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Query: UMLS:C0007097 (carcinoma)
 152,788 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-four patients with endometrial carcinoma received tamoxifen (Nolvadex) for 7 days. Before and after administration, circulating hormones (estradiol, testosterone, progesterone, gonadotropins FSH and LH) were evaluated. Estrogen (ER) and progesterone receptors (PgR) in neoplastic tissue were also assayed. Our results show a net increase in PgR content and a significant decrease in gonadotropin levels after the treatment. The authors suggest that clinical trials be conducted using tamoxifen and progestins for adjuvant therapy after surgery of endometrial carcinoma and for the therapeutic approach of advanced carcinoma.
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PMID:Hormonal and receptor status in postmenopausal women with endometrial carcinoma before and after treatment with tamoxifen. 642 17

Patients with advanced prostatic carcinoma who had received minimal or no prior therapy were treated with tamoxifen citrate in escalating doses from 10 to 50 mg orally twice a day. Twenty-nine courses were evaluated in 17 patients. Entry was limited to patients with measurable sites of disease. There were no objective responses at any dose level in these measurable sites. Acid and alkaline phosphatase were reduced in 0% and 18% of courses, respectively. Serum testosterone increased by an average of 119 ng/ml. Most increases were transient; no tumor flares were observed. Transperineal prostate biopsies in selected patients after completion of treatment showed no evidence of tumor necrosis or alteration in histologic grade of the tumors. Tamoxifen citrate, over the range of doses evaluated, has no activity in metastatic prostatic carcinoma.
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PMID:Tamoxifen in advanced prostatic carcinoma. A dose escalation study. 643 May 41

Seventy patients with advanced breast carcinoma were treated with a loading dose regimen of 160 mg Tamoxifen on day 1 followed by a maintenance dose of 20 mg daily from day 2 onwards. Compliance was 100% and only 3 patients developed mild side effects. In 27% regression of disease was observed within 1 month and in 57% within 2 months. This regimen is recommended for routine clinical use.
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PMID:A clinical assessment of loading dose tamoxifen for advanced breast carcinoma. 650 18

Twenty-four patients with advanced carcinoma of the male breast have been treated with tamoxifen citrate (Nolvadex). An objective regression rate of 37.5% was obtained, with five complete and four partial responses. In addition, two patients had stabilisation of their disease for 24 months each. Regression of disease was noted in soft-tissue disease, bone and lung metastases. The duration of response ranged from 8 months to 60 months with a mean of 21 months. In view of the singular lack of side-effects and the age group of the patients (mean age 63 years), it is suggested that tamoxifen should be the first line of endocrine therapy before orchidectomy or adrenalectomy.
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PMID:Tamoxifen in the treatment of male breast carcinoma. 667 81

Cell proliferation kinetics during growth of an estrogen receptor-positive human breast carcinoma cell line, T-47D, was defined, and some factors which modify its response to tamoxifen were investigated in vitro. T-47D cells were estrogen responsive when grown in charcoal-stripped fetal calf serum, but the addition of 17 beta-estradiol did not fully restore the growth rate to that observed in the same concentration of fetal calf serum. Tamoxifen had both a low-dose, estrogen-reversible, growth-inhibitory effect and a high-dose, estrogen-irreversible, growth-inhibitory and cytotoxic effect on T-47D cells. Tamoxifen-induced growth inhibition was associated with a decrease in the percentage of S-phase cells and, to a lesser extent, G2-M-phase cells and an increase in G0-G1-phase cells. Plateau-phase cells were considerably less sensitive than were exponentially growing cells, and this was accompanied by a fall in unoccupied estrogen receptor content from 4407 +/- 655 (S.E.) sites/cell in exponentially growing cultures to 1420 +/- 315 sites/cell in plateau-phase cultures. T-47D cells were more sensitive to tamoxifen cytostasis when grown in fetal calf serum rather than charcoal-stripped fetal calf serum. However, with both types of growth medium, the sensitivity to tamoxifen was inversely related to the serum concentration, e.g., the 50%-inhibitory dose concentration increased 75-fold as the fetal calf serum concentration was increased from 0.25 to 10%. Addition of insulin to the culture medium had no effect on the growth rate, estrogen receptor content, or tamoxifen sensitivity of T-47D cells. These results illustrate that the conditions under which cells are cultured markedly affect their sensitivity to tamoxifen and highlight the need to specify these conditions when reporting effects of this drug.
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PMID:Factors affecting the sensitivity of T-47D human breast cancer cells to tamoxifen. 672 80

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

Daily treatment of female Sprague-Dawley rats with CB-154 (prolactin suppressor) or Tamoxifen (estrogen antagonist) for 33 days before and after 7,12-dimethylbenzanthracene (DMBA) administration reduced (p less than 0.005) the incidence of mammary carcinomas by 58 and 49%, respectively. A combination of CB-154 and Tamoxifen further reduced (p less than 0.005) mammary carcinoma incidence by an additional 50-59%. Treatment with Tamoxifen for 66 days beginning 33 days after carcinogen treatment reduced (p less than 0.05) the incidence of mammary carcinomas by 65%; CB-154 treatment, during the same time period, did not significantly effect the final yield of mammary carcinomas. The combination of Tamoxifen and CB-154 was comparable to Tamoxifen alone in suppressing the incidence of mammary carcinomas in the latter study. These results demonstrate a substantial suppressive and synergistic effect of Tamoxifen and CB-154 in the initiating phases of mammary carcinogenesis while in the early promoting phases of this oncogenic process, short-term treatment with Tamoxifen was superior to CB-154 treatment; no synergism between these clinically important compounds was observed.
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PMID:2-bromo-alpha-ergocryptine (CB-154) and tamoxifen (ICI 46,474) induced suppression of the genesis of mammary carcinomas in female rats treated with 7,12-dimethylbenzanthracene (DMBA): a comparison. 680 66

