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

Preoperative serum CA 125 levels were measured in 61 patients with various FIGO stage endometrial adenocarcinoma and they were compared with stage of disease, grading and pelvic lymph nodes involvement. Serum CA 125 levels in excess of 35 U/ml were detected in 19 patients (31.1%): circulating levels exceeding 65 U/ml were also found in 15 patients (24.5). Rising concentrations were associated with increasing stages. Grading and lymph nodes involvement were correlated with the presence of elevated serum levels (more than 65% for grade two or three and more than 80% in patients with positive lymph nodes). Preoperative high concentrations of CA 125 suggest the presence and the probability of advanced endometrial cancer. The cases with elevated CA 125 serum levels seems to be a higher risk for extrauterine tumor progression and lymphatic space invasion: the preoperative presence of the antigen imposes an accurate intraoperative surgical staging and a careful follow-up for preventing recurrence or metastases.
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PMID:[Preoperative levels of CA 125 and risk factors in adenocarcinoma of the endometrium]. 263 16

Cytogenetic studies were performed on endometrial specimens of four patients with hyperplasia. Six with adenocarcinoma and one with mixed mesodermal tumor. All 65 cells obtained from hyperplasia specimens excluding one cell, had a normal female karyotype. However, cells from five adenocarcinoma specimens had chromosomal abnormalities, though a specimen of a well differentiated adenocarcinoma showed a normal karyotype. A few numerical abnormalities which were clonal in origin, were noted in one case each. Three kinds of structural abnormalities involving chromosomes 1 were identified as clonal in origin; del (1) (p21), t. dic(1; 16) (p21; q24), and i (lq). Since carcinoma cells had two chromosomes 1 of normal morphology, the presence of the marker chromosome led to the partial trisomy or tetrasomy of the long arm of a chromosome 1, being characteristic of cells from adenocarcinoma of the endometrium. A successively transplantable tumor has been produced from a poorly differentiated carcinoma cells with the t. dic (1; 16) (p21; q24) marker chromosome. Histological and chromosomal examinations were performed in cells from the passage 1, 4 and 5 tumors in order to explore the role of this marker played in the formation of the endometrial carcinoma. Though the degree of differentiation status of tumor cells had been changed during transplantations, the t. dic (1; 16) (p21; q24) marker were observed consistently among these cells. This suggested that the rearrangement of chromosome 1 was not produced as a result of genetic instability due to tumor progression, but rather specifically associated with the endometrial carcinogenesis. None of karyotypic changes excluding the marker and the tetraploid was responsible for these phenotypic changes.
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PMID:[Cytogenetic study of endometrial carcinoma]. 301 54

The serum concentrations of CA 125 were determined in 136 corpus carcinoma patients. Before the primary irradiation therapy in 40.2% (19/47), after the hysterectomy 3.4% (3/89) of the patients had elevated (> 35 U/ml) CA 125 levels. CA 125 values above the normal range were frequently associated with advanced stages. Measuring elevated levels after hysterectomy proved bad prognosis. There were no correlation of CA 125 levels and degree of the histological type and differentiation of the tumor. Serological follow up revealed a correlation with the clinical course of the endometrial carcinoma in 62% (31/50). 18 cases who had tumor progression associated rising CA 125 levels. In 10 patients with tumor progression the CA 125 levels increased before clinical sign of progression with a median lead time of one month. The determination of CA 125 is recommended to check the endometrial carcinoma patients and to detect progression of the tumor.
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PMID:[Serologic monitoring of patients with endometrial carcinoma using ovarian carcinoma antigen (CA 125)]. 846 17

Previous studies have demonstrated that some human endometrial carcinomas contain an activating point mutation in codon 12 of the Ki-ras protooncogene. To examine the hypothesis that this mutation may occur at an earlier stage of neoplastic progression in the endometrium, we analyzed 89 samples of premalignant endometrial hyperplasia and an additional 84 samples of endometrial carcinoma for point mutations of Ki-ras codon 12. Mutations were found in all three types of endometrial hyperplasia, simple, complex, and atypical, with no clear evidence of a differential distribution in any particular type. Furthermore, the overall incidence of Ki-ras mutations in the hyperplasia specimens (16%) was similar to the incidence detected in carcinomas (18%), indicating that ras mutation may represent an early event in a subset of endometrial carcinomas. When the tissue samples were segregated as to country of origin, the frequency of this mutation was approximately 2-fold higher in hyperplasia and carcinoma samples from Japan than from the United States, where the incidence, clinicopathological characteristics, and risk factors for endometrial carcinoma differ dramatically. There was no apparent correlation, however, between ras mutation and any pathological, histological, or clinical parameter examined, except survival. The presence of a ras mutation was inversely associated with death from disease, suggesting that this molecular feature may characterize a subset of endometrial carcinomas with a good prognosis.
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PMID:Mutation of the Ki-ras protooncogene in human endometrial hyperplasia and carcinoma. 846 12

