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

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

The case of a 36-year-old women found to have a hepatic tumor is reported. The patient complained a malaise, weakness, dyspnea, and ankle edema and had been aware of a slowly growing abdominal swelling for 3 years. She had been taking Gynovlar 21 (3 mg norethinsterone acetate with 50 mcg ethinyl estradiol) for 6 years. Laparotomy revealed a solid, vascularized tumor arising from the left lobe of the liver and from part of the right lobe. A 2800 gm mass was excised along with a 40 gm mass from the celiac axis that involved lymphatic tissue. This is the 1st case report of a hepatic malignancy associated with an oral contraceptive that showed histological evidence of secondary spread.
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PMID:Hepatocellular carcinoma associated with oral contraceptives. 20 11

Histological specimens from 150 women with liver tumors are discussed. Of the 150 patients under consideration, 85% had ingested contraceptive steroids, most for more than 3 years. Of these 64% had taken pills containing mestranol, and 18% had used ethinyl estradiol; 18% had taken both. Average age was about 30 years, and pain was the most common presenting symptom. 19 tumors were malignant (hepatoma), 57 were adenoma, 68 were focal nodular hyperplasia, and 6 were unclassified. To date, 12 of the 19 hepatoma patients have died. In addition to presenting numerous figures depicting the pathology material and a discussion of tumor differentiation difficulties, speculation between steroid ingestation and tumor appearance is considered. Since hepatomas are much more common than benign liver tumors, circumspection is in order before indicting steroids as causative. In this group of women studied, none had cirrhosis, for example, whereas cirrhosis is very common in the general population. The authors call for further investigation of estrogens and primary liver tumores.
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PMID:Relation of steroids to liver oncogenesis. 22 96

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 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

Endocrine hormone treatment has been found to be effective in treating metastatic breast cancer in 20-40% of the cases. The effectiveness of this treatment can be predicted to a certain extent by determining whether the hormone receptors in the tumor tissue react positively or negatively when incubated with highly active hormones, e.g. H3-17 beta-estradiol. Estrogen receptors are found in 60-70% of primary tumors and 40-50% of tissue samples from metastatized tumors. Estrogen receptors are more frequently found in post-menopausal women than in women who are still menstruating. Progesterone receptors have been found in 20-40% of all investigations undertaken, androgen receptors in 20-30%, and corticosteroid receptors in 20-50%. A remission rate of 56% has been achieved after endocrine therapy of those with positive estrogen receptor tests, compared to 10% among those with negative tests. The correlation between the receptor test results and (the success of) endocrine therapy is not very high; this could be a factor determined by the cellular constitution of a tumor. The remission rate is 75% among patients with positive receptor tests for both estrogen and progesterone. Faulty lab techniques could be responsible for low correlation. Determination of the receptor activity of both the primary tumor and its metasases, or immunological or immunohistological determination of receptor activity may improve the usefulness of the test in determining tumor reaction to endocrine hormone treatment.
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PMID:[The clinical value of hormone receptors in the treatment of breast neoplasms]. 54 83

Estrogen receptors (ER's) were determined by agar gel electrophoresis in 105 human mammary tumor biopsies. Fifty-three tumor specimens revealed measurable amounts of receptor, and 64% of these patients showed an objective remission after endocrine treatment. If we also include cases with partial remission, previous response, and arrested growth but no actual remission, the benefit rate increases to 87%. The corresponding percentage in the ER-negative groups is 13%. In a retrospective study of 42 patients with human breast cancer, a correlation between ER finding and remission rate after chemotherapy was found. Of the ER-negative patients, 71% showed an objective remission after polychemotherapy, whereas only 43% of the ER-positive cases revealed such remission. The presented data are discussed with special regard to their clinical relevance.
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PMID:Some comments on the necessity of receptor determination in human breast cancer. 69 71

Estrogen receptors (ER) were measured on specimens taken from 27 patients with benign breast conditions and 109 patients with breast cancer. Using sucrose gradient assay, 15% (4/27) of benign lesions and 56% (61/109) of malignant tumors were estrogen receptor-positive (ER-positive means 8S or 8S+4S levels more than 7 fmoles/mg cytosol protein). Progesterone receptors (PR) were tested on specimens from 28 patients and 39% (10/26) of the cancers were PR-positive. ER protein activity was not correlated with stage, histology, size of primary lesions, or extent of axillary or distant metastasis. Tumors with low ER levels are more likely to recur, and recurrent tumors after longer disease-free intervals are more likely to be ER-positive. Detailed analysis showed that ER levels did correlate with age and serum albumin levels. Concentrations of serum alpha1-globulin were decreased, while IgG and IgM were significantly increased among patients with positive ERs. Eighteen evaluable patients with advanced breast cancer had endocrine therapy, 13 had objective response. Twelve of these 13 had 8S receptor above 10 fmoles/mg, or 4S above 15 moles/mg, or 8S+4S above 25 fmoles/mg. The one exceptional patient had tumor with high PR but without detectable ER.
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PMID:Steroid receptors study in breast carcinoma. 74 84

When initiated the same day as dimethylbenzanthracene (DMBA) administration, daily treatment with 8 or 24 mug of the new antiestrogen RU 16117 (11alpha-methoxy ethinyl estradiol) completely prevented the appearance of mammary tumors in all animals up to the last time interval studied (130 days after DMBA administration). At daily doses of 0.5 and 2.0 mug of RU 16117, the tumor incidence was reduced to 78.6% and 40.0%, respectively. 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. While plasma LH levels were decreased after treatment with 8 or 24 mug RU 16117, plasma prolactin levels were slightly increased in animals receiving the highest dose of the antiestrogen. When RU 16117 was given at the daily dose of 24 mug for a period of 4 weeks, RU 16117 led to 65% reduction of the number of already established DMBA-induced mammary tumors. Not only the tumor number but also the tumor size was reduced by RU 16117 in a manner similar to that following ovariectomy. That the inhibitory effect of RU 16117 was not due to its low estrogenic activity is indicated by the absence of inhibitory effect of similar treatment with a range of doses (0.1-12.5 mug per day) of estradiol-17beta which cover the low estrogenic activity of the doses of RU 16117 used. Decreased levels of receptors for estradiol-17beta, progesterone, and prolactin were found in the tumors remaining after ovariectomy while treatment with the dose (24 mug) of RU 16117, efficient to inhibit tumor growth, has a similar inhibitory effect on the levels of estradiol-17beta and prolactin receptors. The present data indicate that the potent inhibitory effect of RU 16117 on the development and growth of DMBA-induced mammary tumors results from actions at both the hypothalamic-pituitary and tumor levels. The action at the peripheral level would be possibly secondary to a reduced sensitivity of the tissue to circulating hormones through lowering of hormone receptor concentrations.
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PMID:Potent inhibitory activity of a new antiestrogen, RU 16 117, on the development and growth of DMBA-induced rat mammary adenocarcinoma. 82 98


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