Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0476089 (endometrial cancer)
 11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immunohistochemical localization of estrogen receptors (ER) using specific monoclonal antibody to human ER, H222, with ABC methods were performed on frozen sections of 22 endometrial carcinoma specimens. Specific nuclear staining of ER was observed in most epithelial, stromal and malignant cells while specific cytoplasmic staining was not observed. ER positive staining (H-Score > 75) was found in 16 of 22 cases (72.7%), and the H-Score of cancer components was significantly associated with the histological grade of endometrial carcinoma (P < 0.05). The data suggest that ER content of endometrial carcinoma reflects the degree of cancer cell differentiation and may be taken as a guideline for hormone therapy.
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PMID:[Immunohistochemical detection of estrogen receptors (ER) in endometrial carcinoma]. 816 83

CD44 is known as an adhesion molecule which is involved in lymphocyte activation and lymphocyte homing. In recent years, its role in the invasion and metastasis of malignant tumors has attracted the attention of investigators. In this study, the expression of CD44 variants was investigated in primary lesions and metastasis into the lymph node in 53 patients with gynecological cancer. The following patients with various types of gynecological carcinoma, established by operation and pre-treatment biopsy, were included in this study: 19 patients with cancer of the uterine cervix, 23 with cancer of the uterine endometrium, and 11 with ovarian cancer. Tissue samples were obtained from a primary lesion and a nodal metastasis of each patient, and immunohistochemical staining was performed by the ABC method through the use of monoclonal antibodies against CD44v1-10. Specimens proving CD44v1-10 positive were then submitted to immunohistochemical staining through the use of monoclonal antibodies against CD44v6 and CD44v9. Expression of CD44v was judged positive when DAB revealed color development, irrespective of the degree of staining intensity. CD44v were all expressed in the cancer cell membrane. In normal endometrium, expression of CD44v1-10 and v9 was observed in the endometrial gland cell membrane. In normal ovarian tissues, CD44v6 and v9 were not detected. The expression of CD44v6 in patients with endometrial cancer was noted in 13 (72.2%) of 18 patients with vascular invasion and in one (20.0%) of 5 patients without it, indicating a significant relation to vascular invasion. It was also remarkably higher in those for whom the invasion exceeded 1/2 of the myometrium than in those for whom the invasion did not exceed 1/2 of the myometrium, and was higher too in advanced stages and in node-positive patients. In one patient, CD44v6 was detected not in the primary lesion but in the nodal metastasis. The expression of CD44v6 in patients with ovarian cancer occurred more frequently in node-positive patients. Our study results suggest that the expression of CD44v6 in endometrial adenocarcinoma cells is involved in the progression of the carcinoma, nodal metastasis, myometrial invasion, and vascular invasion, and that in ovarian cancer, the expression of CD44v6 is involved in nodal metastasis.
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PMID:Expression of CD44 alternative splicing variants in primary and lymph node metastatic lesions of gynecological cancer. 911 64

Adenocarcinomas of the uterine cervix show a wide range of morphological features, and can be confused with endometrial adenocarcinoma in biopsy or curetting specimens. The objective of this study was to use tissue microarray technology to evaluate the immunoprofile of a large set of uterine adenocarcinomas with an extended panel of antibodies, comparing the profile of primary cervical and endometrial adenocarcinomas. A tissue microarray was constructed using paraffin-embedded, formalin-fixed tissues from 141 hysterectomy specimens. Duplicate 0.6-mm cores were obtained from 57 cervical adenocarcinomas (16 in situ and 41 invasive) and 84 endometrial adenocarcinomas. Tissue array sections were immunostained with 21 commercially available antibodies [B72.3, CD 99, carcinoembryonic antigen (CEA), c-kit, pancytokeratin, CK 5/6, CK 7, CK8/18, CK19, CK 20, CK 22, EMA, estrogen receptor (ER), KP-1, melan-A, p53, PLAP, S-100, synaptophysin, TTF-1, and vimentin] utilizing the avidin-biotin (ABC) technique. Hierarchical clustering analysis of the tumors was done based on the immunostaining results. Only ER ( P<0.001), CEA ( P=0.04), vimentin ( P<0.001), and CK 8/18 ( P=0.002) showed a significantly different frequency of positivity in endometrial relative to cervical adenocarcinomas. ER, vimentin, and CK 8/18 were more likely to be expressed in endometrial adenocarcinomas, while cervical adenocarcinomas more frequently expressed CEA. We were able to identify immunoprofiles that were highly specific for endocervical adenocarcinoma (ER(-), vimentin(-), CK 8/18(-), CEA(+)) or endometrial adenocarcinoma (ER(+), vimentin(+), CK 8/18(+), CEA(-)), but most tumors showed an intermediate, non-specific immunophenotype. Hierarchical clustering analysis was useful in the interpretation of these intermediate immunophenotypes. Papillary serous adenocarcinoma of the endometrium was less likely to express vimentin ( P=0.002) than endometrioid carcinoma of the endometrium.
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PMID:Immunoprofile of cervical and endometrial adenocarcinomas using a tissue microarray. 1264 18

