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

Estrogen (ER) and progesterone (PR) receptor levels were assayed in primary tumor samples from 271 premenopausal patients suffering T1,2N1M0 (stage II) breast cancer. Four clinical groups were identified according to steroid receptor levels in which results of adjuvant treatment (chemotherapy or complex treatment) were assessed. ER and PR positivity was associated with longer disease-free and overall survival. Adjuvant hormone therapy proved beneficial in ER+PR+ tumor patients. The latter group was also characterized by a lower relapse rate, particularly, in those aged over 40. It is recommended that: (1) T1,2N1M0 breast cancer patients be given adjuvant chemotherapy whatever tumor receptor status, (2) these patients should not be given adjuvant hormone therapy unless tumor receptor status has been established since prophylactic oophorectomy and subsequent hormone therapy are not justified for operable breast cancer, (3) complex therapy be administered to premenopausal patients aged over 40 years with ER+PR+ tumors only, and (4) PR-positivity be considered a good predictor of hormone sensitivity of cancer.
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PMID:[The role of tumor receptor status in choosing adjuvant therapy for breast cancer patients of reproductive age]. 130 Jul 82

The effects of estrogen, progesterone, and testosterone on the growth of 7,12 dimethylbenz(a)anthracene (DMBA) induced adenocarcinomas in rats (Wistar strain) were evaluated. Estrogen resulted in the highest acceleration of tumor volume. The histologic features were a solid structure associated with a significant proliferation of connective tissues and with many signet ring cells with intracytoplasmic canaliculi. Progesterone changed the histologic features to a more immature adenocarcinoma associated with a notable solid area with many mitotic figures, although the growth rate of the tumor was the same as the controls. On the contrary, testosterone induced the slowest tumor growth and a histologically scirrhus pattern. The results of this preliminary observation indicate a possible role for sex steroids in the ovarian tumorigenic process.
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PMID:A study of the role of sex hormones in rat ovarian cancer. 130 11

Renal cell carcinoma has been reported to contain estrogen and progesterone receptors. Thus, it has been suggested that these tumors are hormone dependent in a similar manner described for the breast and prostate cancers. It has been recently shown that mammary and prostate tumor cells contain gonadotropin-releasing hormone (GnRH) receptors and are growth inhibited directly by GnRH antagonists. In this study we examined for the presence of GnRH, estrogen and progesterone receptors in normal and malignant renal tissues. Estrogen receptors were found both in the normal and malignant kidney while progesterone receptors were present only in the normal tissue. Specific binding of [125I]buserelin, a GnRH agonist, was evident in renal carcinoma and in normal kidney and was displaced with equal efficiency by unlabeled buserelin and by D-Trp6-GnRH, but not by unrelated peptides such as thyrotropin releasing hormone and oxytocin. The non-linear scatchard curve obtained for buserelin binding, suggests the presence of at least two binding sites, one with high affinity in the nanomolar range and another in the micromolar range.
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PMID:Gonadotropin-releasing hormone specific binding sites in normal and malignant renal tissue. 133 44

Ovarian steroids are associated with the proliferation of normal as well as tumorigenically transformed mammary epithelial cells. The experiments performed in this study were designed to establish that (1) tumorigenic transformation induced by the ras oncogene is associated with alterations in estradiol biotransformation, (2) altered endocrine responsiveness persists in the fully transformed tumor cell phenotype and (3) specific perturbations induced by the ras oncogene can be experimentally downregulated. The ras transfectant pH06T and the tumor-derived T1/Pr1 cells exhibited 3- and 43-fold increases, respectively, in C-16 alpha hydroxylation of estradiol relative to the parental mouse mammary epithelial cells (P less than 0.0001). At the cellular level, this alteration corresponded with approximately 90-fold increase in the anchorage-independent growth of T1/Pr1 cells (P less than 0.0001). Estrogen responsiveness of T1/Pr1 cells was demonstrated by their suppression of growth in phenol red-free and/or tamoxifen-supplemented medium and by the reversal of antiproliferative effect of tamoxifen by phenol red and estradiol. Indole-3-carbinol, a naturally occurring tumor suppressive agent, was able to upregulate C-2 hydroxylation at the expense of C-16 alpha hydroxylation of estradiol. Treatment of T1/Pr1 cells with indole-3-carbinol resulted in a substantial decrease in anchorage-independent growth.
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PMID:Persistent estrogen responsiveness of ras oncogene-transformed mouse mammary epithelial cells. 144 Jun 96

