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

HER-2/neu oncogene protein, epidermal growth factor receptor, progesterone receptor, and estrogen receptor were examined immunohistochemically in specimens of normal and neoplastic endometrium. Tissues obtained at the time of hysterectomy were snap-frozen at liquid nitrogen temperature and serially sectioned at 4 microns. Normal endometrial epithelial cells stained with anti-epidermal growth factor receptor and anti-HER-2/neu with intensities graded from 0 to 3+. Of the 49 endometrial malignancies studied, seven (14%) contained tissue exhibiting HER-2/neu staining in excess (4+) of any of the normal tissues or the other 42 cancer specimens. Expression of both HER-2/neu and steroid receptors was heterogeneous within these seven tumors. To examine this heterogeneity more closely, sections of these and other tumors were double-stained for HER-2/neu and progesterone receptor. It was found that the cells exhibiting 4+ HER-2/neu staining were progesterone receptor-negative. Conversely, cells that were progesterone receptor-positive within the same specimen exhibited HER-2/neu immunostaining equal to or less than 3+. All specimens containing 4+ HER-2/neu tissue were graded 1 or 2 adenocarcinomas, stage I. Thus, there is an inverse relationship between overexpression of HER-2/neu and progesterone receptor in endometrial cancer. On the other hand, overexpression of HER-2/neu in endometrial cancer does not seem to be related to loss of other differentiated characteristics. The prognostic value of these observations awaits continued study.
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PMID:Immunohistochemical study of HER-2/neu, epidermal growth factor receptor, and steroid receptor expression in normal and malignant endometrium. 134 72

Thirty specimens of human endometrial carcinoma (n = 23) and cervical adenocarcinoma (n = 7) have been analyzed for c-myc, epidermal growth factor receptor (EGFR) and c-erbB-2 by immunohistochemistry. In endometrial carcinomas, expression of c-myc was observed in all cases, EGFR in 21 of 23 cases (91.3%) and c-erbB-2 in 7 of 23 cases (30.4%). In cervical adenocarcinomas, expression of c-myc was seen in 5 of 7 cases (71.6%), EGFR in all cases and c-erbB-2 in 2 of 7 cases (28.6%). c-myc immunoactivity was observed as nuclear or cytoplasmic stain or both, EGFR as membrane and cytoplasmic stain, c-erbB-2 as membrane stain. There was no relationship between expression of these three oncogenes and clinical prognostic factors in the present study.
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PMID:Expression of c-myc, epidermal growth factor receptor and c-erbB-2 in human endometrial carcinoma and cervical adenocarcinoma. 168 93

Endometriosis has been shown to be associated with increased number and activity of peritoneal macrophages. The peritoneal macrophage-conditioned media from 33 women with or without endometriosis were studied for their effects on an endometrial carcinoma cell line, ECC-1. The media from six of six stage III/IV cases demonstrated a mitogenic effect, which was blocked by an antibody to epidermal growth factor receptor. However, the conditioned media from seven of nine stage I/II cases and 14 of 18 normal women did not show a mitogenic effect. The difference between stage III/IV and the other two groups was significant (p less than 0.01). The incorporation of tritium-thymidine was three times higher with the media from stage III/IV cases, as compared with that of controls. When purified cytokines were tested in the tritium-thymidine uptake assay, only epidermal growth factor-transforming growth factor-alpha was mitogenic on ECC-1, whereas tumor necrosis factor, interleukin-1, and platelet-derived growth factor had no effect. Thus peritoneal macrophages in patients with endometriosis may play an important role in the progression of endometriosis, and the noted effects could be mediated by epidermal growth factor or a related growth factor.
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PMID:Effects of peritoneal macrophages from patients with endometriosis on the proliferation of endometrial carcinoma cell line ECC-1. 175 Apr 84

Some endometrial cancers and endometrial adenocarcinoma cell lines show amplified expression of proto-oncogenes (fos, fms, myc, myb, neu, and erb-B) and augmented production of growth factors (colony-stimulating factor 1, epidermal growth factor, transforming growth factor-alpha, and transforming growth factor beta) and epidermal growth factor receptor. Oncogene expression, the presence of estrogen and progesterone receptors, and the fraction of cells in S phase are useful biochemical prognostic indicators of clinical outcome, and markers recognized by monoclonal antibodies are available for use in following the clinical course of the disease and responses to treatment. In vivo and in vitro studies on normal and neoplastic tissues are providing evidence of paracrine influences on epithelial cell proliferation. Long-term administration of tamoxifen as adjuvant therapy for breast cancer has recently been found to increase the risk for development of endometrial cancer.
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PMID:Endometrial cancer: biochemical and clinical correlates. 199 48