A possible precursor for invasive endometrial carcinoma is an in situ stage, but this notion is very much debated. We present a case of endometrial carcinoma diagnosed in a patient with post-menopausal bleeding. The morphological examination of the hysterectomy specimen, processed by routine technique, put in evidence focal atypias of the glandular epithelium in a group of few endometrial glands, on a background of atrophy without a desmoplastic stromal reaction. The immunohistochemical investigation of the steroid receptors and p53 protein, using monoclonal antibodies in the ABC technique, revealed the p53 positivity and the absence of the receptors in the focal malignant areas. The surface epithelium had the same immunohistochemical aspect. These aspects were decisive in precising that the malignant change was primarily in the surface epithelium with secondary extension in some glands, the final diagnosis being in situ serous papillary carcinoma.
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PMID:[Endometrial carcinoma in situ. Morphological and immunohistochemical aspects]. 1475 81

The endometrium extracellular matrix (ECM) is essential for embryo implantation. Versican, a large chondroitin sulfate proteoglycan that binds hyaluronan and forms large ECM aggregates, can influence fundamental physiological phenomena, such as cell proliferation, adhesion and migration. The present study investigated the possible role of versican in human embryo implantation. Versican V1 expression and secretion in human endometrial epithelial cells (EECs) was most prominent in the mid-secretory phase. Versican expression in EECs significantly increased after treatment with estrogen and progesterone, but not by estrogen alone. We also established versican V1-overexpressing Ishikawa (endometrial cancer cell line) cells (ISKW-V1), versican V3-overexpressing (ISKW-V3) and control GFP-overexpressing (ISKW-GFP) Ishikawa cells. By the in vitro implantation model, the attachment ratio of BeWo (choriocarcinoma cell line) spheroids to the monolayer of ISKW-V1, but not of ISKW-V3, was found significantly enhanced compared with attachment to the ISKW-GFP monolayer. The conditioned medium derived from ISKW-V1 (V1-CM) also promoted the attachment of BeWo spheroids to the ISKW monolayer. However, this attachment-promoting effect was abolished when V1-CM was pretreated with chondroitinase ABC, which degrades chondroitin sulfate. Therefore, out of the ECM components, versican V1 may facilitate human embryo implantation.
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PMID:Versican V1 in human endometrial epithelial cells promotes BeWo spheroid adhesion in vitro. 3039 8

: Initially, patients that respond to cisplatin (DDP) treatment later relapse and develop chemoresistance. Agents that enhance DDP effectiveness will have a significant impact on cancer treatment. We have shown pronounced inhibitory effects of the progesterone-calcitriol combination on endometrial and ovarian cancer cell growth. Here, we examined whether and how progesterone-calcitriol combination potentiates DDP anti-tumor effects in cancer cells. Ovarian and endometrial cancer cells treated with various concentrations of DDP showed a concentration-dependent decrease in cell proliferation. Concurrent treatment of cells with DDP and progesterone-calcitriol ombination potentiated anticancer effects of DDP compared to DDP-calcitriol, or DDP-progesterone treated groups. The anticancer effects were mediated by increased caspase-3, BAX, and decreased BCL2 and PARP-1 expression in DDP and progesterone-calcitriol combination-treated cells. Stimulation of the PI3K/AKT and MAPK/ERK pathways seen in cancer cells was reduced in DDP-progesterone-calcitriol treated cells. Pretreatment of cells with specific inhibitors further diminished AKT and ERK expression. Furthermore, progesterone-calcitriol potentiated the anti-growth effects of DDP on cancer cells by attenuating the expression of SMAD2/3, multidrug resistance protein- 1 (MDR-1), and ABC transporters (ABCG1, and ABCG2), thereby impeding the efflux of chemo drugs from cancer cells. These results suggest a potential clinical benefit of progesterone-calcitriol combination therapy when used in combination with DDP.
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PMID:Progesterone-Calcitriol Combination Enhanced Cytotoxicity of Cisplatin in Ovarian and Endometrial Cancer Cells In Vitro. 3224 45