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Query: UMLS:C0006826 (cancer)
 1,092,456 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study describes the distribution and frequency of estrogen receptor (ER), progesterone receptor (PR), androgen receptor (AR), and glucocorticoid receptor (GR) in a large series of patients with primary metastatic breast cancer. 329 patients were in this series. All 4 steroid hormone receptors were present in the population: ER was positive in 53%, PR was positive in 38%, AR was positive for 31%, and GR was positive in 52%. Next, the distribution of ERs as well as the distributions of PR, AR, and GR values seemed unimodal. There was a very high correlation between any steroid hormone receptor value expressed as either fmol/mg of cytoplasmic protein or fmol/mg of breast tumor. Of more importance was that alternate methods of data expression did not alter the classification of values as positive or negative. No correlation was found between any of the steroid hormone receptors and laterality of the breast tumor, location and size of the primary tumor, extent of disease, or type of tissue assayed. None of the steroid hormone receptors correlated with age. There was a strong correlation noted between ER values and menopausal status. Neither PR, AR, nor GR was significantly associated with menopausal status. ER status was correlated with axillary nodal status, with the ER positive group containing a high proportion of node-negative patients. Finally, quantitative analysis of steroid receptor hormone values demonstrated correlations among other receptors. Plotting values of any 1 receptor vs. any other receptor resulted in a positive Kendall rank test correlation which was highly significant.
Cancer Res 1979 May
PMID:Distribution, frequency, and quantitative analysis of estrogen, progesterone, androgen, and glucocorticoid receptors in human breast cancer. 42 88

The specific estrogen receptor in the cytosol of human breast cancer tissue was assayed in 217 primary cases. The specific progesterone receptor was also assayed in 48 cases as evidence of estrogen action on the tissue. Both receptors were positive in 45.8% of all cases. Plasma 17beta-estradiol and progesterone were assayed concomitantly with these steroid receptors. The higher hormone levels were found in the cases with fewer receptor binding sites. The relationship between 17beta-estradiol levels in tumor cytosol and the number of binding sites was more clearly observed. Plasma prolactin levels, however, showed no correlation with the number of receptor binding sites or the plasma levels of sex steroids. None of these assayed substances had a clear correlation with the histological type of tumor or the clinical stage of the disease.
Cancer Res 1979 May
PMID:Estrogen and progesterone receptors in human breast cancer with concomitant assay of plasma 17beta-estradiol, progesterone, and prolactin levels. 42 16

85 patients with metastatic or surgically unrecsectable primary breast cancer who had had 1 or more steroid hormone receptor assays performed immediately before the institution of endocrine therapy were studied retrospectively to determine any influence of steroid hormone receptors on response rate to endocrine therapy. Included in addition to effects of estrogen receptor (ER) status are the effects of androgen receptor (AR), progesterone receptor (PR), and glucocorticoid receptor (GR) on therapy perfornamce. Of 18 patients whose tumor contained PR, 11 responded to endocrine therapy, compared with 8 of 26 patients with low or absent PR. PR increased the predictive index of the ER in an group of patients who had received no prior therapy, but it did not help in patients who had received prior endocrine therapy. 0 of 4 patients whose tumors were ER negative but PR positive responded to endocrine therapy. Present trends suggest a possible association between AR and GR and response to endocrine therapy. A cut-off value of 10 fmol/mg of cytoplasmic protein was needed to make these trends apparent. The distributions of AR and GR values for responders and nonresponders were not significantly different. Knowledge of AR status does not increase the protective index in ER-positive or ER-negative tumors. GR positivity may increase the predictive index in ER-positive tumors, but not in ER-negative ones.
Cancer Res 1979 Jun
PMID:Relationship between the progesterone, androgen, and glucocorticoid receptor and response rate to endocrine therapy in metastatic breast cancer. 44 96

The stimulation of RNA synthesis induced by estradiol has been studied on 60 breast cancers in short-term cultures. In the same tumors the estrogen receptor (ER) assay was carried out. In 35% of the cases studied the stimulating effect by estradiol in vitro was observed. The frequency of response to in vitro hormone treatment was higher (42%) in ER+ cancers and lower (25%) in ER- cancers. The specificity of the in vitro test was assessed by the use of tamoxifen.
Cancer 1979 Jun
PMID:Short-term tissue culture of human breast cancer: presence of estrogen receptors and 17 beta-estradiol stimulation of RNA synthesis. 45 26

Tissue specimens from 55 female patients with benign breast disease were assayed for estrogen receptor. Twenty-one of 55 patients (38%) had tumors which contained significant amounts of estrogen receptor (greater than 10 femtomoles/mg protein). Fibroadenomas possessed estrogen receptor more frequently than fibrocystic disease or other benign breast tumors. Estrogen receptor positivity did not correlate with laterality of the tumor; location or size of the largest nodule. Patients with estrogen receptor positive tumors had a mean age of 26.9 years compared to 36.4 years for patients with estrogen receptor negative tumors (p less than 0.01). Twenty of 46 (43%) premenopausal patients had benign tumors which were estrogen receptor positive compared to zero of 8 postmenopausal patients (p less than 0.05).
Cancer 1979 Jul
PMID:Estrogen receptor values in patients with benign breast disease. 45 47

