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Query: UMLS:C0476089 (endometrial cancer)
 11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-eight epithelial and 22 nonepithelial feline tumors were studied immunohistochemically. Epithelial tumors were 10 squamous cell carcinomas, two basal cell tumors, two sebaceous gland carcinomas, three apocrine gland carcinomas, three thyroid papillary carcinomas, one thyroid solid carcinoma, one renal clear cell carcinoma, one renal papillary carcinoma, one endometrial carcinoma, and four lung bronchioloalveolar carcinomas. Nonepithelial tumors were 10 fibrosarcomas, one liposarcoma, one leiomyosarcoma, one rhabdomyosarcoma, one hemangiosarcoma, two mast cell tumors, one osteosarcoma, three melanomas, and two lymphomas. Commercially available antibodies directed against high- and low-molecular-weight keratins (keratin, RCK-102, NCL-5D3), vimentin, desmin, glial fibrillary acidic protein (GFAP), and neurofilament intermediate filament (IF) proteins were used in the avidin-biotin-peroxidase complex technique on formalin-fixed, paraffin-embedded tumor tissue samples. All epithelial tumors except the endometrial carcinoma expressed some type of keratin protein. Squamous cell carcinomas expressed high-molecular-weight keratins exclusively. Coexpression of high- and low-molecular-weight keratins was observed in one basal cell tumor, sebaceous and apocrine adenocarcinomas, and thyroid, renal, and lung carcinomas. In addition to keratins, vimentin immunoreactivity was found in all basal cell tumors, all sebaceous gland, thyroid papillary, renal, and lung adenocarcinomas, and one of the apocrine gland adenocarcinomas. Immunoreactivity with GFAP antibody was found in one basal cell tumor and one sebaceous gland adenocarcinoma. The endometrial carcinoma did not react with any of the antibodies applied. Nonepithelial tumors analyzed expressed either vimentin (fibrosarcomas, liposarcoma, haemangiosarcoma, mast cell tumors, osteosarcomas, melanomas) or vimentin and desmin (leiomyosarcoma, rhabdomyosarcoma, one fibrosarcoma) IF proteins exclusively. Lymphomas did not react with any of the antibodies employed. These findings indicate that IF proteins antibodies can be included in diagnostic panels of antibodies for immunocharacterization of feline tumors. In addition, they can be used as a basis for the diagnoses of poorly differentiated or undifferentiated feline neoplasms.
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PMID:Immunohistochemical distribution pattern of intermediate filament proteins in 50 feline neoplasms. 859 5

Angiogenesis plays a critical role in tumor biology and may someday be a target for novel therapeutic interventions. To date, however, relatively few markers have been identified that can specifically distinguish between microvessels in benign versus malignant lesions. Here we report that the cationic heme-protein eosinophil peroxidase (EPO) was localized by in situ immunohistochemistry on the vascular endothelial cells and/or connective tissue stroma in 16 of 16 cases of human endometrial carcinoma and in 12 of 15 cases of ovarian carcinoma. Similar deposits of EPO were not detected in normal endometrial tissues or ovaries from five healthy subjects, in adjacent uninvolved tissues from four tumor-bearing subjects, or in any normal organs from five other subjects. These findings imply that eosinophil degranulation is a significant and previously unappreciated component of the interaction between ovarian and endometrial cancers and the host. Moreover, the abundant and highly specific nature of the EPO deposition near and within the microvessels of these cancers suggests that eosinophil degranulation is a new marker for tumor blood vessels that potentially could be exploited to treat these important types of cancers that currently lack highly effective therapies.
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PMID:New marker for blood vessels in human ovarian and endometrial cancers. 981 42