Estrogen and progesterone receptors (ER, PR) were measured in cytosol fractions from 18 primary canine mammary carcinomas by use of biochemical assays. One or both receptors were detected (> 10 fmol/mg of cytosol protein) in 11 tumors: 5 ER and PR; 2 ER only; 4 PR only. Mean cytoplasmic receptor concentrations (fmol/mg of cytosol protein) were 22.8 +/- 2.9 (SEM) for ER and 51.0 +/- 10.3 for PR in tumors containing ER and PR, 28.8 +/- 12.1 for ER in tumors containing only ER and 13.2 +/- 1.5 for PR in tumors containing only PR. Estrogen or progesterone receptors or both were identified in 6 of 9 tubular adenocarcinomas, 4 of 5 papillary adenocarcinomas, and 1 of 1 squamous cell carcinoma. These receptors were not identified in solid carcinomas (n = 2) or a single spindle cell carcinoma. Although the number of cases was limited, survival times of dogs tended to be longest in those with tumors containing ER alone or in combination with PR, intermediate in those with tumors containing only PR, and shortest in those with tumors without ER or PR. A correlation was not apparent between receptor status and age, presence of ovaries, tumor size, or histologic classification of the tumor. In the analysis of this series, the extent of surgery (mastectomy of the involved gland vs unilateral or bilateral mastectomy) did not appear to influence the outcome of the disease, and metastasis to regional lymph nodes did not appear to be a reliable prognostic indicator.
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PMID:Estrogen and progesterone receptor status of mammary carcinomas and correlation with clinical outcome in dogs. 146 19

Estrogen (ER) and progesterone receptor (PR) contents in primary tumors from 127 advanced breast cancer patients were measured by DCC method. The patients were followed for 2 years and the prognostic value of the receptor levels was evaluated and compared with other tumor and patient characteristics. No relation was found between receptor levels and tumor, first relapse site as well as short-term survival (2 years) which might be due to the advanced stage of disease at diagnosis.
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PMID:Estrogen and progesterone receptor status of primary breast cancer: relationship with the pattern of first metastasis and survival. 149 24

The case is a 77-year-old man who was first examined in August 1980 (at age 67). Prostatic biopsy revealed a poorly-differentiated adenocarcinoma, and clinically, diagnosis was made as stage B. Castration and DES administration were carried out. Subsequent chemotherapy with BLM, MMC, and 5-FU led to CR. A periodical check-up in September 1985 detected a pelvic lymph node metastasis, which was, however, completely remitted by radiotherapy and chemotherapy. In April 1990, local relapse was noted in the left lobe of the prostate. Biopsy revealed a poorly-differentiated adenocarcinoma. Three courses of intravenous administration of CDDP, THP, and VP-16 caused no change. From August 1990 on, anal submucosal injection of MTX was started. 20 mg of MTX administration once a week, for consecutive 5 weeks, followed by 4-week interruption on ambulatory basis formed one course. The tumor was distinctly reduced following one course, disappeared (MRI) following two courses and showed only a few viable cells (biopsy) following four courses. We consider that the present method is a hopeful new therapeutic approach.
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PMID:[The effectiveness of anal submucosal injection of methotrexate for relapsed prostatic cancer--a case report]. 149 7

