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

Several AA, utilizing the biochemical method (DCC) showed the presence or absence of hormonal receptor in either synchronous or metachronous metastatic nodes (N) can reproduce the receptor assessment (AR) of the primary breast tumor (T). We evaluated the AR in T and in synchronous N, by using two morphological methods, immunocytochemical and histofluorescent, to detect the nuclear Estrogen Receptor (ER1) and cytoplasmic sites of the II type (ER2 and PgR2). We studied 50 patients who underwent radical mastectomy for breast cancer N+. In this series we founded a high correlation between AR in T and in N: 82% for ER1, 94% for ER2, and 92% for PgR2. Also we observed 4 cases (2 ER1 and 2 PgR2) which presented the receptor in N only. These data are comparable to results obtained with the DCC method and confirm the opportunity to perform also morphological techniques to evaluate AR in breast cancer to take into consideration also cellularity and tumor heterogeneity informations.
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PMID:[Receptor assessment of primary breast carcinoma and synchronous metastatic lymph nodes: histochemical study]. 186 99

Estrogen (ER) and progesterone receptors (PR) in tumorous mammary gland tissues have been investigated for a long time. The clinical significance of measuring the amount of ER and PR in the normal and pathological endometrium and myometrium was assessed. Endometrial and myometrial tissue obtained by operation was placed in a vessel containing liquid nitrogen an dry ice. Homogenization was performed at 15, 5, and 45 seconds in a buffer solution. After ultracentrifugation at 105 g for 1 hour, cytosol fraction was separated and used for ER, PR, and protein analysis according to the method of Lowry. The ER content of normal endometrium was 4 times higher than that of normal myometrium, however, the PR content in normal endometrium was only 2 times higher than in normal myometrium. The ER content did not differ in cancerous endometrium, but the PR content decreased 1.5 times. ER and PR amounts in myomatous neoplasm tissue increased 3 times compared with healthy myometrium. Robel et al. showed the ER increased to 6000-10,000/cell after ovulation, while the number of PR reached 14,000/cell in the preovulation phase. IN 29 endometrial cancer patients a significant decrease of both were fund. The ratio of PR to ER was 7.9 in the endometrial tissues of healthy women compared with 2.28 in those with endometrial cancer. In the present investigation, the respective ratios were 3.6 and 1.8; this low index was attributed to women in postmenopause without estrogen stimulation. The number of PR seems to be directly influenced by estrogens being higher in women with cyclical activity of the ovaries, thus receptors in uterine tissue change depending on endocrine functions. Endometrium and myometrium are hormone-dependent tissues. The increase of Er and PR is characteristic of benign processes, while the decrease of PR and especially of the PR/ER index indicates the malignant nature of the disease.
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PMID:[Clinical significance of analysis of estrogen and progesterone receptors in human uterine tissues]. 189 75

Estrogen and progesterone receptor phenotypes expressed as "positive" or "negative" are widely used for the determination of estrogen dependence of primary breast tumor. In our opinion the receptor phenotype, so important for biological and clinical behavior of tumor, should consider the quantitative values of receptor content. For this purpose, the correlation between quantitative estrogen versus progesterone receptor content and the distribution of the quantitative estrogen and progesterone receptor content within some parameters of tumor and tumor-host was analyzed. Our results show: There is the same range of correlation between estrogen versus progesterone receptor content in tubular tumor type, invasive ductal and lobular carcinomas, and in all three histologic grades; Histologic type influences the estrogen dependence through histologic grade. There is no difference in distribution of the quantitative estrogen and progesterone receptor content when corresponding grades of tubular tumor type, invasive ductal and lobular carcinomas are compared; In premenopause status histologic grade defines different groups with regard to the quantitative progesterone receptor content; In postmenopause status histologic grade defines different groups with regard to the quantitative estrogen and progesterone receptor content; In tumors with histologic grade I, transition of pre to postmenopause status is connected with a significant increase of the frequency of the high quantitative estrogen receptor content; In tumors with histologic grade III, transition of pre to postmenopause status is connected with a significant increase of the frequency of the low quantitative estrogen and progesterone receptor content.
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PMID:[The importance of hormone receptor determination in breast malignancies]. 191 39

