Expression profiling of endometrial cancer of different grades
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE115810 | GEO | 2018/06/15
REPOSITORIES: GEO
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Project description:The present study has focused on the identification of the differences between expression patterns of kinin-dependent genes in endometrial cancer
2012-03-10 | GSE36389 | GEO
Project description:The present study has focused on the identification of the differences between expression patterns of kinin-dependent genes in endometrial cancer For microarray analysis 20 samples were used: 7 control samples, 3 - G1 samples, 8 - G2 samples and 2 - G3 samples.
2012-03-10 | E-GEOD-36389 | biostudies-arrayexpress
Project description:Expression profiling of endometrial cancer of different grades
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Project description:Transcriptional profiling of rat EAC - comparison of non-/pre-malignant endometrium with endometrial tumors Endometrial cancer develops from the endometrium of the uterus and is the most common pelvic malignancy diagnosed in women in the western countries. Similar to all cancer diseases, endometrial cancer is a genetic disorder that results from complex patterns of genetic and epigenetic alterations involved in the malignant transformation. The genetic heterogeneity inherent in the human population, differences in the environment and life styles poses enormous difficulties when analyzing the complex patterns of genetic alterations contributing to cancer etiology. Inbred animal models constitute unique experimental genetic tools as the genetic heterogeneity and the influence of environmental factors can be readily reduced. The BDII/Han rat model is unique for spontaneous hormonal carcinogenesis since more than 90% of the female virgins spontaneously develop endometrial cancer during their life span. The possibility to perform global gene expression profiling of tumor cells would likely provide important information of the genes and pathways that are involved in EAC susceptibility and carcinogenesis. Keywords: Endometrial tumors developed in crosses with the BDII inbred rat strain (from backcrosses, NUT, and intercrosses, RUT) and Sprague Dawley curley-3 and Brown Norway
2008-10-02 | GSE13003 | GEO
Project description:Transcriptional profiling of rat EAC - comparison of non-/pre-malignant endometrium with endometrial tumors Endometrial cancer develops from the endometrium of the uterus and is the most common pelvic malignancy diagnosed in women in the western countries. Similar to all cancer diseases, endometrial cancer is a genetic disorder that results from complex patterns of genetic and epigenetic alterations involved in the malignant transformation. The genetic heterogeneity inherent in the human population, differences in the environment and life styles poses enormous difficulties when analyzing the complex patterns of genetic alterations contributing to cancer etiology. Inbred animal models constitute unique experimental genetic tools as the genetic heterogeneity and the influence of environmental factors can be readily reduced. The BDII/Han rat model is unique for spontaneous hormonal carcinogenesis since more than 90% of the female virgins spontaneously develop endometrial cancer during their life span. The possibility to perform global gene expression profiling of tumor cells would likely provide important information of the genes and pathways that are involved in EAC susceptibility and carcinogenesis. Keywords: Endometrial tumors developed in crosses with the BDII inbred rat strain (from backcrosses, NUT, and intercrosses, RUT) and Sprague Dawley curley-3 and Brown Norway Common reference design - Universal rat reference (Stratagene) hybridized to all arrays. Biological replicates and technical replicates (3) of each clone printed at random positions on the array.
2010-05-19 | E-GEOD-13003 | biostudies-arrayexpress
Project description:<p>Endometrial diseases are common gynecological diseases that disorder women of childbearing age and perimenopausal women, including endometrial polyps (EP), endometrial cancer (EC), and endometrial hyperplasia (EH). Clinically, biopsy or imaging methods are usually used to screen and diagnose endometrial diseases, but due to their invasiveness and heterogeneity, a noninvasive, convenient, objective and accurate biomarker is needed for the differential diagnosis of EP and EC or EH. In the present study, serum samples from 396 patients with endometrial disease and 225 healthy volunteers were analyzed by UPLC-Q-TOF/MS non-targeted lipidomics. A combination of multivariate (Orthogonal partial least-squares discriminant analysis) and univariate (Student t-test) analyses were used to identify and qualify 6, 8, and 7 potential biomarkers in serum from patients with EP, EC, and EH, respectively. With the aid of logistic regression algorithm and receiver operating characteristic (ROC) curve analysis, A biomarker panel including four specific EP biomarkers, 6-Keto-PGF1α, PA(37:4), LysoPC(20:1) and PS (36:0), had good classification and diagnostic ability in distinguishing EP from EC or EH. The biomarker panel can be used as a rapid diagnostic method to assist imaging examination to effectively differentially diagnose endometrial diseases, and provide a reference for clinicians in the identification and diagnosis of endometrial diseases. </p>
2022-01-14 | MTBLS3444 | MetaboLights
Project description:The objectives of the present study were to determine whether obesity impacts human decidualization and the endometrial control of trophoblast invasion (both of which are required for embryo implantation) and evaluate the potential involvement of endometrial extracellular vesicles (EVs) in the regulation of these physiological processes. Using primary human cell cultures, we first demonstrated that obesity is associated with significantly lower in vitro decidualization of endometrial stromal cells (ESCs). We then showed that the trophoblastic cell line’s invasive ability was greater in the presence of conditioned media from cultures of ESCs from obese women. Using mass-spectrometry-based quantitative proteomics, we found that EVs isolated from uterine supernatants of biopsies from obese women (vs. nonobese women) presented a molecular signature focused on cell remodeling and angiogenesis. Lastly, the results of functional assays indicated that supplementation of the culture medium with EVs from nonobese women can rescue (at least in part) the defect in in vitro decidualization described in ESCs from obese women. Lastly, the addition of endometrial EVs from obese women (vs. nonobese women) was associated with significantly greater invasive activity by HTR-8/SVneo cells. In conclusion, our results provided new insights into the endometrial EVs’ pivotal role in the poor uterine receptivity observed in obese women.
