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Query: UMLS:C0027651 (
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685,946
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The human ovarian carcinoma cell line NIH-OVCAR-3 grown in immunodeficient mice has been reported to be sensitive to estrogen medications and to express progestin receptor. To assess the effects of sex steroids on CA 125 production and survival times in these mice, we administered
Tamoxifen
, estrogen, and progestin. During the first 28 days after inoculation of mice with 2.3 million
tumor
cells ip, serum CA 125 rose exponentially, reaching 4308 +/- 776 and 3905 +/- 1013 units/ml (mean +/- SEM, P greater than 0.1) in placebo- and
Tamoxifen
-treated mice, respectively; median survival times were 41 and 39 days, respectively (P greater than 0.1). Uninoculated mice had nondetectable CA 125, and all outlived the inoculated mice. In
tumor
-inoculated mice, serum CA 125 levels and survival were similar when estrogen or progestin was injected alone and when both were given in combination. We detected no significant differences in production of CA 125 in vitro by
tumor
cells harvested from ascites fluid when the mice were treated with placebo, estrogen, or progestin. We conclude that, for our model, serial measurements of serum CA 125 provide excellent estimates of the relationship between
tumor
burden and survival, and that CA 125 production appears unaffected by estrogen, progestin, or
Tamoxifen
.
...
PMID:Serum CA 125 and survival of mice inoculated with ovarian carcinoma and treated with antiestrogen, estrogen, or progestin. 347 51
Initially somewhat exaggerated expectations about increased cure rates from adjuvant chemotherapy in operable breast cancer have been fulfilled only partially up to this date. However, most of the randomized, prospective and all of the historically controlled trials have revealed significantly decreased relapse and (less impressive) also death rates (expected mortality ratio) 5 and more years after mastectomy. Not all patient subgroups seem to benefit equally from adjuvant chemotherapy: its effectiveness seems to be more pronounced in pre- than in post-menopausal women and in those with only 1-3 instead of 4 and more
tumor
-positive homolateral axillary lymph nodes. Adjuvant combination chemotherapy seems to be more effective than monochemotherapy. Shortening of adjuvant CMF from 12 to 6 cycles gives the same result with definitely less toxicity. Adjuvant
Tamoxifen
probably is yielding similar results as adjuvant CMF (or other combinations) in post-menopausal, hormone-receptor positive women, but neither its long-term impact on survival nor the necessary treatment duration with antiestrogens are clearly known today. The value of adjuvant chemo- and hormone-therapy in node-negative women is still controversial, although at least hormone-receptor negative, node-negative patients exhibit the same risk of relapse and ultimate prognosis as do node-positive women. After 8-15 years of median follow-up in controlled studies, there seems to be no increased, but rather a decreased risk of second malignancies and also late leukemias in women treated with temporary adjuvant chemotherapy. Optimizing effectiveness and practicability of adjuvant chemo- (and also hormono-) therapy requires additional carefully controlled clinical studies, especially in high risk patients with more than 3
tumor
-positive axillary nodes.
...
PMID:[Adjuvant chemotherapy of breast cancer: an international review and the Swiss experience]. 354 40
The clinical response rate of chemotherapy or endocrine therapy for advanced or recurrent breast cancer has been described as being about 30%, regardless of steroid hormone status. However, the response rate for endocrine therapy is about double in patients with positive estrogen receptor. In order to obtain a higher response rate than that for single therapy, experimental attempts were made to combine cytotoxic agents, antiestrogenic agents, ablative therapy and immunotherapy from the viewpoints of
tumor
cell kinetics, natural killer activity and interferon activity of spleen cells.
Tamoxifen
and orchiectomy were shown by flow cytometry to produce a G1 block, increasing the G0, G1 phase and decreasing the S phase, in MCF-7 cells in vitro and in SC 115 cells, in vivo respectively, for a long period. On the other hand, 5-FU showed most effective cytotoxicity in the S phase of both types of
tumor
cells in vitro and in vivo, although the depressed S phase recovered within 24 hours. Therefore, any combined chemo-endocrine therapy should be devised so that the endocrine therapy maintains a G1 block for a long period and performed immediately following chemotherapy during the decreased S phase of the
tumor
cells. N K activity of spleen cells were enhanced, and interferon production in spleen cells was not changed by ovariectomy in C3H/He mice compared with sham-operated mice. It is suggested that endocrine therapy may affect the immunopotentiality of cancer patients.
...