Estrogen synthesis by aromatase occurs in a number of tissues throughout the body. Strategies which reduce production of estrogen offer useful means of treating hormone-dependent breast cancer. Initially, several steroidal compounds were determined to be selective inhibitors of aromatase. The most potent of these, 4-hydroxyandrostenedione (4-OHA) inhibits aromatase competitively but also causes inactivation of the enzyme. A number of other steroidal inhibitors appear to act by this mechanism also. In contrast, the newer imidazole compounds are reversible, competitive inhibitors. In vivo studies demonstrated that 4-OHA inhibited aromatase activity in ovarian and peripheral tissues and reduced plasma estrogen levels in rat and non-human primate species. In rats with mammary tumors, reduction in ovarian estrogen production was correlated with tumor regression. 4-OHA was also found to inhibit gonadotropin levels in animals in a dose-dependent manner. The mechanism of this effect appears to be associated with the weak androgenic activity of the compound. Together with aromatase inhibition, this action may contribute to reducing the growth stimulating effects of estrogen. A series of studies have now been completed in postmenopausal breast cancer patients treated with 4-OHA either 500 mg/2 weeks or weekly, or 250 mg/2 weeks. These doses did not affect gonadotropin levels. Plasma estrogen concentrations were significantly reduced. Complete or partial tumor regression occurred in 26% of the patients and the disease was stabilized in 25% of the patients. The results suggest that 4-OHA is of benefit to postmenopausal patients who have relapsed from prior hormonal therapies. Several of the steroidal inhibitors are now entering clinical trials as well as non-steroidal compounds which are more potent and selective than aminoglutethimide. Aromatase inhibitors should provide several useful additions to the treatment of breast cancer.
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PMID:Aromatase and its inhibitors--an overview. 195 29

The effects of treatment with a somatostatin analog (Sandostatin, SMS201-995) were investigated in female rats with dimethylbenzanthracene (DMBA)-induced rat mammary tumors. A 3-week treatment was performed using sandostatin, the LHRH-agonist buserelin alone, or buserelin in combination with sandostatin. Twice daily sandostatin treatment was performed with dosages of 0.05 microgram, 0.2 microgram, 1 microgram, 5 micrograms, and 20 micrograms. Buserelin was used in a 2 x 5 micrograms/day dosage. The combined results from six different experiments show that the various dosages of sandostatin caused no tumor growth inhibition. Somatostatin receptors could not be demonstrated in these mammary tumors. Sandostatin treatment by daily injections did not suppress levels of growth hormone, prolactin, or epidermal growth factor-like activities. Estrogen (ER) and progesterone (PgR) receptor contents of the mammary tumors were not changed. In contrast, buserelin treatment caused highly significant tumor remission. The combined treatment with sandostatin and buserelin did not alter the treatment results obtained after treatment with buserelin alone. In conclusion, sandostatin treatment in this tumor model had no direct growth inhibitory effect and did not cause an endocrine inhibition of mammary tumor growth. However, these results do not exclude antitumor effects in human breast cancer in view of the presence of somatostatin receptors in approximately 20-45% of human tumors, besides possible different endocrine effects.
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PMID:The somatostatin analog Sandostatin (SMS201-995) in treatment of DMBA-induced rat mammary tumors. 196 5