Human uterine leiomyosarcoma is a rare gynecological malignancy with a generally poor prognosis. We have established a human uterine leiomyosarcoma tumor line in nude mice, designated UTS-1, and describe the characteristics of this tumor. The UTS-1 tumor doubled in 12.1 days and retained the histological characteristics of leiomyosarcoma, even after 14 serial generations. Ultrastructurally, the tumor is characterized by nuclear pleomorphism typical of smooth muscle, intracytoplasmic filaments with dense bodies, a relative paucity of micropinocytotic vesicles, and an incomplete external lamina. Immunohistochemically, the UTS-1 cells reacted with antibodies against vimentin, desmin, smooth-muscle actin and myosin, but not with antibodies against keratin, CEA and S-100 protein. Serum levels of AFP, CA125, CEA and SCC ranged within normal limits in tumor-bearing mice. The serum level of immunosuppressive acidic protein correlated well with an activity of the tumor. Estrogen and progesterone receptors were not detected in the tumor. Chromosomal analysis showed a human karyotype with some marker chromosomes and a modal number of 85 chromosomes. The UTS-1 tumor should prove a useful model to explore the biological characteristics and treatment of human uterine leiomyosarcoma.
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PMID:Establishment and characterization of human uterine leiomyosarcoma heterotransplanted into nude mice. 150 Feb 17

Estrogen is thought to stimulate the proliferation of human breast tumors indirectly, through induced production of autocrine polypeptide growth factors. Constitutive production of such growth factors would lead to the loss of 17 beta-estradiol (E2)-dependence that is associated with progression of the disease. Our data, however, do not support this hypothesis and suggest that hormone-dependent breast tumor cell lines like MCF7 do not react to the growth factors which they produce. Moreover, we provide evidence that E2 directly stimulates proliferation by inducing, like many growth factors, the c-fos proto-oncogene. E2 by itself, however, is poorly mitogenic. This may be caused by the lack of induction of genes from the jun family, whose gene products are necessary for dimerization with the c-fos encoded protein, leading to an important step in growth factor signalling pathways; stimulation of TPA responsive element (TRE)-dependent transcriptional activity. In combination with insulin-like growth factors, efficient inducers of c-jun in these cells, E2 synergistically stimulates proliferation and TRE-activity. Constitutive TRE-activation may lead to loss of E2-dependence.
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PMID:Direct stimulation by estrogen of growth factor signal transduction pathways in human breast cancer cells. 152 51

The effects of 17 beta-estradiol versus tamoxifen on the growth and metabolism of MCF7 human breast cancer cells, in culture and in tumors implanted in nude mice, were studied by 31P and 13C nuclear magnetic resonance spectroscopy and by proton magnetic resonance imaging. In culture, the content of the phosphate metabolites including nucleoside triphosphates (NTP), phosphomonoesters, phosphodiesters and inorganic phosphate (Pi) were not affected by tamoxifen treatment. However, in the presence of estrogen the rate of glucose consumption and lactate production via glycolysis (270 and 280 fmol/cell.h, respectively) were twice that of tamoxifen treated cells. Estrogen rescue of tamoxifen treated cells indicated that glycolysis induction occurs at the early stages of the hormonal response. The in vivo studies included recording of proton images that provided an accurate measure of tumor size and distribution of tumor cells, necrotic regions and stromal tissue. Tamoxifen caused enhanced necrosis extending from the center of the tumor during the first two days of treatment (12 h to 6 days). This was followed by growth of reparative tissue along with tumor regression. Tamoxifen also modified the content of the phosphate metabolites, increasing markedly (P less than 0.0002) the ratio of NTP to Pi from 0.41 before treatment to 1.75 9-19 days after treatment. This change was attributed to the enhanced growth of repair tissue. The results provide new information regarding the response of human breast cancer to hormonal treatment and suggest a mechanism for the induction of tumor regression by tamoxifen.
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PMID:Tamoxifen induced changes in MCF7 human breast cancer: in vitro and in vivo studies using nuclear magnetic resonance spectroscopy and imaging. 152 59


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