The molecular genetics of human endometrial carcinoma have yet to be defined to any significant extent. Cell lines from 11 endometrial carcinomas were examined for alterations in proto-oncogenes that might predictably be present, based on existing data from the better-characterized human carcinomas of the uterine cervix, ovary, and breast. Codons 12, 13, and 61 of the Ha-ras, Ki-ras, and N-ras genes were examined for possible point mutations, and the c-erbB2/neu, c-myc, and epidermal growth factor receptor (EGFR) genes were examined for amplification or overexpression. Ras mutations were found in seven of 11 (64%) tumors, including three in codon 61 of Ha-ras (CAG----CAT) and four in codon 12 of Ki-ras (GGT----GAT in two and GGT----GTT in two). No evidence was found for amplification or overexpression of the c-erbB2 or EGFR genes in any tumor. One tumor contained amplified c-myc sequences and exhibited relative overexpression of c-myc. These data suggest that the amplification or overexpression of several proto-oncogenes frequently observed in other human gynecologic and breast tumors are not prevalent in endometrial carcinoma and that ras gene mutations are relatively common in this tumor type.
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PMID:Analysis of oncogene alterations in human endometrial carcinoma: prevalence of ras mutations. 206 24

UM-EC-2 was established from a patient with poorly differentiated stage IB endometrial carcinoma. This cell line produces tumors in nude mice that have the same histological features as the patient's tumor. UM-EC-2 cells express b2-microglobulin, the epidermal growth factor receptor (EGF), and the H blood group antigen. This membrane antigen phenotype is consistent with cells of human endometrial origin. The karyotype of UM-EC-2 is fairly complex, with rearrangements affecting all chromosomes except 3, 10, 14, 19, and 20. There were two populations of cells, a hyperdiploid population with a modal number of 53-55 and a hypertetraploid population with a modal number of 109. A postulated sequence of events before and after tetraploidization is suggested based on the number of copies of individual chromosomes and rearrangements. Comparison of the UM-EC-2 karyotype to that of UM-EC-1 (a previously described line from a different patient with endometrial carcinoma) revealed that the two lines share eight very similar chromosome changes, which include loss of most of chromosome 4, breakpoints affecting proximal bands on 8p, loss of most of 9q, a breakpoint at 12q22, loss of 13q, breakpoints in proximal bands on 18q, and a breakpoint at 22p11. These changes may represent nonrandom chromosome abnormalities in poorly differentiated endometrial cancer. Estrogen (ER) and progesterone (PgR) receptors were not detected in either the primary tumor or the cell line. Nevertheless, UM-EC-2 cells were very sensitive to growth inhibition by tamoxifen (TAM) in vitro. One micromolar TAM caused 50% inhibition of cell growth, 2.5 microM caused cytostasis, and 5 microM TAM was cytotoxic, killing all cells after 5-7 days of exposure to the drug. Paradoxically, 100 nM estradiol (E2) caused a moderate increase in the growth of the cells but it did not prevent or reverse growth inhibitory effects of TAM. These findings support the concept that in some tumors TAM causes growth inhibition by an ER-independent mechanism. UM-EC-2 cells were also sensitive to growth regulation by EGF. Thus, these cells provide a new in vitro model of human endometrial cancer in which the roles of both TAM and EGF as growth regulatory substances can be investigated.
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PMID:Establishment and characterization of UM-EC-2, a tamoxifen-sensitive, estrogen receptor-negative human endometrial carcinoma cell line. 234 64