MCF-7 human mammary carcinoma cells were inoculated into 150-sq cm flasks at 3 X 10(5) cells/flask, and after a lag period of about 48 hr, these cells grew exponentially for 5 days with a mean population doubling time of about 24 hr. During exponential growth, 80 to 90% of cells were in the "rapidly cycling" pool, the clonogenic fraction was 50 to 60%, and the mean percentage of cells in the G0-G1, S, and G2 + M phases of the cell cycle was 48.9 +/- 0.6% (S.E.), 39.4 +/- 0.6%, and 11.6 +/- 0.3%, respectively. These parameters changed rapidly between Days 7 and 13 when plateau phase was reached. Between Days 13 and 18, 74.8 +/- 0.7% of cells were in G0-G1, 15.3 +/- 0.4% were in S, and 9.8 +/- 0.6% were in G2 + M phase. Only about 30% of these cells were cycling rapidly, and the clonogenic fraction had fallen to less than 10%. Tamoxifen induced a dose-dependent decrease in the growth rate of exponentially growing cells, which was accompanied by a dose-dependent increase in percentage of G0-G1-phase cells, and a decline in percentage of S-phase cells. At doses greater than or equal to 10 microM, a 24-hr pulse of tamoxifen was cytotoxic to exponentially growing cells. Plateau-phase cells were less sensitive to these effects of tamoxifen. In an attempt to define the kinetic basis of the G0-G1 accumulation induced by tamoxifen, asynchronous MCF-7 cells were pretreated for 42 hr with various doses of tamoxifen, and the rate of efflux of cells from the G0-G1 phase of the cell cycle was assessed by blocking their reentry into G1 with ICRF 159. Following treatment of control cultures with ICRF 159, two populations of cells were distinguished by their rates of efflux from G0-G1 phase. The majority of cells left G0-G1 rapidly with a mean t1/2 of 2.3 hr ("rapidly cycling" cells). However, about 18% of cells had a much slower rate of exit with a mean t1/2 of about 30 hr ("slowly cycling" cells). Pretreatment with tamoxifen resulted in a dose-dependent decrease in the proportion of rapidly cycling cells and an increase in the proportion of cells with slow G1 transit times. Although this appeared to be the predominant effect, tamoxifen also decreased the rate at which the slowly cycling cells traversed G1. Simultaneous treatment with estradiol returned these parameters to control values at doses of tamoxifen less than or equal to 5 microM, partially reversed the effect of 7.5 microM tamoxifen, but was without effect on the arrest of cell cycle progression induced by 10 microM tamoxifen. It is concluded that cells accumulate in G0-G1 following tamoxifen treatment due to an increase in the proportion of slowly cycling cells at the expense of a population of rapidly cycling cells, which appear to be relatively uninfluenced by the drug.
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PMID:Cell proliferation kinetics of MCF-7 human mammary carcinoma cells in culture and effects of tamoxifen on exponentially growing and plateau-phase cells. 687 41

Estrogen (ER) and progesterone (PgR) receptor contents were determined in 214 patients with primary mammary carcinoma. Premenopausal and postmenopausal females (43 and 48%, respectively) were found to be ER and PgR positive. ER levels between 100 and 500 fmol/mg protein were observed in 37% postmenopausal and 14% premenopausal patients, respectively. ER distribution between lymph node-positive and -negative patients did not differ significantly. Subjects without detectable ER had recurrences earlier than did subjects with ER. On the other hand, no differences in recurrence rates were noted when PgR-positive and -negative patients were compared. In addition, the determination of ER did not permit selection of patients for adjuvant cytotoxic chemotherapy. Furthermore, the action of tamoxifen was investigated in the rat pituitary as a model system. Tamoxifen was found to act as antiestrogen at the level of transcription by inhibiting the accumulation of estrogen-stimulated preprolactin mRNA. Combined data suggest that patients with positive lymph nodes and positive receptors may benefit from combined endocrine plus cytotoxic adjuvant chemotherapy.
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PMID:Clinical and experimental aspects of hormone receptors in breast carcinoma patients. 688 82

Prostatic Carcinoma is known to be a hormonally responsive neoplasm which contains both estrogen and androgen receptors. Sixty-three heavily pretreated patients with Stage D prostatic adenocarcinoma received tamoxifen (Nolvadex) at a dose of 20 mg twice a day. Patients were examined every 4 weeks at which time they also had a white count, hemoglobin and platelet count, acid phosphatase, SMA-12, and recording of the status of their measurable or evaluable disease. If the evaluable disease was metastatic to bone, the relevant x-rays were repeated every 8 weeks. The median age of the patients was 66. The Karnofsky status of the patients for whom this information was known was 40% (6), 45% (1), 50% (1), 60% (8), 70% (11), 80% (6), 90% (5), and 100% (2). Forty-one patients were eligible for response evaluation; the majority had evaluable bone disease. No serious toxicity was encountered; two patients withdrew from the protocol because of nausea and vomiting and one patient had hot flashes. One complete response was seen in measurable nodal disease which is continuing after 13+ months, 1 minor response was seen in evaluable bone disease, and 4 patients had long (more than 10 months) stability of bone disease with subjective improvement. We conclude that although the response rate was low, patient acceptability was excellent and that tamoxifen may warrant further trial in a less heavily pretreated patient population.
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PMID:A phase II study Nolvadex: tamoxifen citrate in the treatment of advanced prostatic adenocarcinoma. 709 Oct 40


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