bcl-2 expression was examined on paraffin-embedded specimens in proliferative, hyperplastic, and neoplastic human endometrium by immunohistochemistry. The results of bcl-2 immunostaining in endometrial carcinomas were compared with clinicopathological indicators as well as with p53 accumulation. The streptavidin-peroxidase detection system was used and the intensity and the distribution of immunostaining was evaluated semiquantitatively by counting H-score values. Expression of the bcl-2 protein was found in 2 out of 5 cases of proliferative endometrium (mean H-score 0.4, range 0.35-0.45), 4 out of 5 cases of simple hyperplasia (mean H-score 1.23; range 1.0-1.4), 4 out of 5 cases of complex hyperplasia (mean H-score 1.1; range 0.7-1.2) and in 7 out of 25 cases of endometrial carcinoma (mean H-score 0.48; range 0.35-0.65). All bcl-2 positive slides were obtained from patients who had endometrial cancer and who were in the early (stage I due to FIGO) clinical stage of the disease. bcl-2 expression was not related to age, surgical stage or histopathological features, and neither was there an inverse correlation between bcl-2 immunostaining and p53 expression reported in the study of neoplastic endometrium. Our data indicate that mechanisms other than p53 may play a role in the regulation of bcl-2 expression in endometrial carcinomas.
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PMID:bcl-2 protein expression in endometrial carcinoma: the lack of correlation with p53. 992 61

Tamoxifen is a liver carcinogen in rats and has been associated with an increased risk of endometrial cancer in women. Recent reports of DNA adducts in leukocyte and endometrial samples from women treated with tamoxifen suggest that it may be genotoxic to humans. One of the proposed pathways for the metabolic activation of tamoxifen involves oxidation to 4-hydroxytamoxifen, which may be further oxidized to an electrophilic quinone methide. In the present study, we compared the extent of DNA adduct formation in female Sprague-Dawley rats treated by gavage with seven daily doses of 54 micromol/kg tamoxifen or 4-hydroxytamoxifen and killed 24 h after the last dose. Liver weights and microsomal rates of ethoxyresorufin O-deethylation, 4-dimethylaminopyrine N-demethylation and p-nitrophenol oxidation were not altered by tamoxifen or 4-hydroxytamoxifen treatment. Uterine weights were decreased significantly and uterine peroxidase activity was decreased marginally in treated as compared with control rats. DNA adducts were assayed by 32P-post-labeling in combination with HPLC. Two major DNA adducts were detected in liver DNA from rats administered tamoxifen. These adducts had retention times comparable with those obtained from in vitro reactions of alpha-acetoxytamoxifen and 4-hydroxytamoxifen quinone methide with DNA. Hepatic DNA adduct levels in rats administered 4-hydroxytamoxifen did not differ from those observed in control rats. Likewise, adduct levels in uterus DNA from rats treated with tamoxifen or 4-hydroxytamoxifen were not different from those detected in control rats. These data suggest that a metabolic pathway involving 4-hydroxytamoxifen is not a major pathway in the activation of tamoxifen to a DNA-binding derivative in Sprague-Dawley rats.
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PMID:Comparison of the DNA adducts formed by tamoxifen and 4-hydroxytamoxifen in vivo. 1019 May 64

The aim of the current study was to investigate the immunohistochemical expression of the retinoblastoma protein (pRB) in formalin-fixed, paraffin-embedded specimens obtained from 62 patients suffering from endometrial cancer. The avidin-biotin-peroxidase detection system with microwave pretreatment and the mouse anti-human NCL-RB1 monoclonal antibody were used. Heterogeneous nuclear immunostaining for the pRB was generally observed in the glandular cells in 59 out of 62 (95%) endometrial carcinomas, while stromal components were unreactive. In one case of stage Ic endometrioid adenocarcinoma, a small percentage of glandular cells (5%) stained positively with the anti-RB antibody, while two other tumors (stage IIa adenosquamous carcinoma and stage IIIa endometrioid adenocarcinoma) were pRB negative. In the cases with concomitant hyperplastic and neoplastic endometrial lesions, pRB immunoreaction was heterogeneous in the hyperplastic endometrial cells and in the adjacent neoplastic endometrium. Moreover, eight cases of endometrial carcinoma harboring K-ras codon 12 gene point mutation overexpressed pRB (more than 80% of glandular endometrial cells were positive) immunohistochemically, while none of three pRB negative slides had a K-ras gene alteration. Our data support the view that the pRB is expressed in most of the human endometrial neoplasms, but the lack of pRB immunoreactivity may correspond with the retinoblastoma gene rearrangements in a subset of advanced endometrial carcinomas.
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PMID:RB protein expression in human endometrial carcinomas--an immunohistochemical study. 1067 71

