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1,838
datasets available to search
ShareScore release 0.9.0
Dataset results
1,838 results for “Endometrial”
Effect of Physical Activity Intervention on Overweight and Obese Patients With Endometrial Cancer
ClinicalTrials.gov study NCT06312917. IPD Sharing: UNDECIDED. Countries: 1. Publications: 0.
Gonadotropin-releasing Hormone Agonist (GnRHa) Plus Letrozole In Young Women With Early Endometrial Cancer
ClinicalTrials.gov study NCT05247268. IPD Sharing: YES. Countries: 1. Publications: 22.
Studies on the H Pipelle, a New Device for Endometrial Sampling at Hysteroscopy
ClinicalTrials.gov study NCT00755651. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Physical Activity After Endometrial Cancer
ClinicalTrials.gov study NCT00501761. IPD Sharing: Not stated. Countries: 1. Publications: 1.
A Study Comparing Mirena and Systemic Progestin for Endometrial Hyperplasia
ClinicalTrials.gov study NCT01074892. IPD Sharing: Not stated. Countries: 1. Publications: 14.
Sentinel Node Biopsy in Endometrial Cancer
ClinicalTrials.gov study NCT04073706. IPD Sharing: NO. Countries: 7. Publications: 1.
Sentinel Node Mapping in Women With Endometrial and Cervical Cancer
ClinicalTrials.gov study NCT02820506. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Weight Loss Management in Endometrial Cancer Survivors
ClinicalTrials.gov study NCT06877572. IPD Sharing: YES. Countries: 1. Publications: 18.
Comparison of Dilatation & Curettage and Endometrial Aspiration Biopsy Accuracy in Patients Treated With Progestin for Endometrial Hyperplasia: A Korean Gynecologic Oncology Group Study
ClinicalTrials.gov study NCT02412072. IPD Sharing: Not stated. Countries: 1. Publications: 1.
the Effect of Endometrial Compaction Caused by Progesterone Effect on Pregnancy Outcomes
ClinicalTrials.gov study NCT04733235. IPD Sharing: UNDECIDED. Countries: 1. Publications: 1.
Flavopiridol in Treating Patients With Recurrent or Persistent Endometrial Cancer
ClinicalTrials.gov study NCT00023894. IPD Sharing: Not stated. Countries: 5. Publications: 1.
Data from: Poor endometrial proliferation after clomiphene is associated with altered estrogen action
Open the record for dataset details and reuse information.
Proteomic data of endometrial and myometrial hydrogels
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BMP/SMAD1/5 signaling in the endometrial epithelium is essential for receptivity and early pregnancy
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Enhanced stromal H2S production via CBS upregulation promotes estrogen-stimulated human endometrial angiogenesis
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Combining genome-wide studies of breast, prostate, ovarian and endometrial cancers maps cross-cancer susceptibility loci and identifies new genetic associations
<p>Data set linked to the paper, "Combining genome-wide studies of breast, prostate, ovarian and endometrial cancers maps cross-cancer susceptibility loci and identifies new genetic associations". Pre-print of the paper is here: <a href="https://doi.org/10.1101/2020.06.16.146803">https://doi.org/10.1101/2020.06.16.146803</a>.</p> <p> </p> <p>cross_cancer_sum_stats.txt.gz contains summary genome-wide association statistics for susceptibility to single cancers (breast (BR), prostate (PR), ovarian (OV), endometrial (EN), estrogen receptor (ER)-positive breast (POS), ER-negative breast (NEG), and high-grade serous ovarian (HGS) cancers) and from the cross-cancer meta-analysis (main [main] and subtype-focused [sub]). EA in the header refers to the effect allele, OA is the other allele, EAF is the effect allele frequency in the largest of the single cancer data sets (BR), IMPR2 is the imputation quality in the largest of the single cancer data sets (BR), SE is the standard error, PVAL is the P-value, RE2Cs1 is the RE2C statistic mean effect part, RE2Cs2 is the RE2C statistic heterogeneity part, RE2Cp* is the RE2C* P-value. More on RE2Cp* can be found here: <a href="http://software.buhmhan.com/RE2C/index.php?mid=contact&act=dispBoardWrite">http://software.buhmhan.com/RE2C/index.php?mid=contact&act=dispBoardWrite</a> and in <a href="https://academic.oup.com/bioinformatics/article/33/14/i379/3953957">https://academic.oup.com/bioinformatics/article/33/14/i379/3953957</a> SNP names in cross_cancer_sum_stats.txt.gz include the chromosome and build 37 position.</p> <p> </p> <p>main_tetrachoric_corr_matrix.txt and subtype_tetrachoric_corr_matrix.txt provide the tetrachoric correlation matrices used in the main and subtype-focused meta-analyses. These were also used to specify the cryptic.cor argument of the exh.abf function of MetABF. More on MetABF can be found here: <a href="https://github.com/trochet/metabf">https://github.com/trochet/metabf</a> and in <a href="https://onlinelibrary.wiley.com/doi/abs/10.1002/gepi.22202">https://onlinelibrary.wiley.com/doi/abs/10.1002/gepi.22202</a></p> <p> </p> <p>prior_sigmas_for_metabf.txt contains the values used to specify the prior.sigma argument of the exh.abf function in MetABF.