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)

In the therapy of metastatic breast cancer MAP was used with different dosages and different forms of administration. Pharmacokinetics and pharmacodynamics were investigated. MAP plasma concentrations are dose dependent with great interindividual variation. The cortisol suppressive effect is dependent on plasma concentrations with only narrow interindividual variability. The oral administration of the crystal suspension is equivalent to the administration of tablets concerning plasma levels und endocrine effects. The therapy schedule for i.m. application used here leads to lower MAP plasma concentrations and correspondingly to a minor endocrine effect than in oral therapy. Tumor effective and cortisol suppressive plasma concentrations seem to have the same level.
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PMID:[High dose medroxyprogesterone acetate in metastatic breast cancer. Comparative clinical, pharmacokinetic and pharmacodynamic data of different forms of administration]. 621 99

Based upon preliminary observations that tumor response to MPA was correlated to cortisol suppression 42 patients were treated with MPA at different dose levels. 1500 mg MPA p.o. almost completely suppressed endogenous cortisol production in 23 out of 23 patients. Consequently, 51 patients with advanced stage metastatic breast cancer were treated with Medroxyprogesteroneacetate (HD-MAP) at a dosage of 1500 mg p.o. daily or 500 mg i.m. on 5 days per week. There were 5 complete and 7 partical remissions, 23 patients with no change and 10 with progressive disease. 7 patients were not evaluable. Clinical results correlated to plasma cortisol and prolactin blood levels bot not to LH, FSH, TSH, TBI, T3, T4, ACTH and aldosterone measurements. There was no patient with relapse and suppressed cortisol or normal prolactin measurements. The development of pituituary resistance to MPA is suggested. HD-MPA was equally effective in estrogen and/or progesterone receptor positive as in receptor negative patients. It is proposed that cortisol and prolactin determinations are useful to monitor for effective MPA treatment and the early detection of MPA resistance.
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PMID:[High dose medroxyprogesteroneacetate in metastasizing breast cancer: correlations between course of the disease and hormone profiles]. 622 46

In mature male and female SD rats, the anti-weight gain effect of durabolin plus vitamin C or vitamin C alone was statistically significant compared to durabolin-treated and control rats. The anti-tumor and anti-weight gain effects of MAP plus vitamin C on DMBA-induced rat mammary cancer were compared with those of MAP and vitamin C in relation to ER. An anti-tumor effect was noted in the MAP treated groups, irrespective of the ER status; it was more pronounced in the MAP (100 mg/kg) plus vitamin C treated group with ER+tumors. Among the ER+tumor groups, weight gain was remarkable in the MAP-treated (20 mg/kg) animals; an anti-weight gain effect was seen in the MAP (20 mg/kg) plus vitamin C group.
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PMID:[Effect of medroxyprogesterone acetate (MAP) and vitamin C on DMBA induced rat mammary cancer in relation to estrogen receptor(ER)]. 622 84

The Australian Drug Evaluation Committee (ADEC) has never approved Depo-Provera for general use as a contraceptive, but it is approved for the treatment of malignant neoplasia and precocious puberty. Thus, it is available on the drug market. On the market, the drug is being used as a contraceptive under guidelines issued by the ADEC. The guidelines allow the drug to be prescribed as a contraceptive for investigational purposes on the basis of informed consent. The practical effect of this is that doctors are the final arbiters of its use. Evidence exists that Depo-Provera is being given to disadvantaged women in Australia and overseas without their informed consent. Attention has been focused on this medical practice and on the contraceptive itself. Its erratic use for contraception in Australia has attracted the critical gaze of 2 federal ministries. Meanwhile the drug continues to be prescribed as a contraceptive in Australia even though the ADEC, following the lead set by the US Food and Drug Administration (FDA), has not given its approval. Although not approved in the US, Depo-Provera is approved as a contraceptive in about 80 countries. In New Zealand the drug was approved as early as 1968 and now has a higher per capita use in that country than any other in the world. In January this year, as a result of an appeal by Upjohn Pty Limited against the FDA's earlier refusal to approve the drug, Depo-Provera became the subject of the 2nd only public Board of Inquiry convened by the FDA. The results of that inquiry will not be known for several months. The lineup at the inquiry reflected the pattern of opposing forces wherever the drug has been debated. An impressive array of health experts and organizations appeared in favor of approval. Those arguing for disapproval included the FDA scientists themselves, the Public Citizens Health Research Group, and the National Women's Health Network. The key scientific issue in the inquiry involved the validity of animal studies on the drug. The drug company argued that the beagle dog, which had developed breast tumors when tested with the drug, was not an appropriate model for judging the effects of the drug in humans, a view shared by the World Health Organization (WHO). FDA scientists and the medical director of the health research group argued that even if dogs and monkeys do not exactly mimic effects on humans, animal studies are a reliable predictor of carcinogenicity in humans. Even if the FDA was to approve the drug and if the Australian government was to follow suit, consumer groups and women's health groups would be expected to use such an inquiry to press for longterm monitoring of the drug and standard guidelines for informed consent.
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PMID:Testing times for women in body lab. 622 1