Expression of a neoepitope on cytokeratin 18, recognized by the monoclonal antibody M30, is an early indicator of apoptosis in epithelial cells. The aim of this study was to determine the equilibrium between apoptosis (M30), anti-apoptosis (bcl-2), and proliferation (Ki-67) in different endometrial conditions. Paraffin-embedded samples (n = 107), representing proliferative endometrium (18), secretory endometrium (19), postmenopausal endometrium (15), disordered proliferative endometrium (6), simple hyperplasia (12), complex hyperplasia (8), and endometrial adenocarcinoma (29), were evaluated immunohistochemically. The indirect streptavidin-biotin-horseradish peroxidase technique, with 3-amino-9-ethylcarbazole as the chromogen, was used to visualize the reactions. Proliferative endometrium showed high bcl-2 and Ki-67 expression levels with no M30. In the secretory phase, the balance was tipped in favor of M30 with a decrease of bcl-2 and Ki-67. Postmenopausal endometrium revealed high Ki-67 and bcl-2 expression levels and no M30. In complex hyperplasia, M30, bcl-2, and Ki-67 showed increased expression. In endometrial carcinoma, an increasing reactivity for M30 and Ki-67 was seen as the grade progressed. bcl-2 reacted weakly and only in grade 1 cancer. Immunohistochemistry facilitates the study of the expression of proteins related to cyclic endometrial activity. Interruption of these cyclic events is associated with specific disturbances in the expression patterns of these proteins.
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PMID:The patterns of expression of an apoptosis-related CK18 neoepitope, the bcl-2 proto-oncogene, and the Ki67 proliferation marker in normal, hyperplastic, and malignant endometrium. 1078 7

Degranulating eosinophils have been described in most endometrial cancers. We hypothesized that endometriosis (ectopic, nonneoplastic endometrial tissue) would be an appropriate model system for determining whether eosinophil degranulation is part of a specific immune response to endometrial cancer or if it is related to the more general phenomenon of tissue remodeling (wound healing) that is common to both disorders. To test this hypothesis, we performed immunohistochemistry and Western blotting to evaluate the presence of eosinophil peroxidase (a marker of eosinophil degranulation) in normal endometrium (n = 20) and endometriosis samples (n = 24) and to define the coexpression of three eosinophil chemoattractants: interleukin-5 (IL-5), eotaxin, and regulated on activator-normal T cell expressed and secreted (RANTES). There was focally intense deposition of eosinophil peroxidase in the fibrotic connective tissue and blood vessels of 21 of 24 human endometriosis specimens; two samples showed weak staining, and only one tissue was negative for eosinophil degranulation. None of the 10 normal proliferative endometrial specimens had evidence of eosinophil degranulation, and four of 10 secretory tissues stained only weakly for eosinophil peroxidase. The presence of degranulating eosinophils was also associated with the presence of eotaxin and IL-5 in some samples and with RANTES in others. We conclude that the abundant presence of degranulating eosinophils in the fibrous regions of endometriosis supports the interpretation that eosinophils are involved in general tissue remodeling and wound healing rather than a tissue-directed immune response.
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PMID:Degranulating eosinophils in human endometriosis. 1079 70