PMID:[Experimental studies on the enhanced effects of chemoendocrine therapy in breast cancer]. 356 91
Tamoxifen
is a nonsteroidal antiestrogen whose mode of action is, as yet, unclear. The purpose of this report is to investigate the effects of
Tamoxifen
on endometrial adenocarcinoma ultrastructurally. Five patients with endometrial adenocarcinoma, 3 cases well differentiated and the others undifferentiated, were treated with 20mg
Tamoxifen
per os a day for 7 days, and the following changes were observed: The cells became roundish and slightly swollen. Development of cytoplasmic organelles was observed. In the cytoplasm, glycogen granules did not increase. These results suggest that an anti-cancer effect is brought about by the induction of the tissue toward functional differentiation as well as inhibition of glycogen metabolism in
tumor
cells.
...
PMID:Effect of tamoxifen on ultrastructure of endometrial carcinoma. 358 11
The influence of
Tamoxifen
on the lymphocyte mediated auto-
tumor
lysis was tested in vitro. The drug caused an induction or enhancement of auto-
tumor
lysis in a considerable number of experiments, whereas a reduction of this function was observed in 2 experiments.
...
PMID:Effect of tamoxifen on cell-mediated auto-tumor lysis. 359 62
A 37-year-old female, who had undergone a left standard mastectomy in May, 1983 for breast cancer, was treated with
Tamoxifen
and FT-207 postoperatively. The patient had no further evidence of disease until two and one-half years later, when a routine chest film showed a single, half-rounded density 6.5 cm in diameter in the hilus of her left lung. Bestrabucil, the benzoate of an estradiol-chlorambucil conjugate, was administered p.o. at a daily dose of 200 mg for four weeks. Thereafter, the
tumor
greatly decreased in size to 3.0 cm in diameter. When a left upper lobectomy was performed, the
tumor
was found to be necrotic tissue. Microscopically, a small cancer nest similar to the primary breast carcinoma was observed in the center of the necrosis. The necrotic tissue was surrounded with cellular infiltrate, markedly consisting of histiocytes.
...
PMID:[A case of breast carcinoma with lung metastasis]. 359 80
The 6-day subrenal capsule assay was used to determine chemotherapeutic sensitivities of brain tumors. Twenty-nine brain tumors were obtained at the time of surgical resection. A minced
tumor
fragment (1-mm cube) was implanted under the renal capsule of 5- to 8- week-old normal female ddY mice. Each fragment was measured at two diameters using ocular micrometer unit (10 omu = 1.0 mm). The animals were randomized, usually 5 to 7 per group, and treated with anticancer drugs on day 1 through 5. On day 6, the mice were killed. The kidney was exteriorized and the
tumor
was again measured. The change in
tumor
size was obtained for each animal by ratio of the final
tumor
size/the initial
tumor
size. Sensitivities of tumors to anticancer agents were determined by comparing differences in mean values of the change in
tumor
size between control and treated group. Twenty-seven out of 29 specimens (93%) were submitted to evaluable assay. The response rate of 11 malignant gliomas (grade 3 and 4) was 44% and that to anticancer drugs tested were as follow: 5-FU 78%, ACNU and CPA 50%, VCR 40%, CDDP 36%. The response rate of 3 medulloblastomas was 36%: MTX 67%, CPA 50%, ACNU and CDDP 33%. That of two low-grade gliomas (grade 2) was 29%, while that of 4 malignant brain tumors (2 metastasis, chordoma, malignant fibrous histiocytoma) was 60%. Four neurinomas and 3 meningiomas were not sensitive to
Tamoxifen
and none were determined for estrogen receptor. In histological analysis, the transplanted
tumor
retained similar characteristics to the original
tumor
in the cases of neurinomas, meningiomas and some gliomas. Lymphocytic infiltration was observed in many cases. In the cases of metastasis (adenocarcinomas), considerable mesenchymation and lymphocytic infiltration was observed,
tumor
cells were reduced in number with poor preservation. Clinical response in 9 cases treated with sensitive drugs were 1 complete response, 2 partial response, 5 stable and 1 progressive disease in CT examination. The subrenal capsule assay is therefore considered to be very useful for determining suitable chemotherapeutic agents for brain tumors.
...
