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Results for “Neoplasms, Hormone-Dependent”

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At least 19 recordsLinked to original sources
PubMed1978

Dihydrotestosterone concentration in prostate cancer tissue as a predictor of tumor differentiation and hormonal dependency.

Tissue dihydrotestosterone and 5alpha-reductase (delta4-3-ketosteroid-5alpha-oxidoreductase) levels have been measured in prostates of patients with cancer and benign prostatic hypertrophy; significant decreases in average values for both of these biochemical parameters were noted in prostate cancer compared to benign prostatic hypertrophy, although individual values overlapped in both groups. Prostate cancer tissue dihydrotestosterone levels appeared to correlate better than did either histological tumor grading or 5alpha-reductase with the ultimate clinical response to antiandrogen therapy. These results suggest that assay of tissue dihydrotestosterone levels in prostate cancer should be further explored as a possible marker for tumor differentiation.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1978

Platelet derived growth factor(s) for a hormone-responsive rat mammary tumor cell line.

Mammary tumor cell growth factor(s) has been identified in extracts of platelets from both male and female rats, as well as in extracts prepared from pooled outdated human platelets. When assayed by the growth promotion of MTW9/PL rat mammary tumor cells in culture, platelet extracts alone were able to support growth 50--75% as well as whole serum. The mitogenic activity from crude human platelet lysates was shown to be trypsin sensitive, relatively stable to extremes of pH, labile to heat treatment at 70 degrees, non-dialysable, ammonium sulfate precipitable, not removed by 56 degrees charcoal treatment, and of apparent molecular weight of 30,000 to 50,000 daltons as estimated by G-100 Sephadex chromatography. The platelet derived mammary growth factor activity was not replaced or potentiated by thrombin or known hormones and growth factors such as prolactin, insulin, 17-beta-estradiol, progesterone, hydrocortisone, L-thyroxine, and mouse epidermal growth factor. The experimental report demonstrates that platelets are a rich source growth factor activity for rat epithelial mammary tumor cells, and that the activity appears to be a polypeptide(s) different from other mitogenic activities known to influence growth of mammary tissue.

Animals↗
PubMed1978

Isolation and purification of rat mammary tumor peroxidase.

7,12-Dimethylbenz(a)anthracene-induced rat mammary tumors often contain high levels of the enzyme perioxidase, a putative marker of estrogen dependence. This enzyme can be effectively extracted with 0.5 M CaCl2, giving rise to a soluble peroxidase with a molecular weight of about 50,000 as determined by gel filtration. This is the same size as the estrogen-induced peroxidase of rat uterus but smaller than other mammalian peroxidases. Further purification of the rat mammary tumor peroxidase by concanavalin A-Sepharose chromatography and hydrophobic interaction chromatography on phenyl Sepharose provides a 640-fold purification of the enzyme.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1978

Vasopressin stimulation of acetate incorporation into lipids in a dimethylbenz(a)anthracene-induced rat mammary tumor cell line.

In a preliminary report we described the effects of rat prolactin on the incorporation of [14C]acetate into lipids by a cell line from a dimethylbenz(a)anthracene-induced rat mammary tumor. The characteristics of the response to prolactin were very similar to those described for the normal rat mammary gland; namely, insulin was required for full expression of the response, maximal activity was not seen until 36 hr after the addition of the hormones, and growth hormone was able to elicit the same response. However, we were unable to detect binding of 125I-labeled prolactin to these cells, and furthermore, other more purified prolactin preparations were inactive. Upon further investigation we discovered that the activity resided in a low-molecular-weight fraction of the rat prolactin B-1 preparation and was probably either vasopressin or oxytocin or both. These data suggest the possibility that vasopressin may play a role in rodent mammary tumorigenesis.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1978

[Early effect of estradiol on ultrastructure of chromatin in the endometrium and hormone-dependent mammary tumors].

After in vivo and in vitro administration of aestradiol, the chromatin of lamb endometrium and of hormone-dependent 7,12-dimethylbenzanthracene Rat mammary tumors is rapidly transformed from a condensed into a diffuse chromatin. A stimulation of 3H leucine incorporation into protein was also observed. These modifications were specific for estrogen receptor ligands and for estrogen responsive tissues. In vitro tamoxifen induced pycnosis. These changes could be used to improve the prediction of hormone dependency of human breast and uterine cancers.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1979

Effect of catechol estrogens on rat mammary tumors.

