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

The number of plasma membrane receptors for TRH on tumor-derived mammotropic cells in culture, GH3 and GC cells, but not their affinity for TRH, was increased by estrogens. For GH3 cells, exposure to 10 nM 17 beta-estradiol for 48 h increased the receptor level from 54,000 to 90,000 sites/cell, while for GC cells, the number of receptors increased from 29,000 to 46,000 after 28 h. PRL accumulation in the medium was also increased by 17 beta-estradiol. 17 beta-Estradiol and diethylstilbestrol were equally potent in increasing the TRH receptor level, while estrone was only 1/10th as potent. Diethylstilbestrol bound to the cytoplasmic estrogen receptor with an apparent affinity approximately 2.5 times higher than 17 beta-estradiol in GH3 and GC cells, while the affinity for estrone was only 1/12th to 1/20th that of 17 beta-estradiol. Tamoxifen, an antiestrogenic compound, inhibited the increase in TRH receptor number induced by 0.3 nM 17 beta-estradiol and was capable of binding to the estrogen receptor. Modulation of the TRH receptor level on mammotropic cells by estrogens, which is likely mediated through cytoplasmic estrogen receptors, may be an important mechanism for regulation of TRH action.
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PMID:Estrogens increase the number of thyrotropin-releasing hormone receptors on mammotropic cells in culture. 22 Nov 99

Effects of 12 chemical cancerogenic agents have been studied in 910 anuran amphibia of the grass frog Rana temporaria. Tumors developed by administration of 8 of the agents studied. Dimethyl, diethyl and dibutylnitrosamines dissolved in water induced tumors in 44.2, 43.6 and 50% of animals, respectively; benzidine and 2-acetylaminofluorene administered subcutaneously and per os--in 46.6 and 41.2%, respectively, whereas p-dimethylaminoazobenzene and orthoaminoazotoluene (per os and subcutaneously)-in 30--33.3% of cases. Diethylstilbestrol-propionate induced tumors in 21% of cases. All the tumors developed within relatively short periods of time (15.6--31.9 weeks) and were located in the liver (hepatocellular cancer, hepatoadenomas) and the haemopoetic system (hemocytoblastosis). In control group of animals 3 amphibia developed multiple tumors of skin-cystadenopapillomas. The results obtained testify to the common mechanism of cancerogenesis in classes of vertebrates. In addition, the findings presented indicate to the suitability of amphibia as a new experimental object in oncology as well as to the applicability of these animals for purposes of express diagnostics of cancerogenicity. It may successfully serve as a biological indicator of environmental pollution with blastomogenic agents.
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PMID:Tumor induction by carcinogenic agents in anuran amphibian Rana temporaria. 30 91

Breast cancer is often hormone responsive, since growth or regression of tumors can often be modulated by appropriate endocrine manipulations. Estrogen and progesterone appear to be major hormones involved in regulation of breast tumor growth. It has been recently argued that a more accurate marker of hormonal responsiveness might result if an end product of an intact estrogen response system were measured instead of the initial hormone binding step. Progesterone receptor (PgR) has been investigated in this regard since it can be readily measured in human breast tumors and there is clear evidence in experimental breast tumor model systems that PgR is under acute estrogen control. PgR is rarely found in ER- metastatic breast tumors but is present in approximately 59% of ER+ metastatic tumors, especially in those tumors with high levels of ER. Preliminary clinical correlation of ER, PgR and response to endocrine therapy is encouraging. The response rate is significantly higher if the tumor contains both ER and PgR than if the tumor contains ER alone.
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PMID:Current status of estrogen and progesterone receptors in breast cancer. 32 86