Certain oncogenic viruses have been implicated in human breast cancer, including the murine mammary tumor virus (MuMTV) and the Mason-Pfizer monkey virus (MPMV). We have used the leukocyte migration inhibition (LMI) response to assay the response to several potential breast cancer-related antigens, including MuMTV, MPMV, and a breast cancer cultured cell line, MCF-7, in 96 breast cancer patients, in 32 women with benign breast disease, and in 67 normal women. The lowest tenth percentile of control (LMI) responses was used as the cutoff point to designate responders. Breast cancer patients showed significant responses to MuMTV (49% and to MCF-7 (50%), but not to MPMV (29%). In a paired-antigen study using MuMTV and MCF-7, 75% of the breast cancer patients responded, versus 18% of the normal women (P less than 0.0050). The potential for this assay to distinguish "normal" from "breast cancer" was analyzed using a migration index derived from discriminant analysis. The ability of the assay to discriminate "normal" from "cancer" was significant (P less than 0.001) and showed a sensitivity of detecting "cancer" of 75%. The overall responses to MuMTV and MCF-7 were analyzed with reference to certain prognostic factors, but showed no relation to age, menstrual status, estrogen receptor status, or stage of disease. The above reactions suggest that a large proportion of breast cancer patients exhibit presensitization to antigenfs found in MuMTV and MCF-7, which may be cross-reactive with antigens in the primary cancer. These responses appear to be independent of major prognostic variables. Further refinement of this assay may yield one which is more highly discriminating for breast cancer.
 ...
PMID:The leukocyte migration inhibition response to certain breast cancer-related antigens (MCF-7 and MuMTV): their potential as discriminants. 46 74

The proliferative activity of breast cancer has been analyzed in relation to the hormonal characteristics of the host and of the tumor for 199 patients. The analyses of labeling index frequency distributions of estrogen receptor positive (ER+) and negative (ER-) cancers from premenopausal and postmenopausal patients have allowed us to identify three different kinetic groups. A first group, with a very low proliferative activity, includes ER+ cancers from postmenopausal patients; a second group, with an intermediate proliferative activity, includes ER+ cancers from premenopausal and ER- cancers from postmenopausal patients; and a third group, with a very high proliferative activity, includes ER- cancers from premenopausal patients. Generally, the amount of estrogen receptors in ER+ cancers is inversely correlated with the proliferative activity. Lower levels of ER in premenopausal in comparison to postmenopausal patients were found in low proliferative activity tumors.
Cancer 1979 Aug
PMID:Relationship between proliferative activity and estrogen receptors in breast cancer. 47 75

The estrogen receptor status in 335 primary breast carcinomas was correlated with disease-free interval, survival and site of recurrent disease. Estrogen receptor positive carcinomas had a longer disease-free interval, a longer survival (mastectomy-death) and a longer time interval between recurrence and death. These parameters were also influenced by the lymph node status at mastectomy. Estrogen receptor positive cancers had a significantly better chance of survival independent of lymph node status. Estrogen receptors also delayed recurrence in node-positive carcinomas, but this advantage gradually disappeared with increasing interval after mastectomy. Estrogen receptor positive or estrogen receptor negative primary carcinomas did not show any predilection for spread to any particular site.
Cancer 1979 Aug
PMID:Prognostic value of estrogen receptors in primary breast cancer. 47 76

The involvement of rotenone in rat mammary carcinogenesis has been suggested to occur through estrogenic effects. This hypothesis was tested by determining the extent of rotenone inhibition of 17 beta-estradiol binding to the estrogen receptor and of the 17 beta-estradiol-induced uterotrophic response in ovariectomized Sprague-Dawley rats. Estradiol binding to the uterine estrogen receptor in the presence of rotenone was determined by charcoal assay and Scatchard analysis. Additionally, 17 beta-estradiol-receptor interactions were assessed on sucrose density gradients. No inhibition of binding was observed in either assay with ratios of rotenone/17 beta-estradiol in excess of 10,000. Finally, an in vivo approach was used to extend the in vitro data. Silastic capsules containing rotenone or 17 beta-estradiol were implanted in various combinations into eight groups of ovariectomized Sprague-Dawley rats (four rats/group). After five days, uteri were removed and weighed. An analysis of variance revealed that rotenone neither interfered with 17 beta-estradiol-induced uterine weight gain nor displayed any uterotrophic properties by itself. Results from these three procedures demonstrate that rotenone does not act as an estrogen or as an estrogen antagonist. Additionally, there were no other effects attributable to rotenone.
Cancer Res 1979 Nov
PMID:Failure of rotenone to interfere with 17 beta-estradiol action in the rat uterus. 49 75

Results of a study of estrogen Rc receptors in 32 primary human breast cancer cytosol preparations are presented. Tritiated sulfate activation to tritiated adenosine 3'-phosphate 5'-phosphosulfate and subsequent formation of tritiated estrogen sulfotranferase levels was assessed in these preparations. 2 groups of tumors were identified: a low estrogen sulfurylation which was predominantly Rc negative, and a high estrogen sulfurylation with almost exclusive Rc -positivity. In the 1st type of tumor, in which estrogen sulfotranferase levels were low (40 pmol of 17beta-estradiol 3-sulfate formed/mg of protein/2 hours) and were independent of tritiated adenosine 3'-phosphate 5'-phosphosulfate production from tritiated sulfate and adenosine triphosphate, and in the 2nd type of tumor, in which estrogen sulfotransferase levels ranged from 50-200 pmol of 17 beta-estradiol 3-sulfate/mg of protein/2 hours, there was a correlation between the 2 in terms of tritiated adenosine 3'-phosphate 5'-phosphosulfate formation (P.005). 11 of 16 of the 1st type of tumor were estrogen receptor negative, whereas 2 of 16 of the 2nd tumor type were receptor negative. In receptor-negative tumors, the estrogen sulfotransferasse levels were significantly lower than those in receptor-positive tumors (rho=.025).
Cancer Res 1979 Dec
PMID:A correlation between estrogen sulfotransferase levels and estrogen receptor status in human primary breast carcinoma. 49 39


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