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

The cumulative effects of Lentinan and endocrine therapy on the growth of DMBA (7, 12-dimethyl benzanthracene)-induced mammary tumors of rats were studied. Multiple injection of Lentinan alone resulted in a slight degree of regression of the tumor growth, when administered to rats bearing mammary tumors of about 1 cm in size. Ovariectomy-adrenalectomy, ovariectomy, and adrenalectomy, which are performed as surgical endocrine therapy, resulted in a more marked regression of the tumor than that produced by Lentinan treatment alone. Furthermore, multiple injection of Lentinan performed on these mammary tumor-bearing rats which had received surgical endocrine therapy 2 weeks previously evoked a marked regression of tumor growth. However, no changes in growth curves and survival rates, compared with those of saline controls were observed, indicating that Lentinan might be a useful agent when combined with surgical endocrine therapy. Concurrent injection of Lentinan resulted in a slight augmentation, although the histamine sensitivity of tumor bearing rats which had previously received surgical endocrine therapy elevated greatly, compared with that of controls. By contrast administration of Tamoxifen, which is used for medical endocrine therapy, resulted in a lesser degree of regression than that observed following surgical endocrine therapy, and was also not greatly affected by Lentinan injection.
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PMID:[Cumulative effects of lentinan and endocrine therapy on the growth of DMBA-induced mammary tumor in rats]. 643 Feb 43

The efficacy of tamoxifen treatment was studied in 46 postmenopausal patients with localized and disseminated breast cancer. Objective remissions were observed in 47.8, stabilization of tumor process-in 21.7%, mostly in cases of metastasis into the skin, subcutaneous fat, lymph nodes, pleura and bones. Tamoxifen proved sufficiently effective both in primary treatment and as a measure taken when the effect of a specific therapy (radiation, cytostatic or hormonal) was over. Side-effects were slight and were registered in 19.6%.
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PMID:[Use of tamoxifen in patients with disseminated and local breast neoplasms]. 649 91

It is known from previous investigations by other authors that the non-steroidal molecule Tamoxifen competes for estradiol binding sites in target tissues and displays partial agonist-antagonist effects. It is able to bind a cytosol protein distinct from ER which has been detected in target tissues, as well as in fetal target and non-target organs. The present work investigates the antiestrogen binding activity of human breast cancer cell lines and tumor biopsies. It is found that BT-20 and MDA-MB 231 cell lines devoid of ER and PGR contain a cytosol protein component able to bind antiestrogens with a high affinity (= 2 X 10(-9) M). The 3H-labeled complex prepared in hypotonic buffer sediments at 6.25 S in a sucrose gradient. A substantial amount of antiestrogen binding sites is found to be linked to the microsomal cell fraction, in agreement with previous data from other investigators. In experiments using whole cells incubated at 37 C, the complex is depleted from the cytosol compartment. A low amount of radioactivity is extracted from the purified nuclei. In the cytosol of human breast tumor biopsies the presence of antiestrogen binding sites is not exclusively associated with the presence of ER and PGR. The identity of the natural ligand which binds to these sites under physiological conditions merits investigation.
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PMID:High affinity cytosol binding site(s) for antiestrogens in two human breast cancer cell lines and in biopsy specimens devoid of estrogen receptors. 652 39

The effect of tamoxifen on the growth of malignant melanoma was investigated using human cell lines and single-cell suspensions prepared from patients' tumours cultured in soft agar. Tamoxifen stimulated both [3H]-thymidine incorporation and cell numbers in all of the cell lines tested. Cytoplasmic oestrogen receptor (ER) was detected in one of the responding lines and progesterone receptor (PR) in another. Tumour colony formation in soft agar culture was satisfactorily established from tumour cell suspensions from 13 of 21 patients, only one of which had detectable cytoplasmic ER. Greater than 50% reduction in colony formation with 5 X 10(-7) M tamoxifen occurred in two tumours, neither of which contained ER. These results indicate that tamoxifen has the potential to either retard or accelerate the growth of human malignant melanoma.
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PMID:The effect of tamoxifen on the growth of human malignant melanoma in vitro. 654 Jan 81

Human pituitary tumors were studied in vitro using the clonogenic stem cell assay. Mechanical dispersion was used to prepare single cell suspensions for plating. Colony formation occurred in 21 of 24 tumors plated. Bromocriptine (Brc; 10 nM) added to the medium resulted in a significant decrease in the number of colonies formed in 5 of 10 prolactinomas and in 1 tumor secreting both PRL and GH. However, PRL secretion was decreased in 8 of 9 tumors tested. Brc had no effect on either colony formation or hormone secretion in other tumors secreting GH (n = 2), ACTH (n = 2), or FSH (n = 1) or in nonsecreting tumors (n = 4). Tamoxifen (Tam; 10(-7) M) inhibited colony formation in 6 of 10 prolactinomas and in 1 tumor secreting GH and PRL. PRL secretion into the medium correlated with the changes in the number of colonies. Tam was not effective in any other tumor tested. In only 1 instance was there a synergistic action between Brc and Tam on inhibition of colony formation. Brc, but not Tam, caused a significant decrease in the size of the colonies formed from cells of PRL-secreting tumors. The least numbers of colonies per plate were found in 3 prolactinomas from patients treated preoperatively with Brc. We conclude that the soft agar clonogenic assay technique is a feasible method to study human pituitary tumors in vitro. Both Brc and Tam inhibited colony formation in this system in a significant proportion of tumors. The potential antiproliferative action of Tam in vivo needs to be studied in view of these results.
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PMID:Inhibitory action of bromocriptine and tamoxifen on the growth of human pituitary tumors in soft agar. 661 72

