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

The relation between the histological type and thepresence of estrogen receptor or response to oophorectomy in the mammary cancers induced by 7,12-dimethylbanz(a)anthracene in Sprague-Dawley rats is discussed. 23 tumors were evaluated for histological classification. 4 were poorly differentiated (Type A), 16 were well-differentiated (Type B), none was atrophic (Type C), and 3 were secretory (Type D). Of the 4 Type A tumors, 3 had the estrogen receptor. Of the 16 Type B tumors, 10 were with the receptor. 3 secretory Type D tumors showed binding. The response to oophorectomy in each group showed no coorelation to the histological type of the tumor. However, there was a good correlation b etween the presence of estrogen receptor and response to oophorectomy in that 12 of 14 tumors that contained the estrogen receptor responded well. None of the 9 tumors that did not show the binding capacity had a good response. The biochemical feature of estrogen receptor has not been shown to exert influence on structural difference of these tumor cells.
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PMID:Lack of correlation between the presence of estrogen receptor and histological type of mammary cancer induced by 7,12-dimethylbenz[alpha]anthracene. 17 60

Retention of estrogen receptor in regrowing tumors long after endocrine ablation in rat and human breast cancer is reported. Mammary cancer was induced in Sprague-Dawley rats by 7,12-dimethylbenz(a)anthracene (DMBA). More than 10 weeks after oophorectomy, tumors that were continuously growing or recurrent after regression were again submitted to estrogen receptor assay. 4 of the 8 tumors did not contain estrogen receptor before oophorectomy; 2 of these responded temporarily and the other 2 did not respond. The estrogen receptor was not found after oophorectomy in any of these 4. In the other 4 with presence of estrogen receptor all showed some response to oophorectomy. All the recurrent tumors in these 4 rats maintained their ability to bind titrated estradiol specifically. There were no definite change of Ks or (Ns) values. In the 4 patients with breast cancer, the metastatic or recurrent tumors disappeared once or regressed after a major endocrine ablation operation. After a relatively long period of regression, the malignancy had recurred. Assay of estrogen receptor and estimation of associated constant (Ks) and concentration of binding sites ((Ns)) continued the same as determined before the ablative therapy. It is assumed that these tumors initially contained cells of 2 types: sensitive and autonomous. The recurrent tumor is thought to be composed of autonomous cells while the sensitive cells have been eliminated by withdrawal of their supporting hormone. Results seem to be contradictory to the concept of autonomy in recurrent breast cancer after hormonal manipulation. The secondary recurrent cancer may sometim es be successfully checked by another hormonal manipulation or by some blocking agents that compete with the estrogen-receptor complex formation.
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PMID:Possible retention of the estrogen-binding capacity after endocrine ablation therapy in the rat and human breast cancer. 17 62

The estrogen receptor was assayed, using the 2,000g supernatant and dextran-coated charcoal method, in 243 tissue samples from human breast cancer, benign breast diseases, macroscopically normal breast tissues, normal uterine myometrium, and uterine myoma. The estrogen receptor was found to be positive in 52.1% of 98 primary breast cancer and in 54.1% of 24 metastatic tumors. The receptor in the breast cancer was found to be similar to that in normal uterine myometrium in the binding character; that is, the dissociation constant of 10(-9) approximately 10(-11) M and number of binding sites of 0 approximately 2,800 fmol/mg protein. There was no correlation between the presence of the receptor and some clinical factors such as menopausal status, age of the patient, urinary 17-ketosteroid excretion, clinical stage of cancer, tumor size, positive or negative axillary lymph node metastasis, histological type, metastatic site of the cancer, or disease-free interval. The estrogen receptor appeared to be retained by metastasis of cancer, and this may lead to the use of the receptor assay with mastectomy specimens for the prediction of response to hormonal therapy in future recurrence of malignancy. Furthermore, it may be possible by this assay to select patients suitable for adjuvant therapy with hormones at the time of mastectomy. A good correlation was found between the presence of the receptor and response to the major endocrine ablation therapy in patients with advanced or metastatic breast cancer. When the receptor was negative in the cancer tissue, the change of response to the endocrine therapy was minimum. On the other hand, if the cancer contained the receptor, approximately 60% of the patients with metastatic or advanced breast cancer responded well to the major endocrine ablation therapy. Thus, the estrogen receptor of breast cancer in Japanese patients appears to bear a close resemblance to that reported in Western patients in its incidence and the correlation to some biological characteristics of the cancer.
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PMID:Estrogen receptor in breast cancer of the Japanese. 19 78