The expression of epidermal growth factor receptor (EGFr) and transforming growth factor alpha (TGF-alpha) was compared with the presence of "squamous differentiation" (SD) visualized in various histotypes of endometrial carcinoma by using a panel of monoclonal antibodies. The results of the current study demonstrate that EGFr and TGF-alpha are present in routinely processed endometrial carcinoma. The highest positive EGFr and TGF-alpha expression was seen in the group of adenocarcinomas with SD. The more intense EGFr and TGF-alpha immunoreactivity was observed in "squamous" foci both in adenoacanthomas (AA) and in adenosquamous carcinomas (AS). These EGFr- and TGF-alpha-positive squamous areas prevalently displayed a "stratification-related" cytokeratin (CK) immunoprofile characterized by the expression of CKs 1, 4, 5, 10, 13, 14, and 16. No correlation was found between EGFr- and TGF-alpha-positive status and depth of myometrial invasion or surgical stage. These results clearly demonstrate that EGFr and TGF-alpha expression is related remarkably to endometrial carcinoma with "squamous" areas both morphologically and immunophenotypically. This specific association leads us to suggest that EGFr and TGF-alpha expression in endometrial carcinoma may be prevalently involved in the equilibrium of cell differentiation of the "squamous" foci commonly observed in this group of neoplasias.
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PMID:Immunocytochemical study of epidermal growth factor receptor, transforming growth factor alpha, and "squamous differentiation" in human endometrial carcinoma. 752 64

We report here a retrospective study of epidermal growth factor receptor (EGFR) expression in 140 patients with human endometrioid endometrial carcinoma (median period of follow-up, 43.8 months; ranging from 1 to 155 months). Tumor specimens were immunohistochemically examined for the overexpression of EGFR, and the correlation among EGFR status, various clinicopathologic parameters, and prognosis was statistically evaluated. Monoclonal antibody (clone 31 G 7), which recognizes the extracellular domain of the EGFR molecule, was used for immunostaining. Ninety-four of 140 cases were immunohistochemically positive for EGFR (67.1%). The presence or absence of EGFR did not correlate with surgical stage, depth of myometrial invasion (DI), or lymph node involvement, but did correlate with histological grade and patient's age. Furthermore, patients with EGFR-positive endometrial carcinoma had a statistically significant shorter length of survival than those with EGFR-negative tumors (P = .018). This trend is more apparent among the patients more than 50 years old (P = .003). When adjusted for surgical stage, DI, and patient age, EGFR status retained prognostic value by multivariate analysis. However, when adjusted for surgical stage, histological grade, DI, and patient age, EGFR status failed to retain prognostic value by multivariate analysis. The results of this study suggest that EGFR expression is correlated with histological grade and greater invasiveness of human endometrioid endometrial carcinoma.
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PMID:Prognostic value of epidermal growth factor receptor expression in endometrioid endometrial carcinoma. 763 51

The role of epidermal growth factor receptor (EGF-R) and transforming growth factor alpha (TGFA) in endometrial cancer is still controversial. In this study the immunostaining of EGF-R and TGFA, investigated in 44 cases, proved to be related to endometrial cancer histotype regardless of the tumor grade or the extent of myometrial invasion. In fact, EGF-R expression was observed in 12.5% (1/8) of cases with classical endometrioid adenocarcinoma, in 91% (10/11) with endometrial adenocarcinoma and benign squamous metaplasia, and in 35% (6/17) with adenosquamous carcinoma. TGFA expression was concomitant with EGF-R in the first two histotypes, and was present in about 50% (9/17) of the latter. Conversely, in mucinous and serous papillary adenocarcinoma, EGF-R and TGFA immunostaining was not observed. In conclusion, EGF-R positivity was observed in endometrial cancer with squamous differentiation, especially in those cases with benign squamous metaplasia. EGF-R and TGFA coexpression appeared as a constant feature of benign squamous metaplasia.
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PMID:Epidermal growth factor receptor (EGF-R) and transforming growth factor alpha (TGFA) expression in different endometrial cancers. 765 16

We studied the expressions of aberrant epidermal growth factor receptor (EGFR) gene or erbB-2, which is highly homologous to EGFR gene, and erbA or estrogen receptor (ER) gene, which is highly homologous to erbA, as a preliminary study, to know which oncogene expressions are associated with the development of endometrial cancers. ErbB-2 mRNA lacked only extracellular domain (EX), suggesting the lack of downregulation of erbB-2 expression by a ligand, which led to regulated tyrosine kinase activity. Mutated DNA binding domain of ER mRNA were found in 3 of the 13 cases, suggesting the promotion disorder of estrogen-inducible proteins in these 3 endometrial cancers. The behavior of aberrant erbB-2 and ER gene co-expressions is considered of similar to that of erbA and erbB co-expressions in the chicken introduced by the avian erythroblastosis virus, which leads to the development of erythroblastosis in the chick, and seems to be associated with the development of endometrial cancer.
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PMID:Preliminary study of oncogene expressions in endometrial cancers. Aberrant estrogen receptor gene and erbB-2 expressions. 774 15


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