Forty-eight of 81 (59%) of N-nitrosomethylurea-induced rat mammary tumors regressed in average to almost one-half of the original size 10 days after ovariectomy (ovax) (hormone responsive), while 33 remained essentially unchanged (hormone resistant). AT 20 days after ovax, further decline in hormone-responsive tumors was observed when the rats were treated daily with 0.9% NaCl solution on the tenth day after ovax. Treatment for the same length of time with estrogen either alone or in combination with bromocryptine (to effectively suppress serum prolactin level) prevented tumor regression in hormone-responsive tumors. A similar effect was observed when rats were treated with perphenazine (to stimulate endogenous prolactin secretion) either alone or in combination with the antiestrogen tamoxifen. Estrogen receptors (ERs) significantly declined after ovax. Treatment with estrogen or perphenazine did not have any significant effect on ER level. Progesterone receptors (PGRs) became virtually undetectable after ovax. Treatments with estrogen, estrogen plus bromocryptine, and perphenazine plus tamoxifen but not perphenazine alone were able to partially restore PGRs although this effect was of borderline statistical significance. ER and PGR levels were not significantly different between hormone-responsive and -resistant tumors within each group. We conclude that both estrogen and prolactin play a role in the growth of the N-nitrosomethylurea-induced rat mammary tumor. Changes in ER and PGR levels did not correlate with tumor growth under the present experimental conditions.
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PMID:Role of estrogen and prolactin in the growth and receptor levels of N-nitrosomethylurea-induced rat mammary tumors. 628 7

The estrogen receptor was assayed in 8 intracranial meningiomas, 14 lung cancers, 3 thymomas and 2 malignant lymphomas using the dextran-charcoal method. Progesterone and androgen receptors were also assayed in all the cases of lung cancer. The estrogen receptor assay was positive in 3 meningiomas, 2 lung cancers, and all thymomas and malignant lymphomas. The androgen receptor assay was positive in one case of lung cancer but the progesterone receptor was negative in all assayed cases. No cases showed multiple receptor positivity. An antiestrogen (tamoxifen) was administered to one case each of intracranial meningioma and lung cancer with positive estrogen receptor. The receptor content was decreased to an undetectable level in the former after 4 months of administration. This finding suggests the estrogen dependency of the tumor. The lung cancer patient, however, died 2 weeks later without any evidence of hormone dependency.
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PMID:Sex steroid receptors in diverse human tumors. 629 Mar 6

Estrogen receptors (ER) in breast cancer patients were determined histologically with estradiol-BSA-FITC and biochemically both by sucrose density gradient and dextran coated charcoal methods. Either 8 S or 4 S ER was found clinically to be related to estrogen dependency. ER-positive cells were in clumps or intermixed with ER-negative cells in cancer tissue, which may be one of the reasons for the fact that surgical ablation of breast cancer patients rarely resulted in complete regression of tumors. High dose administration of Hexestrol of Medroxyprogesterone acetate was occasionally effective for ER-negative human and rat breast cancer, which suggests that there is another endocrinological tumor suppressing mechanism besides the mechanism involving the estrogen-ER system.
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PMID:[Histochemical and biochemical assays of estrogen receptors in breast cancer and significance of endocrine therapy]. 630 7

