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

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).
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PMID:A correlation between estrogen sulfotransferase levels and estrogen receptor status in human primary breast carcinoma. 49 39

Two patients with squamous cell carcinoma of the breast are described. In one patient the lesion represented a primary breast tumor; in the second, a metastases from primary bonchogenic carcinoma. Neither lesion possessed estrogen receptor protein. This report emphasizes the rarity of epidermoid lesions of the breast and the importance of identifying an extramammary primary source of metastases to the breast.
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PMID:Epidermoid carcinoma of the breast. 50 63

Estrogen receptor (ER) assays in human breast cancer tissue have proved useful in selecting patients for endocrine therapies. The absence of ER indicates hormone independent tumors and precludes the use of endocrine therapy. Patients with positive tumor ER respond to endocrine therapy at nearly twice the rate of those patients chosen by clinical criteria, although about a third of ER positive tumors in patients still do not respond. Recently, research has been directed toward increasing the accuracy of the ER assay in the ER positive group. The absolute tumor ER value and the presence of progesterone receptor appear promising in this regard. The significance of nuclear estrogen receptor is being studied. Finally, the ER status of a primary breast tumor appears to be a marker for the length of time until recurrence after mastectomy, and for survival. The ER assay may prove valuable in planning new adjuvants in the treatment of breast cancer.
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PMID:Therapy for cancer of the breast. Current status of steroid hormone receptors. 51 64

The presence or absence of steroid hormone receptors has been associated with predicting response to exogenous hormone therapy in breast tumors and in the treatment of metastases. This study was conducted to determine whether hormone receptors are present in cervical epithelium showing intraepithelial neoplasia. 18 biopsies of normal cervical epithelium were collected from hysterectomy patients with normal cervical cytology. 32 abnormal epithelium specimens were similarly obtained from patients with abnormal cervical cytology. An assay method using dextran-coated charcoal was performed to determine the values of estrogen and progesterone receptors in the cervical samples. Among those with normal epithelium, 67% were found to be estrogen receptor + compared to 77% of those with cervical intraepithelial neoplasia (CIN). Progesterone receptor sites were found in 61% of normal patients and 65% of CIN patients. The % of tumors (invasive cervical carcinoma) that are estrogen receptor positive have been found to vary from 0 to 25%. This study suggests a higher % of estrogen and progesterone receptor positivity in CIN than in invasive carcinoma with increasing concentration of receptors proportionate to the degree of dedifferentiation. Further studies should be done to determine whether hormone manipulation of cervical epithelium is of therapeutic and clinical value.
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PMID:Hormone receptors in cervical intraepithelial neoplasia. 52 46

On the basis of estrogen receptor assays, breast carcinomas are presently classified as estrogen-dependent tumors, which respond to endocrine therapy, and autonomous tumors, for which endocrine therapy is useless. This paper presents a short review of the biochemical principles of estrogen dependence, the procedures used to determine estrogen receptors, and the clinical applications of the findings of these assay procedures. Biobhemically, the estroogen dependence of normal breast cells is explained as a biochemical reaction occurring between the circulating estradiol and the breast cell, which occurs in 3 steps: 1) circulating estradiol penetrates the cellular membrane by passive diffusion, followed by 2) combining of estradiol with the estrogen-binding protein (estrophilin) and formation of an estrogen receptor complex which undergoes activation and translocation into the nucleus, to result in 3) the activated steroid receptor which combines with the nuclear charomatin and stimulates ribonucleic acid synthesis for the formation of estradiol binding proteins or estradiol receptors. The cytosol method of Wittliff et al. is described in brief and entails radioactive competitive analysis; the other available laboratory procedure is immunofluorescence of tumor sections. Quantification of estrogen receptor content can be used clinically to decide on ablative endocrine therapy, to determine the effectiveness of anti-estrogen administration, to determine the primary site of metastatic carcinoma, and as a screenng device.
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PMID:Estrogen receptors in breast carcinoma. 53 21