PMID:[Responsiveness of brain tumors to chemotherapeutic agents in the subrenal capsule assay]. 372 48
Between May 1980 and November 1983, 46 eligible patients with advanced, objectively evaluable endometrial carcinoma were treated with tamoxifen, 10 mg twice daily. Twenty-two of the patients had previously received progestational agents. None of the progestin-refractory patients experienced
tumor
regression on tamoxifen treatment, while five of the 24 previously untreated with progestins did experience tamoxifen-induced
tumor
regression. Of the five patients previously treated with cytotoxic drugs, only one experienced objective
tumor
regression on tamoxifen. Although 28 of these 46 patients were completely ambulatory at the beginning of tamoxifen treatment, only 26% were alive 1 year later; median survival for the entire group was only 120 days.
Tamoxifen
in this dose cannot be recommended routinely as effective secondary treatment for patients with progestin-refractory advanced endometrial carcinoma.
...
PMID:Ineffectiveness of tamoxifen in advanced endometrial carcinoma after failure of progestin treatment. 373 Nov 47
The human breast cancer cell line MCF-7 can be growth stimulated by estradiol (10(-8) M) when grown in the presence of high concentration of newborn calf serum (NCS, 10%) or high concentration of estrogen depleted fetal calf serum (FCS, 10%). Estradiol stimulated cultures grow with an increased growth rate and also the final cell number in the culture flasks is increased. Analysis of the cell cycle parameters revealed that the proportion of cells in the G1 phase is decreased and the proportion of S phase cells is increased. In comparison, the increase in growth fraction is less significant. These results show that estradiol stimulated cultures grow with a shorter cell cycle time and a shortening of the G1 transit time may explain the observed changes in cell cycle parameters. We assume that the shorter cell cycle time as well as the ability to grow without density inhibition may be prerequisites for
tumor
formation. MCF-7 cells can be growth inhibited by the antiestrogen tamoxifen (10(-6) M). The growth inhibition is estrogen reversible, but estradiol has no growth stimulatory effect under the described growth conditions (0.5% FCS). Growth inhibited cultures accumulate cells with a G1 amount of DNA and the majority of this accumulation is due to non cycling cells.
Tamoxifen
is not a cell cycle phase specific growth inhibitory agent since cells with a G2 amount of DNA are non cycling. Long term treatment with tamoxifen results in cell death, but a few colonies of cells survive more than 10 days' treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Cell cycle analysis of estrogen stimulation and antiestrogen inhibition of growth of the human breast cancer cell line MCF-7. 374 66
Tamoxifen
(
TAM
) has previously been shown to inhibit growth of the Dunning R3327 rat prostate adenocarcinoma and to elevate serum prolactin levels. The purpose of this study was to determine the role of prolactin in modulating the effects of tamoxifen on growth of the R3327 prostatic adenocarcinoma. Intact and castrated Copenhagen-Fischer male rats bearing the Dunning R3327 rat prostatic
tumor
were divided into groups and injected sc five times per week for 16 weeks as follows: vehicle;
TAM
(0.5 mg/kg); haloperidol (HALO; 0.5 mg/kg); bromocriptine (CB-154; 5 mg/kg);
TAM
plus HALO; or
TAM
plus CB-154. In both intact and castrated rats, agents that either raised (HALO) or lowered (CB-154) serum prolactin had little effect on prostatic tumor growth when administered singly. In intact rats, average
tumor
diameter in vehicle-treated controls increased 421% 16 weeks after the start of the experiment, and treatment with
TAM
or
TAM
plus HALO reduced this tumor growth by approximately one-half. Interestingly, CB-154 administered in combination with
TAM
completely blocked
TAM
inhibition of tumor growth in intact rats. In contrast to these results in intact rats, average
tumor
diameter increased 129% in
TAM
- and 118% in
TAM
plus HALO-treated castrated rats and was significantly greater than the characteristic retardation of tumor growth (49% increase) that occurred in the vehicle-treated castrate controls. In addition, combined treatment of
TAM
plus CB-154 in castrate rats resulted in an even greater increase (188%) in average
tumor
diameter. The inhibitory effect of
TAM
on R3327 prostatic tumor growth in intact rats appears to be an indirect effect resulting from its ability to reduce serum testosterone levels. In contrast, the stimulatory effect of
TAM
in castrate rats appears to result directly from an estrogen-like action, which can directly enhance prostatic tumor growth in the presence of low levels of circulating androgens; this stimulatory effect of
TAM
is more pronounced when prolactin levels are suppressed by CB-154. Clearly, castration alone is more effective than
TAM
therapy alone or in combination with castration in the retardation of the growth of the androgen-dependent R3327 prostatic
tumor
in rats.
...
PMID:Role of prolactin in modulating the effects of tamoxifen on growth of the Dunning R3327 rat prostate adenocarcinoma. 382 18
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