The hormone-dependent 7,12-dimethylbenz(a)anthracene rat mammary tumor has been shown to regress when administered pharmacological doses of testosterone propionate. Tumor regression was correlated with estrogen receptor before and 15 to 20 days following testosterone therapy. A dramatic decline of receptor occurred in all regressing tumors, whereas those administered sesame oil alone maintained both growth and receptor content. Although receptor in regressing tumor was significantly less than in the untreated biopsies, the small amount of remaining receptor maintained the same binding affinity to estradiol, showing that testosterone affects the number and not estrogen affinity of the estrogen receptor. These studies suggest that testosterone depletion of estrogen receptor may be causally related to tumor regression.
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PMID:Estrogen receptors in androgen-induced breast tumor regression. 19 56

The number of plasma membrane receptors for TRH on tumor-derived mammotropic cells in culture, GH3 and GC cells, but not their affinity for TRH, was increased by estrogens. For GH3 cells, exposure to 10 nM 17 beta-estradiol for 48 h increased the receptor level from 54,000 to 90,000 sites/cell, while for GC cells, the number of receptors increased from 29,000 to 46,000 after 28 h. PRL accumulation in the medium was also increased by 17 beta-estradiol. 17 beta-Estradiol and diethylstilbestrol were equally potent in increasing the TRH receptor level, while estrone was only 1/10th as potent. Diethylstilbestrol bound to the cytoplasmic estrogen receptor with an apparent affinity approximately 2.5 times higher than 17 beta-estradiol in GH3 and GC cells, while the affinity for estrone was only 1/12th to 1/20th that of 17 beta-estradiol. Tamoxifen, an antiestrogenic compound, inhibited the increase in TRH receptor number induced by 0.3 nM 17 beta-estradiol and was capable of binding to the estrogen receptor. Modulation of the TRH receptor level on mammotropic cells by estrogens, which is likely mediated through cytoplasmic estrogen receptors, may be an important mechanism for regulation of TRH action.
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PMID:Estrogens increase the number of thyrotropin-releasing hormone receptors on mammotropic cells in culture. 22 Nov 99

Histologic and cytomorphologic features of mammary carcinoma have been correlated with estrogen receptor (ER) levels determined by the dextran-coated charcoal (Scatchard) analysis in 51 primary mammary carcinomas. The results were expressed as follows: ER-positive above and ER-negative below 10 fmol/mg protein and ER-rich above and ER-poor below 250 fmol/g tissue for premenopausal patients (750 fmol for postmenopausal patients). Most lobular carcinomas were ER-positive and ER-rich (84.6%). A similarly high percentage (88.9%) of ER-positive and ER-rich determinations was seen in ductal carcinomas with tubular features, whereas only about half of the remaining ductal tumors were ER-positive or ER-rich. The highest ER values were obtained in the lobular carcinomas and in ductal carcinomas with tubular features. Three cytomorphologic indices independent of variation in tumor histology showed a strong correlation with ER values: maximal epithelial cellularity of the tumor (P less than 0.001); cellular size (P less than 0.05); nuclear size (P less than 0.05).
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PMID:Correlation of estrogen receptor levels with histology and cytomorphology in human mammary cancer. 22 29

