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

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

Eelectron microscopy has disclosed the presence of intracytoplasmic lumina within breast cancer cells. These structures can be recognized with the light microscope by their sharp, round outlines and thick walls. Their identification in large numbers may provide additional support for the breast origin of a metastatic tumor. Three illustrative cases in which demonstration of intracytoplasmic lumina was diagnostically helpful are presented.
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PMID:Intracytoplasmic lumina in breast carcinoma: a helpful histopathologic feature. 17 16

Since metastasizing breast cancer is hormone-related, hormonal therapy is based on control of tumor growth by elimination of the hormonal influence, hormone ablatives, or administration of steroid hormones to change the hormonal milieu of thehost organism. The time span during which hormonal therapy may be effective is extremely limited; therefore, this is not recommended for patients with an interval of less than 2 years between primary treatment and 1st manifestation of metastasis, patients with visceral metastasis, or women less than 5 years in the postmenopause. According to cooperative European and American studies remission rates for different types of endocrine therapy include: ovariectomy, 25-40%; adrenalectomy, 30-40%; hypophysectomy, 30-40%; androgen, 20%; and estrogens, 20-35%. Studies are underway concerning the use of antiestrogens (Nafoxidine and Tamoxifen) andinhibition of prolactin secretion. Investigations have shown that patients with proven estrogen receptors in the tumor tissue are particularly responsive to hormonal therapy. For patients with no determinable estrogen receptors, however, chemotherapy is perferable. Ovariectomy is recommended as the 1st measure for women in the premenopause, hormone additives for women longer than 5 years in the postmenopause, and for women in the 1st years after menopause ovariectomy in combination with a form of polychemotherapy. For patients with short free intervals polychemotherapy with another endocrine measure, for pleuracarcinosis and liver metastosis high corticosteroid dosages, and for metastases in the central nervous system radiatio treatment with high corticosteroid dosages are recommended.
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PMID:[Hormone therapy of breast cancer]. 18 Mar 75

Sixty patients with metastatic or primary inoperable breast cancer not suitable for hormone alteration therapy were blindly randomized between weekly 5-fluorouracil, intravenously, and daily physiologic doses of conjugated estrogens by mouth against weekly 5-fluorouracil, intravenously, and placebo. There was no difference in the survival or the effect on the tumor in the two groups. Numerous factors were analyzed as to their effect on the course of the disease. The number of organ sites of tumor involvement, age of the host, and previous treatment for the disseminated disease were not shown to influence the survival or the results of therapy of either group. However, the duration of the clinical cancer-free period from primary treatment to recurrence, the sites of organ involvement, and the performance status of the patients at the time of entry into the study significantly did influence the survival. There is no evidence in this study that physiologic doses of conjugated estrogens deleteriously influenced the course of the disease.
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PMID:Clinical studies of 5-fluorouracil + premarin in the treatment of breast cancer. 18 Mar 93

The average age of 1891 women at the start of estrogen therapy was 49 years; long-term replacement was the usual goal. At the end of the study (mean, 12 years) 1573 women were alive, 132 had died, and 186 (9.8%) were lost to the study. The study involved 22,717 person-years. Breast cancer developed in 49 women during this period vs. 39.1 expected on the basis of rates among similar women in the general population, a relative risk of 1.3. The relative risk increased with duration of follow-up, being .9 for the first 5 years after starting estrogen, 1.2 from 5 to 9 years, 1.3 from 10 to 14 years, and 2.9 after 15 years. This trend was considered statistically significant (p less than .02). The excess risk became manifest after about 12 years. Reduced risk with increased parity was noted during the first 10 years only. Most of these patients had undergone hysterectomy and bilateral oophorectomy. The increased breast cancer risk was unrelated to ovarian status. Those with a history of benign breast tumor showed a higher relative risk than others, particularly if the benign disease had developed after estrogen was given. Although a dose-response relation was not observed, the risk was highest among those who took the medication in other than a daily regimen. Findings suggest that menopausal estrogen therapy raises the risk of breast cancer. Data indicate that evaluation of these agents will necessitate the incorporation of several factors lacking in previous studies, e.g., latent period risk indicators, type of therapeutic regimen, and total accumulated dosage.
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PMID:Menopausal estrogens and breast cancer. 18 Apr 9