The effect of 1,3,5(10)-estratriene-3, 16 alpha, 17 beta-triol (estriol), 1, 3, 5(10)-estratriene-2,3-diol-17-one (2-hydroxyestrone), and 1,3,5(10)-estratriene-2,3,17 beta-triol (2-hydroxyestradiol) on the growth of dimethylbenz(a)anthracene-induced mammary tumor and of R3230AC-transplantable mammary tumor was compared with that produced by estradiol benzoate treatment. Estriol showed minimal inhibition of tumor growth in dimethylbenz(a)anthracene-induced tumor and no effect on R3230AC tumor while 2-hydroxyestrone showed no effect of tumor inhibition. On the other hand, 2-hydroxyestradiol showed appreciable inhibition of tumor growth in both tumors studied. That 2-hydroxyestradiol has been found to bind to estrogen receptors in mammary tumors and is uterotropic suggests that the inhibition of tumor growth by 2-hydroxyestradiol may be similar to the mechanism of inhibition of mammary tumors by high concentrations of estradiol.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1979

Inhibition of mammary tumorigenesis in carcinogen-treated Lewis rats by suppression of prolactin secretion.

One hundred sixty-eight female Lewis rats were treated intragastrically with 10 mg 7,12-dimethylbenz[a]anthracene at 56 and 63 days of age. Pituitary prolactin secretion was suppressed in one-half of these rats by daily sc administrations of 2-bromoergocryptine mesylate (CB-154; 0.4 mg/100 g body wt) from 29 to 90 days of age (series 1) and from 90 to 140 days of age (series 2). Treatment with CB-154 was initiated prior to the onset of palpable mammary carcinomas. Control rats were given injections of saline. Inguinal mammary glands were excised from 10 control and 10 CB-154-treated rats at the cessation of saline and CB-154 treatments and examined for hyperplastic nodules (HN). The remaining rats were palpated weekly for mammary carcinomas (MC) and killed at 200 days of age. Mean number of HN per rat, mean number of MC per rat, and percent of rats with MC were, respectively: series 1--controls, 0.6, 1.5, and 68; CB-154 treatment, 0.5, 1.1, and 62; series 2--controls, 10.4, 2.0, and 94; CB-154 treatment, 5.1, 1.1, and 56. The number of HN and MC was only slightly reduced in rats when prolactin was suppressed during carcinogen treatment (series 1) but markedly reduced when prolactin was suppressed after carcinogen treatment (series 2). These results provide evidence that prolactin is involved in the early development of mammary dysplasias in the carcinogen-treated female Lewis rat.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1979

Hormone dependency of rat mammary carcinoma--a comparison of two assay systems.

Succinic dehydrogenase activity of the DMBA induced tumor explants cultured with or without hormones was assessed histochemically while receptors for estrogen (ER) and progesterone (PgR) were estimated from the cytosol fraction of the tumor tissue. Tumor regression following ovariectomy (OVX) was kept as the end point for determining hormone dependency. By in vitro method positive correlation was observed in 5 of 6 responsive or hormone dependent tumors, and 13 out of 14 independent tumors. Presence of receptors (ER + PgR, PgR) correlated with responsiveness in 4 of 6 tumors while their absence in the non-responsive group correlated in 6 of 14 tumors. Prolactin responsive tumors did not regress following OVX even if ER + PgR or ER/PgR were present. Using the same tumor tissue the results of hormone dependency by the two methods were identical in only 9 of 20 tumors.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1978

Estradiol receptor analysis in human breast cancer tissue by isoelectric focusing in polyacrylamide gel.

Isoelectric focusing in polyacrylamide gel combined with limited proteolysis is a simple and specific method for quantitation of estradiol receptors in breast cancer tissue. At least eight different samples can be analyzed simultaneously on one gel, and the whole procedure, including sample preparation, takes less than 7 hr. In comparison with sucrose gradient centrifugation, isoelectric focusing is more sensitive, possibly due to the short time (1.5 to 2 hr) needed for the analysis. Furthermore, only one incubation with tritium-labeled estradiol is needed for an analysis, which means that a smaller amount of tumor tissue is needed than for most other methods. This fact allows analysis of the estrogen receptor content in tumor material obtained from fine-needle biopsy.

Breast Neoplasms↗