Estrogen receptor level expressed as percentages of estrogen receptor-positive cancer cells in the infiltrating cancer cell populations was analyzed with a fluorescent estradiol histochemical technique in fifty-two primary infiltrating and metastatic human mammary carcinomas. The estrogen receptor-positive cancer cells equaled or exceeded the estrogen receptor-negative in number in twelve tumors (23%). The remaining (77%) tumors contained largely estrogen receptor-negative cancer cells. Comparison of the estrogen receptor value in the cytosol derived from tumor tissue homogenates with the histochemical finding in forty cases failed to obtain parallel correlation. Noninvasive intraductal carcinomas were found to be consistently composed of estrogen receptor-negative cancer cells even when present in the vicinity of foci of infiltrating cancer cells with high estrogen receptor activity. In contrast, benign intraductal hyperplastic lesions and papillomas were frequently characterized by piling up of estrogen receptor-positive epithelial cells in the mammary ducts. These observations suggest that when malignant transformation takes place, the cancer cells lose most or all of the progenitors' ability to synthesize estrogen receptors during the intraductal stage of proliferation. This ability is only regained, if ever, by some of the cancer cells during the subsequent infiltrating phase in the stroma. Only occasionally, proliferation of the estrogen receptor-positive cancer cells becomes a prevailing tendency in a human mammary cancer.
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PMID:Cancer cell estrogen receptor of human mammary carcinoma. 22 28

This study measured receptor and deoxyribonucleic acid (DNA) contents in 2 different samples of the same tumor from a human breast cancer to test if results from 1 fragment to the other differ enough to require tumor reclassification. Measurements were taken in 2 samples from 33 primary infiltrating ductal carcinomas. DNA content was found to vary among different subjects and within the same tumor. Receptor distribution also varied; in 45% of the cases, the receptor distribution was homogeneous, and in 55% it was not. In 15% of the cases, 1 fragment was estrogen receptor negative and another was positive, regardless of the parameter to which results were related (DNA or protein). These results showed that there is often no relationship between receptor and DNA contents, since a higher receptor concentration does not always correspond to higher DNA concentrations. No correlation between DNA and receptors was found. The implications of these findings on the use of single biopsy for breast cancer determinations are obvious and are discussed.
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PMID:DNA and oestradiol receptor distribution in human breast cancer. 23 23

Antiestrogen compounds are relatively new in the treatment of breast cancer. A clinical trial of Nafoxidine therapy is being pursued in our institution. In a selected group of patients with metastatic breast cancer who had, in the past, undergone adrenalectomy, Nafoxidine therapy produced objective tumor regression in six out of ten patients. Of the six patients whose tumors contained demonstrable estrogen receptors, four showed regression (67%), one patient had stable disease, and one showed tumor progression. Of the four patients in whom estrogen receptor estimation was not done, two had, in the past, shown regression after endocrine therapy and they also showed regression of tumor with Nafoxidine therapy. In patients with metastatic breast carcinoma, who have undergone adrenalectomy in the past, a therapeutic trial with Nafoxidine may be worthwhile particularly in patients who have demonstrable estrogen receptor in the tumor of those who have in the past shown regression of tumor after endocrine therapy.
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PMID:Clinical trial of nafoxidine in adrenalectomized patients with advanced breast cancer. 33 79

From laboratory studies presented, iodine appears to be a requisite for the normalcy of breast tissue in higher vertebrates. When lacking, the parenchyma in rodents and humans show atypia, dysplasia, and even neoplasia. Iodine-deficient breast tissues are also more susceptible to carcinogen action and promote lesions earlier and in greater profusion. Metabolically, iodine-deficient breasts show changes in RNA/DNA ratios, estrogen receptor proteins, and cytosol iodine levels. Clinically, radionuclide studies have shown that breast atypia and malignancy have increased radioactive iodine uptakes. Imaging of the breasts in high-risk women has localized breast tumors. The potential use of breast iodine determination to determine estrogen dependence of breast cancer has been considered and the role of iodide therapy discussed. In conclusion, iodine appears to be a compulsory element for the breast tissue growth and development. It presents great potential for its use in research directed toward the prevention, diagnosis, and treatment of breast cancer.
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PMID:Iodine and mammary cancer. 34 35


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