The effects of the endocrine milieu on growth, invasion and metastasis, associated with neovascularization of endometrial cancer, the expression of plasminogen activator inhibitor 1 (PAI-1), and its mRNA in endometrial atypical hyperplasia and cancer, and normal endometria as controls were determined in premenopausal and postmenopausal women. In premenopausal women, the levels of PAI-1 and its mRNA in normal endometria were significantly higher than in endometrial atypical hyperplasia and cancer. On the other hand, in postmenopausal women, the results were reversed. There was no difference in the expression of PAI-1 and its mRNA in the various histological grades and clinical stages in endometrial cancers, while the expression of PAI-1 in other cancers increased during tumor progression. In our previous study, the expression of PAI-1 and its mRNA in well-differentiated endometrial cancer cell lines was dependent upon estrogen and progesterone. This might be partially related to the endocrine milieu, especially in endometrial atypical hyperplasia and well-differentiated endometrial cancer, which seems to be dependent on sex steroids. Therefore, endometrial cancer of any histological grade and clinical stage might maintain PAI-1 expression in both premenopausal and postmenopausal women, which may modulate, at least in part, growth, invasion and metastasis associated with neovascularization of endometrial cancer.
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PMID:Comparative study on expression of plasminogen activator inhibitor 1 and its mRNA in endometrial cancers and normal endometria. 898 21

The purpose of this work was to study changes in serum levels of interleukins, growth factors and angiogenin during different stages of endometrial cancer progression. Serum levels were assayed by enzyme-linked immunosorbant assay in 59 women with stages I-IV of endometrial cancer (study subjects: stage I, n = 20; stage II, n = 8; stage III, n = 5; stage IV, n = 6) and compared to the serum levels in 20 women without cancer as control subjects. Patients with endometrial cancer had varied serum levels of interleukins and growth factors. There was a significant increase in serum levels of angiogenin in all stages of tumor progression. Levels of interleukin-8 (IL-8), IL-10 and transforming growth factor beta (TGF beta) were significantly elevated in patients with stages I and II carcinoma. The serum levels of tumor necrosis factor alpha (TNF alpha), granulocyte/macrophage-colony-stimulating factor, basic fibroblast growth factor (BFGF), IL-7 and IL-2 were significantly elevated in patients with stages II and III carcinoma and the serum level of tumor necrosis factor beta (TNF beta) was slightly elevated in patients with stage II carcinoma only. The serum levels of IL-1 alpha, IL-1 beta and IL-6 were not elevated in endometrial cancer patients in any of the clinical stages. The results showed that progression of endometrial cancer is associated with increased serum levels of cytokines, growth factors and angiogenin, which possibly amplify angiogenesis during different clinical stages.
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PMID:Serum levels of interleukins, growth factors and angiogenin in patients with endometrial cancer. 911 82

Clinicopathological, immunohistochemical and molecular genetic analyses of endometrial carcinoma suggest different pathogenetic pathways for endometrioid and serous carcinoma. Most endometrioid carcinomas are associated with endometrial hyperplasia, are ER/PR positive, p53 negative and express low Ki-67. In contrast, almost all serous carcinomas develop from endometrial intraepithelial carcinoma (EIC) in a background of atrophy. These tumors are ER/PR negative, strongly express p53 and show high Ki-67 labeling. On the molecular genetic level, 25-30% of endometrioid carcinomas show microsatellite instability (MI), 25-30% harbor mutant K-ras and less than 10% have mutant p53. In contrast, more than 90% of serous carcinomas have p53 mutations, 2% K-ras mutations and none MI. Among endometrioid carcinomas, K-ras mutations occur most frequently in FIGO grade 2 and 3 tumors and p53 mutations in FIGO grade 3 tumors. In contrast, MI is equally distributed among all FIGO grades. These findings support the view that endometrioid carcinoma develops slowly in a progressive fashion from endometrial hyperplasia. Mutation of p53 occurs late in tumor progression. Thus, endometrioid carcinogenesis resembles the proposed model for colorectal carcinogenesis. In contrast, serous carcinoma develops rapidly from EIC in a background of atrophy. Mutation of p53 occurs early in serous carcinogenesis and this may account for the highly aggressive behavior of this tumor.
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PMID:A dualistic model for endometrial carcinogenesis based on immunohistochemical and molecular genetic analyses. 947 74