Cryostat sections of 50 breast cancer specimens and several lymphoid organs were investigated with antisera against human T-lymphocyte antigen, human lymphocytes, and human immunoglobulins using the immunofluorescence technique and the immunoperoxidase technique. These methods proved to make it possible to discriminate between T and B cells in lymphocytic infiltrates in tissue sections. In nearly all mammary carcinomas studied, T cells were found to predominate in and around tumor cell nests. Only the intraductal carcinomas of this series contained a substantial number of B cells in addition to T cells. The presence of T cells indicates that the host-tumor interaction in vivo mall-mediated immune reaction. The role of the B cells found in the lymphocytic infiltrates of the intraductal carcinomas is still a matter of speculation. Moreover, these findings enhance the value of established histologic classifications. These classifications may have to be modified to provide them with a more functional basis.
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PMID:Identification of T and B lymphocytes in human breast cancer with immunohistochemical techniques. 18 7

Assays of estrophile protein (ER) in 161 patients with no previous additive or ablative hormonal therapy have been analyzed; 47.2 percent were ER positive; 52.8 percent ER negative. A total of 37.5 percent of premenopausal and 50.8 percent of postmenopausal patients had ER-positive tumors. The effects of additive and ablaive hormonal therapy were observed in 75 patients; 63.5 percent of the ER-positive group and 8.6 percent of the ER-negative group responded, but the incidence in the ER-negative group is thought to be spuriously high. The level of the ER content in the ER-positive group did not influence the degree of response. The ER-negative group had a shorter life span after discovery of the tumor and was more likely to develop dominant visceral metastases. Of 15 patients followed with sequential ER assays after hormonal therapy (additive and/or ablative), 14 demonstrated substantial falls in ER levels but these did not correlate with the clinical response. Tumor assayed in nine patients after irradiation of the lesion contained no demonstrable ER. ER assays of breast cancer tissue proved to be a useful but imperfect tool in predicting clinical progress following hormonal maneuvers but some readings may be spuriously low due to imperfect techniques of measurement, prior exogenous hormonal administration or hormonal ablation, and previous irradiation of the tumor.
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PMID:The surgical implications of estrophile protein estimations in carcinoma of the breast. 18 56

There were 700 tissue biopsies of the breast with and without carcinomas examined simultaneously by intraoperative histology and imprint cytology. In 20.2% of the cases with carcinoma the tumor cells showed peculiar intracytoplasmic inclusions, whereas in only 0.43% of the biopsies of the mamma without carcinoma such inclusions were to be found. Their morphologic variation and the histochemical pattern are discussed. It is pointed out that these intracytoplasmic inclusions may be a helpful histopathologic feature in the diagnosis of breast cancer.
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PMID:[Intracytoplasmic inclusions within cells of the breast and their diagnostic significance (author's transl)]. 18 83

Specific iodine-125-labeled prolactin binding was measured in membrane particles prepared from R3230AC mammary carcinoma and liver of tumor-bearing Fischer rats after either prolactin, estrogen, or lergotrile mesylate treatment, or after the induction of diabetes by streptozotocin. Hormone binding to tumors was decreased by treatment with prolactin (.5 or 1 mg/day) or estradiol valerate (7.5 mg/kg/week). In contrast, prolactin treatment was without affect on prolactin binding to liver membrane particles, but estradiol valerate treatment resulted in a 4-fold increase in prolactin binding to this tissue. Lergotrile mesylate, which lowers plasma prolactin levels, had no affect on tumor growth or prolactin binding to either tumor or liver. Prolactin binding to both tumor and liver was significantly reduced in diabetic rats, suggesting that insulin may play an important role in controlling tissue sensitivity to prolactin. Specific binding of iodine-labeled prolactin to enzymatically dissociated cells from R3230AC tumors was demonstrated in vitro. The binding capacity of the cells was found to be of the same order of magnitude as the binding capacity in membrane preparations when appropriate corrections were applied for yields of cells and membranes. R3230AC tumor, which is responsive to prolactin, appears therefore to be a useful model system for further study aimed at elucidation of growth and metabolic response to the hormone prolactin in breast cancer.
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PMID:Prolactin binding to R3230AC mammary carcinoma and liver in hormone-treated and diabetic rats. 18 51

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


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