Endocrine hormone treatment has been found to be effective in treating metastatic breast cancer in 20-40% of the cases. The effectiveness of this treatment can be predicted to a certain extent by determining whether the hormone receptors in the tumor tissue react positively or negatively when incubated with highly active hormones, e.g. H3-17 beta-estradiol. Estrogen receptors are found in 60-70% of primary tumors and 40-50% of tissue samples from metastatized tumors. Estrogen receptors are more frequently found in post-menopausal women than in women who are still menstruating. Progesterone receptors have been found in 20-40% of all investigations undertaken, androgen receptors in 20-30%, and corticosteroid receptors in 20-50%. A remission rate of 56% has been achieved after endocrine therapy of those with positive estrogen receptor tests, compared to 10% among those with negative tests. The correlation between the receptor test results and (the success of) endocrine therapy is not very high; this could be a factor determined by the cellular constitution of a tumor. The remission rate is 75% among patients with positive receptor tests for both estrogen and progesterone. Faulty lab techniques could be responsible for low correlation. Determination of the receptor activity of both the primary tumor and its metasases, or immunological or immunohistological determination of receptor activity may improve the usefulness of the test in determining tumor reaction to endocrine hormone treatment.
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PMID:[The clinical value of hormone receptors in the treatment of breast neoplasms]. 54 83

Because material for biopsy among breast cancer patients is often scarce, a new procedure using material obtained from percutaneous bone marrow biopsy was developed and is presented. Bone marrow biopsy was the source of neoplastic material in 42 patients and was used to determine whether percutaneous bone marrow biopsy specimens could provide the necessary neoplastic tissue for estrogen receptor (ER) determination. Of the 42 patients, specimens from 11 (26%) were found to have insufficient tumor material for further evaluation; of the remaining 31 patients, 12 (39%) contained quantitatively ( 7 fmol) or qualitatively significant estrogen binding. All 12 patients were treated with endocrine therapy alone. Of the 12 patients, 8 (67%) responded to hormonal manipulation. The majority of patients evaluated were without other measureable signs of recurrent disease. All data obtained served to corroborate the usefulness of routine percutaneous bone marrow specimen for receptor analysis. This use of bone marrow represents an important application of improved technology to clinical practice.
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PMID:Estrogen receptor determination in percutaneous bone marrow biopsies of patients with metastatic breast cancer. 54 92

A permanent cell line derived from rat endometrium which contains a specific, low capacity, high affinity estrogen binding protein in cytosol and nuclear fractions (estrogen receptor) is available. Extracts of cells from this line did not appreciably bind the tumor promoter, 12-0-tetradecanoylphorbol-13-acetate. The result suggests that the action of the promoter does not involve translocation to the cell nucleus via binding to the specific estrogen receptor.
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PMID:Failure of tumor promoter 12-O-tetradecanoylphorbol-13-acetate to displace estradiol from its specific receptor. 54 71

The interactions of phytoestrogens with estrogen receptors were studied in the human breast cancer cell line, MCF-7. The compounds tested were coumestrol, genistein, and formononetin and the mycotoxins, zearalenone and its reduced derivative, zearalenol. All but formononetin compete for binding of [3H]-estradiol to unfilled cytoplasmic estrogen receptor or unfilled nuclear estrogen receptor sites. Relative binding affinities are zearalenol HMP (high melting point isomer) greater than zearalenol LMP (low melting point isomer) greater than zearalenone = coumestrol greater than genistein greater than formononetin. Dissociation constants estimated from competition curves show that binding affinities are high. In contrast to estradiol, phytoestrogens bind only weakly to sex steroid-binding globulin; they also do not bind to corticosteroid-binding globulin. These compounds translocate the cytoplasmic estrogen receptor and bind to unfilled nuclear estrogen receptors in whole cells. Bound nuclear receptors are then processed in a manner similar to estradiol in a step which rapidly decreases total cellular estrogen receptors. The phytoestrogens are also biologically active; they can markedly enhance tumor cell proliferation. In sum, phytoestrogens interact with the estrogen receptors of human breast cancer cells in culture and, therefore, may affect estrogen-mediated events in these cells.
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PMID:Phytoestrogen interaction with estrogen receptors in human breast cancer cells. 57 Sep 14

One hundred nine pre- and postmenopausal mammary carcinoma cases were studied to elucidate the role of sex hormone binding globulin (SHBG) in the hormone dependence of human breast cancer. Our findings indicate that there is a significant negative correlation between SHBG binding capacity and plasma testosterone concentration. All patients with high SHBG titers were found to be cytosol estrogen receptor (CER) positive and the plasma SHBG binding capacity of CER positive was significantly higher than that of CER negative patients. We also found that the level of pretherapy plasma SHBG concentration is a reliable indicator in predicting the efficacy of hormone therapy. Our findings also confirm that, for a tumor to be hormone dependent, high plasma SHBG concentration and estrogen receptors must be present simultaneously. The present pretherapy determination of SHBG titers is easier and more reliable than previous methods for determining the hormone dependence of human breast tumors.
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PMID:Sex hormone binding globulin as a reliable indicator of hormone dependence in human breast cancer. 57 61


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