Microsatellite instability (MI) has been observed in endometrioid adenocarcinomas of the endometrium, either arising sporadically or in association with the hereditary colon cancer syndrome. Genes known to contain mononucleotide short tracts in their coding sequence are regarded as targets for mutations in these tumors. BAX is a proapoptotic gene that contains a tract of eight consecutive deoxyguanosines in its third coding exon. DNA of 26 patients with endometrial carcinoma was extracted from blood and from fresh-frozen and paraffin-embedded tumor tissue. For MI analysis, microsatellite loci on chromosomes 3, 5, 10, 12, and 18 were amplified by PCR. Frameshift mutations in the (G)8 tract of BAX were detected by single-strand conformation polymorphism (SSCP) analysis. MI at three or more loci was detected in 13 cases. BAX frameshift mutations were detected in seven MI+ tumors (53.8%), but in none of the 13 MI- neoplasms. In two cases, identical BAX frameshift mutations were detected in different areas of the neoplasm, whereas in the other five cases, BAX mutations were heterogeneously distributed throughout the tumor. Immunostaining with antibodies against the carboxy terminus of BAX protein was very useful in assessing the heterogeneous distribution of BAX frameshift mutations in the neoplasms. The results suggest that BAX frameshift mutations are frequent in endometrial carcinomas with MI, probably playing a role in the process of tumor progression of these neoplasms.
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PMID:BAX somatic frameshift mutations in endometrioid adenocarcinomas of the endometrium: evidence for a tumor progression role in endometrial carcinomas with microsatellite instability. 984 Jun 18

While the role of steroid hormones in the regulation of endometrial proliferation and differentiation is well established, the effects of growth factors and their receptors in normal and neoplastic endometrium remain a matter of debate. Previous studies have documented the positive effects of insulin-like growth factor-I (IGF-I) on epithelial cell proliferation and the active production of this growth factor in endometrial tissues. In view of decreased expression of transforming growth factor-beta1 (TGF-beta1), an antagonist of IGF-I, in endometrial carcinoma, we investigated the expression of IGF-I, at both the mRNA and protein levels, and the immunoreactivity for type I IGF-I receptor in 30 formalin-fixed, paraffin-embedded tissue samples of normal and neoplastic endometrium, in order to possibly clarify the role of IGF-I in endometrial proliferation and differentiation. Our results demonstrate a reduced expression of IGF-I mRNA in endometrial carcinomas compared with non-neoplastic tissues, despite equivalent immunohistochemical expression of IGF-I and IGF-I receptor. Our data suggest that IGF-I and its corresponding receptor may not be directly involved in endometrial cancer cell proliferation and differentiation in vivo, though other components of the IGF-I system (e.g., IGF binding proteins) may affect endometrial malignant transformation and tumor progression.
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PMID:Insulin-like growth factor-I expression in normal and diseased endometrium. 993 98

Telomerase activity has been implicated in the progression of various human tumors. Our aim was to evaluate telomerase activity and to compare it with histo-pathological factors in uterine endometrial carcinoma, to look for possible correlations. Telomerase activity was measured by dilution analysis using a PCR-based telomeric repeat amplification method and detected in 31 of 35 primary endometrial carcinoma tumor specimens. High telomerase activity, detected after 100-fold dilution of extracts, was identified in 15 specimens. There was no significant correlation between the positive telomerase activity and tumor surgical stage or histo-pathological factors. However, high telomerase activity was significantly correlated with advanced surgical stage and with pelvic lymph node metastasis. Our findings suggest that an increase in telomerase activity may be associated with tumor progression and that its level may have a prognostic value in endometrial carcinoma.
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PMID:Telomerase activity correlates with histo-pathological factors in uterine endometrial carcinoma. 1050 33


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