The role of prolactin (PRL) and estrogen in the growth of 7,12-dimethylbenz(a)-anthracene (DMBA)-induced rat mammary tumors was investigated. Tumor growth was suppressed by both bromocriptine and tamoxifen. Combined administration of ovine PRL and tamoxifen attenuated the inhibitory action of tamoxifen on tumor growth. Serum PRL levels were decreased by both bromocriptine and tamoxifen administration. Estrogen receptors (ER) in tumor tissues were decreased in number by tamoxifen, but not by bromocriptine. Progesterone receptors (PgR) in DMBA-induced mammary tumors were abolished by tamoxifen and significantly reduced by bromocriptine. Combined administration of ovine PRL with tamoxifen attenuated the inhibition of PgR induced by tamoxifen alone, while ER remained undetectable. Specific PRL binding to the liver was significantly reduced by treatment with bromocriptine, tamoxifen and tamoxifen plus ovine PRL, whereas PRL receptors in mammary tumor were not influenced by these drugs. These results suggest that PRL may stimulate DMBA-induced tumor growth independently of ER and that a part of the inhibiting effect of tamoxifen on tumor growth may be explained by the decreased PRL secretion.
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PMID:Effects of bromocriptine and tamoxifen on growth and hormone receptor levels of 7,12-dimethylbenz(a)anthracene-induced mammary tumors in rats. 632 51

In this discussion of Depo-Provera (DMPA) attention is directed to the following: pharmacology and mode of action; clinical considerations; cervical dysplasia; breast cancer; and endometrial carcinoma. DMPA, a microcrystalline suspension of medroxy-progesterone acetate, is used widely around the world as a contraceptive, particularly in developing countries. MPA (medroxy-progesterone acetate) is a synthetic progesterone which in its mycrocrystalline depot form can be delivered by simple intramuscular injection or jet injector to that depending on the dose administered plateau contraceptive blood levels will be maintained for 90-180 days when doses of 150 mg and 300 mg respectively are used. The effect of DMPA in suppressing ovulation is at the hypothalmic level where it inhibits the gonadotrophic release responsible for the midcycle surge in luteinizing hormone responsible for ovulation. When 150 mg is administered every 3 months pregnancy rates range from 0.0-1.2/100 women years. The pregnancy rates range from 0.0-3.8/100 women years when 300 mg is administered every 6 months. The drug is usually administered initially in the first 7 days of the menstrual cycle to avoid possible effects on an established pregnancy. Menstrual disturbances are the major reason for discontinuation of DMPA. The usual side effects are amenorrhea, irregular but infrequent bleeding, and a few instances of prolonged or heavy bleeding. There is no evidence to suggest that DMPA increases the risk of invasive cancer of the cervix, but the evidence regarding the incidence of cervical dysplasia is ambiguous. There have not been any cases of breast cancer that can be related to DMPA use, but DMPA toxicology studies on beagle bitches revealed an increased incidence of benign and malignant breast tumors. It is well established that in adenocarcinoma of the endometrium DMPA is effective in causing regression and preventing recurrence of this tumor.
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PMID:Depo provera in perspective. 646 84

The presence of steroid hormone receptors was investigated in rat colonic tumors, experimentally induced by 1,2-dimethylhydrazine, and in adjacent normal tissues. Estrogen, progesterone, glucocorticoid, and 5-alpha-dihydrotestosterone receptor levels were measured by the dextran charcoal competitive binding assay. Estrogen receptors were present in 25% of tumors, although not in adjacent normal tissue. Higher levels of glucocorticoid binding in tumor versus adjacent normal tissue were demonstrated in 5 out of 8 cases. Progesterone and 5-alpha-dihydrotestosterone levels in tumor versus adjacent normal tissue were not significantly different. The results reflect the possible endocrine dependence of colonic tumors.
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PMID:Steroid hormone receptors in dimethylhydrazine-induced rat colonic tumors. 651 32


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