To see whether progestins prevent estrogen action in breast cancer cells, we have studied in vitro the effect of R5020 on the cell growth and the synthesis of secreted proteins in T47D and R27 human breast cancer cells. While R5020 had no effect on cell growth when tested alone, it significantly inhibited the growth of both cell lines in the presence of estradiol (1 nM). The effect was most clear-cut after 10-12 days of treatment and was dose dependent, a half-maximal inhibition occurred with 1 nM R5020. R27, a cloned MCF7 variant resistant to Tamoxifen, remained responsive to R5020, which prevented the effect of 17 beta-estradiol (E2) and inhibited cell growth in the presence of Tamoxifen. This suggests that the two antiestrogens are acting through different mechanisms. Dihydrotestosterone and dexamethasone did not reproduce or inhibit the effect of R5020 on cell growth. R5020 was ineffective in a rat tumor cell line containing androgen and glucocorticoid receptors but lacking progesterone receptors and estrogen receptors. These results suggest that R5020 is probably acting via progesterone receptors rather than via the androgen or glucocorticoid receptors. Using sodium dodecyl sulfate-polyacrylamide gel electrophoresis, we have shown that R5020 specifically decreases the production of the 52K protein, a major protein released by R27 cells after E2 stimulation. We conclude that R5020 has an antiestrogenic activity on breast cancer cells in culture, since it prevents the stimulation of cell growth and protein synthesis by E2.
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PMID:Antiestrogenic effect of R5020, a synthetic progestin in human breast cancer cells in culture. 668 24

Experiments were performed to observe the role of estrogen receptor in the proliferation of androgen-dependent mouse tumor, Shionogi carcinoma 115. Estradiol and diethylstilbestrol inhibited tumor growth as well as the weight gain of seminal vesicles and prostate glands in intact male mice. Tamoxifen decreased the tumor weight in intact males. Both nitromifene given to intact mice and tamoxifen given to castrated androgenized mice decreased the weight of seminal vesicles, but increased tumor weight. Estradiol was bound to the androgen receptor of the tumor cytosol with relatively high affinity, whereas diethylstilbestrol, tamoxifen and nitromifene were not. These were effective competitors in the estrogen receptor present in the tumor cytosol. These results suggest that the estrogen receptor system in Shionogi carcinoma 115 inhibits the proliferation of tumor cells.
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PMID:Effects of estrogens and antiestrogens on androgen-dependent growth of Shionogi carcinoma 115: role of estrogen receptor. 674 83

Tamoxifen-induced fluorescence was used as a marker of hormone receptors in breast tumor cytology. Patients receiving Tamoxifen were compared to patients without such a therapy. Only those receiving this treatment showed fluorescence in their malignant cells. Moreover, in this group, such a fluorescence was noticed only in those patients with hormonal receptors in their tumor cells and not in the patients without estrogen and progesterone receptors. Such a technique seems to be a good method for predicting response to hormonal therapy.
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PMID:[Tamoxifen induced fluorescence as a marker of hormone receptors: cytological study of fine needle biopsy of malignant breast tumors in treated women]. 680 16

An ovarian-responsive mammary tumor subline, T4-OR26, was isolated from an outgrowth of a progressed TPDMT-4 pregnancy-dependent mammary tumor in a virgin DDD mouse. T4-OR26 tumors were characterized by significantly faster growth in virgin mice than in ovariectomized mice. Both estrogen and progesterone were important for growth of the subline, as they were for that of the parent. Tamoxifen (TAM), with estrogenic activity, and epithiostanol (EPI) and testosterone propionate, with androgenic activity, which all caused TPDMT-4 tumors to regress, were compared for antitumor potency against the new subline by 3 s.c. injections weekly in virgins. EPI at 300 micrograms and testosterone propionate at 1000 micrograms elicited immediate tumor growth suppression with subsequent slight regression as did ovariectomy. TAM at 1000 micrograms caused tumor growth suppression after 2 weeks without subsequent regression. At 600 micrograms, EPI but not TAM significantly inhibited 17 beta-estradiol plus progesterone-induced tumor growth; at 400 micrograms, neither had any significant effect on the tumor growth induced by 17 beta-estradiol alone. With regard to their effect on hormone receptors, it was noted that EPI and testosterone propionate treatments with tumor regression caused significant reduction in cytoplasmic progesterone receptor, but TAM treatment, which does not influence tumor growth, did not cause such reduction. The results provide evidence that hormone-dependent mammary tumors may acquire greater resistance to estrogenic than to androgenic therapeutics with progression.
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PMID:Differential response of an ovarian-responsive mouse mammary tumor to androgenic and estrogenic agents. 686 Nov 37

The fluorescent binding of tamoxifen to eosin is used on Papanicolaou-stained smears as a marker of cell responsiveness to the antiestrogen molecule. Forty-two cases of human breast carcinomas were submitted to tamoxifen treatment between first diagnosis and surgery (4 to 30 days). Tamoxifen-induced fluorescence is observed in 17 of 42 cases (40%). There is a highly significant correlation between progesterone receptor content of the tumor and cellular fluorescence (0.01 greater than p greater than 0.001). Ultrastructural changes of such tumors (820 cells observed in 28 treated patients and 840 cells in 32 untreated controls) are observed in 42% of treated cells versus 10% of untreated cells. These ultrastructural alterations can be significantly correlated with cellular fluorescence induced by tamoxifen treatment and with progesterone receptor content of human breast cancers. These data suggest that a short pretreatment with tamoxifen before surgery can give useful additional information at the biochemical, cytochemical, and ultrastructural levels regarding cell responsiveness to hormonal manipulation.
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PMID:Tamoxifen-induced fluorescence as a marker of human breast tumor cell responsiveness to hormonal manipulations: correlation with progesterone receptor content and ultrastructural alterations. 686 Nov 57


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