Correlation between plasminogen activator activity of immunizing tumor cells and complement-mediated cytotoxic antibodies secreted by cloned hybrid cells. 719 36

The influence of individual stages of the rat estrous cycle during exposure to I-nitroso-I-methylurea (NMU) on mammary tumor incidence, latency, number, and cytosol receptor dynamics for estrogen and progesterone was determined. Virgin female Buffalo rats were separated into three groups on Day 53 according to their vaginal smear pattern. NMU (5 mg/100 g body weight, i.v.) was administered in three monthly doses beginning at 53 to 55 days of age on diestrus, proestrus, or estrus between 9:00 and 11:00 a.m. Groups of rats had their second and third injections of NMU on the same day of the estrous cycle as their initial injection. All animals were killed during the morning on a diestrus day. Receptors for estrogen and progesterone were determined by a modified dextran-coated charcoal method and by sucrose density gradient analysis. Mean latencies to first tumor appearance in diestrus, proestrus, and estrus groups were 104.4, 83.6, and 91.4 days, respectively (p less than 0.05, diestrus versus estrus and proestrus) following the first NMU injection. The mean number of tumors per rat was significantly higher in rats injected on proestrus (4.5) or estrus (4.3) than on diestrus (2.0). Estradiol bound to receptor sedimented at 8 and 4 s and was suppressed by diethylstilbestrol and estradiol. Progesterone receptor migrated to 7.8 and 4 s regions. Estrogen receptor incidence (100%) and content (16.7 fmol/mg cytosol protein) was highest in rats injected on diestrus. In the proestrus and estrus injected groups, estrogen receptor incidence was 95 and 63% and content was 10.2 and 11.2 fmol/mg protein, respectively. The affinity of estradiol for its receptor was not significantly altered in any group. Although there were no statistically significant difference in progesterone receptor incidence or affinity between groups, progesterone receptor content (74.6 fmol/mg cytosol protein) was significantly higher in tumors from rats injected on proestrus than on diestrus. These data suggest that the prevailing hormonal milieu of the estrous cycle during NMU exposure may be critically important to the subsequent biological behavior and steroid receptor status of carcinogen-induced rat mammary tumors.
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PMID:Influence of the estrous cycle during carcinogen exposure on nitrosomethylurea-induced rat mammary carcinoma. 719 91

Steroidogenic function of a locally invasive hilus cell tumor of the ovary was studied. Serum levels of testosterone, androstenedione, dihydrotestosterone, 17 alpha-hydroxyprogesterone, progesterone, and estradiol were measured in blood samples from the peripheral and the ovarian vein. The tumor was secreting all but estradiol. Concentrations of progesterone and 17 alpha-hydroxyprogesterone were greatly elevated. Testosterone and dihydrotestosterone were the predominant androgens secreted by the tumor. Estradiol concentrations were elevated but without a significant peripheral-ovarian gradient. Concentrations of all the steroids coming from the tumor were increased paradoxically in the peripheral circulation after administration of dexamethasone, and the tumor was responsive to stimulation by human chorionic gonadotropin.
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PMID:Steroid section patterns of a hilus cell tumor of the ovary. 727 48

Tissue steroid levels in 48 needle-biopsy samples of adenocarcinoma of the prostate were quantified by radioimmunoassay (RIA). Tissue levels of dihydrotestosterone (DHT), estradiol-17 beta, and estrone were correlated with the tumor stage, histologic grade, and patient response to endocrine therapy. All patients with well-differentiated carcinoma of the prostate had tissue DHT content greater than 2.0 ng/g while 35% of patients with moderately differentiated or poorly differentiated tumors had tissue DHT content less than 2.0 ng/g. DHT content appeared to be unrelated to tumor stage. Estradiol and estrone content correlated well with tumor grade but not with tumor stage. DHT levels were measured in 17 patients with symptomatic Stage D2 carcinoma of the prostate. Thirteen patients with DHT content greater than 2.0 ng/g initially had an objective and/or subjective response to endocrine therapy. Four patients with tissue DHT levels below 2.0 ng/g had no response to hormonal therapy. Quantification of tissue DHT content by RIA is a promising method for predicting initial response to hormonal therapy in adenocarcinoma of the prostate.
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PMID:Radioimmunoassay of tissue steroids in adenocarcinoma of the prostate. 729 91


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