Tamoxifen (TAM) is a highly effective selective estrogen receptor (ER) modulator used extensively for the treatment and prevention of breast cancer. However, prolonged treatment of women with TAM may be a risk factor for endometrial cancer, and research in our laboratory is focused on the development of selective aryl hydrocarbon receptor modulators that can be used in combination with TAM to improve its efficacy in the breast and inhibit TAM-induced endometrial effects. This study investigated the effects of the selective aryl hydrocarbon receptor modulators 6-methyl-1,3,8-trichlorodibenzofuran (6-MCDF) alone and in combination with TAM in the carcinogen-induced mammary tumor model and in the ovariectomized uterotropic assay using female Sprague Dawley rats. The lowest effective dose of 6-MCDF that inhibited tumor growth was 50 microg/kg/day, and TAM was antitumorigenic at a dose of 100 microg/kg/day. In animals cotreated with TAM + 6-MCDF at doses of 100, 50, or 25 microg/kg/day of each compound, complete inhibition of mammary tumor growth was observed at all doses, and the results are consistent with a more than additive antitumorigenic response for the low dose group (25 + 25 microg/kg) and additive interactions at the 50 and 100 microg/kg doses. In a separate experiment, 6-MCDF (800 microg/kg) inhibited TAM-induced peroxidase activity and progesterone receptor binding in the ovariectomized rat uterus but did not affect TAM-induced bone growth in ovariectomized rats. This study also investigated the effects of TAM and 6-MCDF alone and in combination on ERalpha protein levels in MCF-7 human breast cancer cells as a model for studying interactions between these compounds. The results show that 6-MCDF decreased TAM-induced ERalpha levels in the absence or presence of 17beta-estradiol through proteasome activation, and these interactions may contribute to the observed combined antitumorigenic effects of these compounds.
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PMID:Tamoxifen-induced antitumorigenic/antiestrogenic action synergized by a selective aryl hydrocarbon receptor modulator. 1135 3

Peroxidase activity was determined in 98 patients with endometrial cancers. In 34 patients with endometrial cancers, the activity of the enzyme was also detected in the neighbouring unchanged (normal) tissues. It was shown that in tumor tissues the level of peroxidase activity was higher than in normal ones. The peroxidase activity increased both in tumor and normal endometrium when clinical and morphological characteristics of tumor were unfavourable, i.e. at later stages of the disease, deeper invasion to myometrium, lower levels of differentiation of tumors. The peroxidase activity was somewhat higher in post-menopausal women; however, no direct was found between the activity of this enzyme in malignant and normal tissues, on the one hand, and the menstrual status of patients with different clinical and morphological characteristics of endometrial cancer, on the other relationship. The level of peroxidase activity in normal and malignant tissues was more pronounced in advanced and poorly-differentiated tumors. It seems important to use peroxidase activity as a prognostic factor and as a possible marker of endometrial cancer hormone-dependence that needs further investigation.
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PMID:[Peroxidase activity in human uterine tissue: connection with clinico-morphological features of endometrial cancer]. 1178 99

Aromatase expression has been described in stromal cells of endometriosis, adenomyosis and endometrial cancer. We analyzed aromatase expression in a series of 23 low-grade endometrial stromal sarcomas. Archival formalin-fixed and paraffin-embedded material was analyzed with immunohistochemistry. Aromatase expression was evaluated with a monoclonal and a polyclonal antibody using the peroxidase-antiperoxidase method. A score was calculated based on the percentage of positive tumor cells and the staining intensity. Aromatase was seen in 19 (83%) of 23 tumors with monoclonal antibody and 20 (87%) of 23 tumors with polyclonal antibody. Aromatase expression using the monoclonal antibody was scored as high in five (22%), moderate in nine (39%) and low in five (22%) tumors. Four (17%) low-grade endometrial stromal sarcomas did not stain for aromatase. Aromatase expression with the polyclonal antibody was scored as high in seven (31%), moderate in four (17%) and low in nine (39%) tumors. Three (13%) low-grade endometrial stromal sarcomas did not stain for aromatase. Little or no aromatase expression tended to correlate with stage I disease, while higher scores were more frequently associated with advanced disease. Our results demonstrate that most low-grade endometrial stromal sarcomas express aromatase. The staining pattern, however, is heterogeneous. The high percentage of aromatase positivity in low-grade endometrial stromal sarcomas may have implications in the management of these tumors and offer new treatment modalities such as hormonal therapy with aromatase inhibitors.
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PMID:Aromatase expression in low-grade endometrial stromal sarcomas: an immunohistochemical study. 1463 63


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