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At least 325 records · Page 18Linked to original sources
PubMed1988

Antiandrogen effects in models of androgen responsive cancer.

The ability of antiandrogens to antagonize androgen effects in androgen responsive tissues is well established. Antiandrogens may diminish in vivo or in vitro proliferation of some androgen responsive cancer cells without causing cessation of multiplication. These model studies are representative of clinical experience in treatment of human prostate cancer with antiandrogen therapy. Recent studies in the AXC/SSh rat prostate cancer model show that these cancer cells elaborate polypeptide growth factors which stimulate their proliferation. If growth factor production by these cells is androgen independent, this may provide an explanation for failure of androgen ablation or antiandrogen treatment to effectively halt prostate cancer cell proliferation.

Androgen Antagonists↗
PubMed1980

Effect of antiestrogens on pituitary prolactin production in normal and pituitary tumor-bearing rats.

Administration of the antiestrogen tamoxifen to normal Buffalo female rats caused a 45% reduction (p less than 0.01) in 3H-prolactin synthesis and release in vitro. Radioimmunoassayable prolactin in incubated glands and medium also decreased significantly. Similar results were observed in Wistar-Furth animals except for in vitro radioimmunoassayable prolactin, which decreased less markedly (by 33%, p less than 0.01). Serum prolactin concentration in treated rats was unchanged. Tamoxifen did not affect the extremely high serum prolactin concentration in rats bearing mammotropic tumors. It further reduced in vitro synthesis of radioactive prolactin but not of the radioimmunoassayable hormone. No interaction between antiestrogens and the dopamine agonist bromocriptine was observed. These observations suggest that the nonsteroidal antiestrogens decrease the synthesis of prolactin but have little effect on release of the hormone. Tamoxifen inhibits growth of transplantable mammotropic tumors MtTW15 and 7315a potently without altering tumor prolactin production. In vivo treatment of adult female rats with tamoxifen did not affect in vitro synthesis and release of radioactive growth hormone, but reversed the elevated growth hormone production of rats bearing 7315a tumors.

Animals↗
PubMed1975

Carcinogenicity of the antineoplastic agent, 5-(3,3-dimethyl-1-triazeno)-imidazole-4-carboxamide, and its metabolites in rats.

Chronic oral administration of the antineoplastic agent, 5-(3,3-dimethyl-1-triazeno)imidazole-4-carboxamide (NSC-45388, DTIC), induced predominantly thymic and mammary tumors as demonstrated previously. Male and female Sprague-Dawley and female Buffalo rats were susceptible to the carcinogenicity of DTIC. A 50% incidence of mammary adenocarcinomas was induced in males within 18 weeks. Type of tumor and tumor incidence were dose dependent. Single and multiple intraperitoneal injections of DTIC did not alter organ specificity. DTIC-induced thymic lymphosarcomas and mammary adenocarcinomas were transplantable. Tissue distribution studies revealed no correlation between uptake of DTIC by a given tissue and its susceptibility to carcinogenicity. Metabolites of DTIC were tested for carcinogenic activity. Animals administered 5-diazoimidazole-4-carboxamide orally, intraperitoneally, or intragastrically developed low incidences of thymic, stomach, bladder, or mammary tumors. A low incidence of mammary tumors developed in rats fed 2-azahypoxanthine. A variety of tumors, including several ependymoblastomas, were induced in rats that received 5-aminoimidazole-4-carboxamide orally. 5-(3-Methyl-1-triazeno)imidazole-4-carboxamide (MTIC), when fed or given in single or multiple intraperitoneal injections, induced a high incidence of mammary adenofibromas and a low incidence of uterine leiomyosarcomas. Control rats had low incidences of mammary adenocarcinomas and adenofibromas after 52 weeks. These data show that the carcinogenic properties of DTIC resemble those of carcinogenic N-nitroso compounds, hydrazine, azo, and azoxy-alkanes and aryltriazenes and thus suggest similar mechanism(s) of action. These data also indicate that MTIC is involved in the induction of mammary adenofibromas and uterine leiomyosarcomas by DTIC.

Adenofibroma↗
PubMed1981

Effect of exogenous angiotensin-II on local blood flow in kidneys with neoplasm. Experiments in the rat.

The effect of angiotensin-II on the local renal blood flow and arterial blood pressure was investigated in the rat with the H2 gas washout technique. Increasing intravenous infusion rates gave a decreasing blood flow and increasing blood pressure, renal vascular resistance being close to proportional to the log of infusion rate. In kidneys with experimental neoplasm, the flow reduction was proportionally less in the tumor than in intact renal tissue. The respective flow levels were maintained for 10 to 45 min without tendency to change.

Angiotensin II↗
PubMed1976

An inhibitory effect of salivary gland extirpation on the induction of mammary tumors in rats by N,N'-2,7-fluorenylenebisacetamide.

N,N'2-2,7-Flourenylenebisacetamide (2.7-FAA) was administered orally to 34 female, strain AXC/I rats. Nineteen were pretreated with the extirpation of the salivary glands. The remaining 15 rats received no surgical treatment. Six of these 15 unoperated rats developed mammary carcinomas and seven developed tumors at other sites, whereas none of 19 operated rats had mammary tumors but 8 rats had tumors at other sites. No tumor developed in 4 operated control rats that were on normal diet. The results demonstrate that pretreatment with extirpation of the salivary glands inhibited mammary tumor induction in rats by 2,7-FAA although it did not inhibit induction of other type tumors. The mechanism by which induction of mammary tumors was inhibited is not clear. Ovarian atrophy and hepatic necrosis were observed in both operated and unoperated rats ingesting 2,7-FAA but did not seem to affect carcinogenesis by the carcinogen. Lower body weight was observed in operated rats but it is not considered to be the major cause of a complete inhibition of mammary tumor induction.

2-Acetylaminofluorene↗
PubMed1978

[Blastomogenesis in repeated administration of DMBA in rats during different life periods].

Three groups of rats were given DMBA emulsion during different periods of the life. The first group received the carcinogen transplacentally, the second- at the age of three months, the third was given the agent twice during the mentioned terms. The third group showed a summation of the blastomogenic effect which was manifested in the frequency of tumors, including neurogenic, renal and mammary gland tumors, in the index of neoplasms multiplicity as well as in shorter average life terms. The results were compared with pure control findings.

9,10-Dimethyl-1,2-benzanthracene↗