Insulin and estrogen binding have been determined in 7,12-dimethylbenz(a)anthracene-induced mammary tumors of rats in various endocrine states. Hormonal therapy, such as diabetes and ovariectomy, resulted in differential effects on growth patterns and hormone binding of tumors coexisting in the same host or in different hosts. It was observed that tumors that continued to grow after the host was made diabetic (insulin independent) or started to regress after ovariectomy (ovarian dependent) demonstrated decreased insulin binding. Tumors that regressed in diabetic hosts (insulin dependent) or continued to grow in ovariectomized animals (ovarian independent) showed an increased insulin-binding capacity. No significant change in insulin binding was observed in tumors that remained static after ovariectomy or induction of diabetes. Estrogen binding in tumor cells from diabetic rats paralleled the pattern of tumor growth response to diabetes; insulin-independent tumors demonstrated a significant increase in binding compared to tumors from intact hosts, and insulin-dependent tumors showed decreased estrogen receptor levels. From these results, we conclude that (a) insulin plays a positive role in regulating estrogen-binding capacity, (b) ovarian hormones may play a role in regulating insulin-binding capacity, and (c) a relationship between insulin and ovarian hormones and the growth of 7,12-dimethylbenz(a)anthracene-induced tumors is strongly suggested and may have therapeutic implications.
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PMID:Relationship between insulin and estrogen binding to growth response in 7,12-dimethylbenz(a)anthracene-induced rat mammary tumors. 41 34

The effect of diethylstilbestrol propionate (DES; 1 mg/kg body wt. was studied in the female offspring of rats exposed subcutaneously on the 19th day of gestation. Examination of vaginal smears showed persistent estrus in adult rats treated prenatally with DES. Compensatory ovarian hypertrophy (COH) induced by hemicastration of these rats was not suppressed by estrogens. A per oral test for glucose-tolerance revealed decreased utilization of glucose in the offspring of DES-treated rats. Preliminary observations demonstrated that tumors developed in 14 of 18 (77.8%) progeny transplacentally expoed to DES and in 9 of 34 (26.5%) intact control rats. Tumors of the ovary and the endometrium were found only in the rats treated prenatally with DES; no tumors of the uterine cervix or vagina were observed in either experimental or control groups. It is suggested that a transplacental effect of DES in the female is impairment of the sex differentiation of the hypothalamus. The resulting hormonal and metabolic shifts might promote tumorigenesis.
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PMID:Transplacental effect of diethylstilbestrol in female rats. 43 10

Data are presented from studies on Syrian golden hamsters with the ENU precursors, EU, and NaNO2, given transplacentally and in adulthood, and with transplacentally administered DES. Hormone modification by gonadectomy of offspring prenatally exposed to ENU caused a significantly greater incidence and multiplicity of PNS neoplasms and other tumor types in orchidectomized males, compared with intact males, and in ovariectomized and intact females. That PNS tumors in gonadectomized males appeared within a significantly shorter latency period indicated that endogenously generated androgens inhibited neoplastic development. The endocrine imbalance also induced a higher incidence of neoplasia in other tissues and organs, e.g., skin melanomas, thyroid and adrenal cortex tumors, and notably gliomas in the CNS of ovariectomized female siblings. Exposure to single doses of ENU on days 12, 13, 14, and/or 15 caused PNS tumors predominantly in females and with an increased frequency in progeny treated during the final days of gestation. The spectrum of neoplasms was greater and their incidence significant in ENU-treated adult hamsters; the tumor types different from those of transplacentally treated animals (i.e., vascular, vaginal, and ovarian tumors and fore-stomach papillomas were seen). Determining factors in carcinogenesis at the time of carcinogen treatment possibly included stage of ontogenic development, degree of cell differentiation, hormone state of host, age, total dose, and duration of treatment. DES results indicated that the haster may be a useful model for reproducing lesions similar to those observed in children of mothers treated with this drug during pregnancy.
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PMID:Role of hormone imbalance in transplacental carcinogenesis induced in Syrian golden hamsters by sex hormones. 48 84