Estrogen and progesterone receptors were studied in fine-needle aspiration biopsy specimens of 56 patients with primary, recurrent, or metastatic breast carcinoma. The ligands, 17 B-estradiol-6-carboxymethyloxine-bovine serum albumin fluorescein isothiocyanate (FITC-BSA estradiol) and hydroxyprogesterone hemisuccinate bovine serum albumin tetramethyl rhodamine isothiocyanate (TMRITC-BSA progesterone), were used in the fluorescent cytochemical method. The findings obtained from the aspirated cells with the use of the fluorescent cytochemical technique were compared with results obtained from the cell population of the same tumor after removal with the use of both the fluorescent cytochemical technique and the biochemical dextran-coated charcoal (DCC) assay. For the needle aspirates, there was 89% concordance for estrogen receptor and 86% concordance for progesterone receptor between biochemical and cytochemical results. A high degree of correlation was also demonstrated between fine-needle aspirates and imprint preparations with the use of the cytochemical technique. This study suggests that the fluorescent cytochemical technique is an effective tool in assessment of estrogen and progesterone receptor content in fine-needle aspirates of primary and metastatic breast cancer. The fluorescent cytochemical technique can be performed easily at community hospitals and is well suited for specimens of insufficient size for biochemical assay.
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PMID:Fluorescent cytochemical detection of estrogen and progesterone receptors in breast fine-needle aspirates. 198 50

Estrogen-induced pituitary lesions in rats were studied in time-sequence experiments using magnetic resonance imaging (MRI), hormone determinations and light microscopy. The main purpose of the study was to evaluate the usefulness of MRI in comparison with conventional biochemical and histopathological methods for detecting the pituitary lesions as early as possible and to follow their development. Measurements were made at 15 time points, ranging from 1 h to 272 days after s.c. implantation of the estrogen pellet. High-resolution T1 weighted sagittal images with 2 mm slice thickness were made with a 2 Tesla 30 cm small-bore MRI system. Radioimmunoassay (RIA) was used to determine the different pituitary hormones. Conventional histopathology and immunoperoxidase staining methods were used to characterize the pituitary lesions and visualize the hormone-producing pituitary cells respectively. The first histopathological pituitary changes (enlarged acidophilic cells with increased number of vacuoles) were seen at day 2 after initiation of the estrogen treatment, while at day 4 the first immunohistochemical changes (increased number of prolactin-positive cells) were encountered. Significantly increased prolactin levels in blood plasma occurred from day 9 onwards. Also at day 9, changes of the pituitary gland were first visible on MR images, showing rounding of the anterior edge of the gland. Gradual enlargement of the pituitary caused by hyperplasia of hypertrophic prolactin-positive cells could be followed by MRI, and later on pituitary tumors were recognized, their images being heterogeneous due to great differences in signal intensity ranging from hypo- or iso- to hyperintense. Signal intensities of hemorrhagic tumor areas varies widely due to variation in the blood flow maintained in these areas. In was concluded that MRI is a powerful tool for detecting enlargement and tumors of the pituitary gland in rats. This method allows the development of such lesions to be followed in one and the same animal, thereby reducing the need of interim kills and thus the number of animals to be used.
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PMID:Magnetic resonance imaging compared with hormonal effects and histopathology of estrogen-induced pituitary lesions in the rat. 199 94

Syrian hamsters were treated with diethylstilbestrol (DES), a potent estrogen and kidney carcinogen, or ethinyl estradiol (EE), a strong estrogen but weak carcinogen, for 1-9 months. At monthly intervals their kidneys were studied using light, immunoperoxidase, and electron microscopic techniques. At 5 months, DES-treated animals exhibited interstitial lesions composed of small round cells with a high nuclear:cytoplasmic ratio. Immunoperoxidase and ultrastructural studies showed these cells to be similar to cells in fully formed tumors at 9 months. Early lesions in EE-treated animals (seen as early as 1 month) were dissimilar, these lesions appeared in the deep cortex adjacent to the renal pelvis, where proximal tubules underwent hyperplastic changes, showing columnar cells with large nuclei, occasional mitoses, and sloughing of apical cytoplasm. Cells in early lesions of EE-treated animals did not resemble the fully developed tumor in either immunoperoxidase or ultrastructural features; although with longer treatment these tubular lesions progressed to dysplasia (3-5 months) and severe dysplasia/carcinoma in situ (7 months), they did not form grossly visible tumors during the 9-month study. Both early lesions identified were specific, inasmuch as they were not observed in control animals and animals treated with beta-dienestrol and 17 alpha-estradiol (noncarcinogenic weak estrogens). Animals given a combination of DES and EE showed tubular hyperplasia but not interstitial lesions; this finding was of particular interest because hamsters given this combination of estrogens do not develop gross renal tumors. These results strongly implicate the primitive interstitial cell in the hamster kidney as the cell of origin of the DES-induced neoplasm.
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PMID:Characterization of early kidney lesions in estrogen-induced tumors in the Syrian hamster. 200 77