2023-10-09 | PXD039568 | Pride
Project description:Human endometrial organoid cultures were established from the decidual samples. We analyzed the global expression profiles of the endometrial organoids. Next, we determined the global expression patterns upon estrogen treatment and compared them to untreated controls.
2021-01-27 | GSE128605 | GEO
Project description:Integrated genomic profiling of endometrial carcinoma associates aggressive tumors with indicators of PI3 kinase activation Although 75% of endometrial cancers are treated at an early stage, 15% to 20% of these recur. We performed an integrated analysis of genome-wide expression and copy-number data for primary endometrial carcinomas with extensive clinical and histopathological data to detect features predictive of recurrent disease. Unsupervised analysis of the expression data distinguished 2 major clusters with strikingly different phenotypes, including significant differences in disease-free survival. To identify possible mechanisms for these differences, we performed a global genomic survey of amplifications, deletions, and loss of heterozygosity, which identified 11 significantly amplified and 13 significantly deleted regions. Amplifications of 3q26.32 harboring the oncogene PIK3CA were associated with poor prognosis and segregated with the aggressive transcriptional cluster. Moreover, samples with PIK3CA amplification carried signatures associated with in vitro activation of PI3 kinase (PI3K), a signature that was shared by aggressive tumors without PIK3CA amplification. Tumors with loss of PTEN expression or PIK3CA overexpression that did not have PIK3CA amplification also shared the PI3K activation signature, high protein expression of the PI3K pathway member STMN1, and an aggressive phenotype in test and validation datasets. However, mutations of PTEN or PIK3CA were not associated with the same expression profile or aggressive phenotype. STMN1 expression had independent prognostic value. The results affirm the utility of systematic characterization of the cancer genome in clinically annotated specimens and suggest the particular importance of the PI3K pathway in patients who have aggressive endometrial cancer. 84 endometrial cancers (including 9 cell lines) were subject to 100K SNP analysis. 57 endometrial cancers were subject to expression analysis.
2009-03-23 | E-GEOD-14860 | biostudies-arrayexpress
Project description:Integrated genomic profiling of endometrial carcinoma associates aggressive tumors with indicators of PI3 kinase activation Although 75% of endometrial cancers are treated at an early stage, 15% to 20% of these recur. We performed an integrated analysis of genome-wide expression and copy-number data for primary endometrial carcinomas with extensive clinical and histopathological data to detect features predictive of recurrent disease. Unsupervised analysis of the expression data distinguished 2 major clusters with strikingly different phenotypes, including significant differences in disease-free survival. To identify possible mechanisms for these differences, we performed a global genomic survey of amplifications, deletions, and loss of heterozygosity, which identified 11 significantly amplified and 13 significantly deleted regions. Amplifications of 3q26.32 harboring the oncogene PIK3CA were associated with poor prognosis and segregated with the aggressive transcriptional cluster. Moreover, samples with PIK3CA amplification carried signatures associated with in vitro activation of PI3 kinase (PI3K), a signature that was shared by aggressive tumors without PIK3CA amplification. Tumors with loss of PTEN expression or PIK3CA overexpression that did not have PIK3CA amplification also shared the PI3K activation signature, high protein expression of the PI3K pathway member STMN1, and an aggressive phenotype in test and validation datasets. However, mutations of PTEN or PIK3CA were not associated with the same expression profile or aggressive phenotype. STMN1 expression had independent prognostic value. The results affirm the utility of systematic characterization of the cancer genome in clinically annotated specimens and suggest the particular importance of the PI3K pathway in patients who have aggressive endometrial cancer.
2009-03-24 | GSE14860 | GEO