The activities of enzymes which synthesize and metabolize catecholestrogens were studied in biopsy samples of human breast neoplasms. Estrogen 2-hydroxylase, a cytochrome P-450-dependent enzyme, was present in both benign and malignant neoplasms but not in normal breast tissue. Catechol O-methyltransferase activity was present in all samples examined and was significantly higher in malignant tumors [549 +/- 31 (S.E.) pmol/20 min/mg protein] than in benign neoplasms (226 +/- 41 pmol/20 min/mg protein) or in normal breast tissue (133 +/- 28 pmol/20 min/mg protein). There was no correlation, however, between estrogen 2-hydroxylase and catechol O-methyltransferase activities. The enzymes responsible for the synthesis and metabolism of catecholestrogens are present in some breast tumor specimens, suggesting that in such tissues these metabolites may be formed in vivo.
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PMID:Catecholestrogen synthesis and metabolism by human breast tumors in vitro. 49 88

Assay conditions which, if varied, may affect the performance of the dextran-coated charcoal assay for estradiol receptor in breast cancer specimens, are reviewed. Incubation time and temperature influence the rate of binding and receptor stability. Lower temperatures preserve receptor integrity, so 2 hours of incubation at 4 degrees were chosen as standard. Various reducing agents (thiols) were tested for their effects on supernatants from high-speed centrifugations, and the following optimum levels were established: dithriothreitol, 7.5 mM for MCF cell line homogenates; and 1 mM for human breast tumor homogenates. Duration of dextran-coated charcoal extraction of the cytosol-tritiated estradiol incubation had no effect on receptor level up to 21 hours. Minimum levels of nonspecific binding could be seen by 4 hours. To overcome artifactual nonspecific binding by the charcoal, albumin is recommended as a supplement to the incubation (200 mcg or more). The dextran:charcoal ratio (1:10 by weight) recommended prevented receptor loss in the order: 1:1 1:10 1:100. 1 mg of dextran-coated charcoal (1:10) has the capacity to absorb .3-.4 mg of free estradiol. Diethylstilbestrol was as efficient as estradiol at displacing unlabeled competitors, but U11, 100A, and estrone were inefficient competitors.
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PMID:Characteristics of the dextran-coated charcoal assay for estradiol receptor in breast cancer preparations. 50 Dec 5

The biological effect of DES (diethylstilbestrol) administered during the organogenetic period of pregnancy is teratogenic rather than carcinogenic. A series of 420 women exposed to DES during the 1st trimester of pregnancy were studied. Colposcopic examination revealed that the original squamocolumnar junction occurred in the vagina in 82% of the cases. During the process of squamous metaplasia, there is danger that neoplastic transformation by carcinogens may occur in the vagina or cervix. Reports of the incidence of squamous intraepithelial neoplasia in DES-exposed women vary widely due to differences in patient selection, numbers in the series, and histologic interpretations. Diagnostic accuracy may be improved through the use of spectrophotometric evaluation of DNA content. The possibility that DES-exposed women have a higher risk of squamous neoplasia should be considered.
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PMID:Squamous neoplasia in DES-exposed women. 52 33

To determine the true prevalence of vaginal epithelial changes in DES-exposed offspring, the National Cancer Institute funded the DESAD Project, a study designed to follow up these women for 4 years and to determine the prevalence of cancer and various other abnormalities in DES-exposed women. 3339 women have constituted the project study cohort as of 12/31/76. Each woman in the DESAD Project undergoes breast, pelvic and colposcopic examinations, as well as vaginal and cervical cytology. Details of her gynecologic, sexual, and reproductive history are also obtained. 34% of the record review participants had vaginal epithelial changes (this rate is much lower than previously reported); no clear cell adenocarcinoma nor severe dysplasia or carcinoma in situ of either the vagina or cervix had been found in any of the women participants. A multivariate analysis of various factors of participant history and examination findings indicate that timing of onset of exposure to DES; total dosage of DES; duration of DES exposure; and age at initial examination correlated with vaginal epitheliel changes. Vaginal epithelial changes were also found to occur less frequently after 26 years of age. Maternal history (indication for use of DES); maternal age; and exposure to other hormones did not correlate with vaginal epithelial changes. The DESAD Project is currently investigating the changes in vaginal epithelium over time, and is also examining women for any evidence of neoplasia of the lower reproductive tract.
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PMID:Vaginal epithelial changes associated with in utero DES exposure. 52 34


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