The role of cell death as a determinant for tumor growth and regression was studied using an estrogen-dependent, transplantable kidney tumor designated H301. H301 cells were injected s.c. into diethylstilbestrol(DES)-treated male Syrian hamsters and developed solid tumors of 1-2 g within 2-3 weeks. Upon withdrawal of estrogen the tumors regressed by 80-90% within 4 days. Mitoses, necrotic areas and single-cell death indicated by small, condensed cell residues, were counted in hematoxylin and eosin stained histological sections of the tumors. Coincident with tumor regression after DES withdrawal, mitotic activity decreased by approximately 90%; the rate of single-cell death increased (by approximately 2-fold at its maximum). The incidence of necrotic areas was not affected by DES withdrawal. DES re-treatment resulted in reduction of single-cell death by 80% within 8 h. Mitotic activity increased within 24 h to the level observed before DES withdrawal. Again, the incidence of necrotic areas did not change. As a result, tumors re-grew to their previous size within 2 days after resumption of DES treatment. These results led to the following conclusions: (i) DES treatment inhibits and DES withdrawal enhances single-cell death of H301 tumor cells. (ii) Both this functional property and its morphology characterize single-cell death in the tumors as apoptosis. (iii) Estrogen-dependent cell death determines, in addition to mitosis and necrosis, the growth rate of H301 tumors. (iv) This experimental model may provide a useful tool to study the interaction of potential anti-tumor drugs with apoptosis in neoplasia.
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PMID:Control of cell death (apoptosis) by diethylstilbestrol in an estrogen-dependent kidney tumor. 202 49

Foci, nodules of cellular overgrowth, that appear after confluence are an in vitro characteristic of malignant transformation. A well-studied in vitro model of estrogen-dependent tumors is the MCF-7 cell line, derived from a pleural metastasis of a human breast adenocarcinoma. We report that cultivation of MCF-7 cells, using routine methods, results in extensive estrogen-stimulated postconfluent cell accumulation characterized by discrete three-dimensional arrays. Side view Nomarski optical sections revealed these to be principally multicellular foci with occasional domes and pseudoacinar vacuoles. This effect on MCF-7 cell growth occurs in media containing fetal bovine serum but not with calf serum or charcoal-dextran-treated fetal bovine serum unless supplemented with estrogens. Foci formation starts 5-6 days after confluence, and the number of foci generated is a function of the concentration of added estrogens. Foci formation is suppressed by the antiestrogens Tamoxifen and LY 156758. Addition of progesterone, testosterone, or dexamethasone had little or no effect, while various estrogens (ethinyl estradiol, diethylstilbestrol, and moxestrol) induced foci development. Clones derived from single cells of the initial MCF-7 population revealed a wide variance in estrogen-induced foci formation, demonstrating heterogeneity of this tumor cell line. The postconfluent cell growth of the estrogen receptor-deficient cell line, MDA-MB-231, contrasted with MCF-7 by developing an extensive multilayer morphology devoid of discrete structures. The tumorigenic potential of the MCF-7 cells used in our experiments was confirmed by their estrogen-dependent growth in immunosuppressed male BDF1 mice. These data suggest an estrogen receptor-based mechanism for the development of multicellular foci during postconfluent growth of MCF-7 cells. After confluence, foci, in contrast to the quiescent surrounding monolayer, retain proliferating cells. Focus formation, therefore, reflects the heterogeneous responsiveness of these cells to estrogens and should provide a model permitting in vitro comparisons between the progenitor cells of multicellular foci and the monolayer population.
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PMID:Estrogen-stimulation of postconfluent cell accumulation and foci formation of human MCF-7 breast cancer cells. 205 45


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