</p> <p> </p> <p>The breast cancer data used are described in <a href="https://pubmed.ncbi.nlm.nih.gov/29059683/"><strong>PMID 29059683</strong></a> and can be downloaded from <a href="http://bcac.ccge.medschl.cam.ac.uk/bcacdata/oncoarray/oncoarray-and-combined-summary-result/gwas- summary-results-breast-cancer-risk-2017/">http://bcac.ccge.medschl.cam.ac.uk/bcacdata/oncoarray/oncoarray-and-combined-summary-result/gwas- summary-results-breast-cancer-risk-2017/</a> (this link also includes acknowledgements). The prostate cancer data are described in <a href="https://pubmed.ncbi.nlm.nih.gov/29892016/"><strong>PMID 29892016</strong></a> and can be downloaded from: <a href="http://practical.icr.ac.uk/blog/?page_id=8164">http://practical.icr.ac.uk/blog/?page_id=8164</a> (this link also includes acknowledgements). The ovarian cancer data used are described in <a href="https://pubmed.ncbi.nlm.nih.gov/28346442/"><strong>PMID 28346442</strong></a> and can be downloaded from <a href="https://www.ebi.ac.uk/gwas/studies/GCST004415">https://www.ebi.ac.uk/gwas/studies/GCST004415</a>. The endometrial cancer data are described in <a href="https://pubmed.ncbi.nlm.nih.gov/30093612/"><strong>PMID 30093612</strong></a> and can be downloaded from <a href="https://www.ebi.ac.uk/gwas/studies/GCST006464">https://www.ebi.ac.uk/gwas/studies/GCST006464</a>. These links point to the same data that form the basis of the cross_cancer_sum_stats.txt.gz file.</p> <p> </p> <p><strong>The sample size and precision of the data presented should preclude identification of any individual study participant. However, in downloading these data, you undertake not to attempt to identify individual study participant and not to re-post these data to a third-party website. Please cite the PMIDs highlighted above along with the appropriate acknowledements if you use the cross_cancer_sum_stats.txt.gz file.</strong></p> <p> </p> <p>If you have any questions about this repository, please email Siddhartha Kar at siddhartha dot kar at bristol dot ac dot uk</p>
Single cell transcriptomes of of primary tumors and normal endometrial derived organoids treated with DBZ
<p>Endometrial carcinoma, the most common gynecologic cancer, develops from endometrial epithelium which is composed of secretory and ciliated cells. Pathologic classification is unreliable and there is a need for prognostic tools. We used single cell sequencing to study organoid model systems derived from normal endometrial endometrium to discover novel markers specific for endometrial ciliated or secretory cells. We performed 10X based single cell sequencing on both normal and DBZ treated organoids, and on endometrial and ovarian tumours.</p>
Data from: Prognostic and clinical significance of miRNA-205 in endometrioid endometrial cancer
Endometrial cancer is one of the most common malignancies of the reproductive female tract, with endometrioid endometrial cancer being the most frequent type. Despite the relatively favourable prognosis in cases of endometrial cancer, there is a necessity to evaluate clinical and prognostic utility of new molecular markers. MiRNAs are small, non-coding RNA molecules that take part in RNA silencing and post-transcriptional regulation of gene expression. Altered expression of miRNAs may be associated with cancer initiation, progression and metastatic capabilities. MiRNA-205 seems to be one of the key regulators of gene expression in endometrial cancer. In this study, we investigated clinical and prognostic role of miRNA-205 in endometrioid endometrial cancer. After total RNA extraction from 100 archival formalin-fixed paraffin-embedded tissues, real-time quantitative RT-PCR was used to define miRNA-205 expression levels. The aim of the study was to evaluate miRNA-205 expression levels in regard to patients' clinical and histopathological features, such as: survival rate, recurrence rate, staging, myometrial invasion, grading and lymph nodes involvement. Higher levels of miRNA-205 expression were observed in tumours with less than half of myometrial invasion and non-advanced cancers. Kaplan-Maier analysis revealed that higher levels of miRNA-205 were associated with better overall survival (p = 0,034). These results indicate potential clinical utility of miRNA-205 as a prognostic marker.
Data from: Downregulation of endometrial mesenchymal marker SUSD2 causes cell senescence and cell death in endometrial carcinoma cells
The cause of death among the majority of endometrial cancer patients involves migration of cancer cells within the peritoneal cavity and subsequent implantation of cancer spheroids into neighbouring organs. It is, thereby, important to identify factors that mediate metastasis. Cell adhesion and migration are modified by the mesenchymal stem cell (MSC) marker Sushi domain containing 2 (SUSD2), a type I transmembrane protein that participates in the orchestration of cell adhesion and migration through interaction with its partner Galactosidase-binding soluble-1 (LGALS1). MSCs have emerged as attractive targets in cancer therapy. Human endometrial adenocarcinoma (Ishikawa) cells were treated with TGFβ (10ng/ml) for 72h. SUSD2, LGALS1 and MKI67 transcript levels were quantified using qRT-PCR. The proportion of SUSD2 positive (SUSD2+) cells and SMAD2/3 abundance were quantified by FACS and Western blotting, respectively. Senescent cells were identified with β-galactosidase staining; cell cycle and cell death were quantified using Propidium Iodide staining. Treatment of endometrial cancer cells (Ishikawa cells) with TGFβ (10ng/ml) significantly decreased SUSD2 transcript levels and the proportion of SUSD2 positive cells. Silencing of SUSD2 using siRNA resulted in senescence and cell death of Ishikawa cells via activation of SMAD2/3. These findings suggest that SUSD2 counteracts senescence and cell death and is thus a potential chemotherapeutic target in human endometrial cancer.
Data from: Perturbing the cellular cevels of steroid receptor coactivator-2 impairs murine endometrial function
As pleiotropic coregulators, members of the p160/steroid receptor coactivator (SRC) family control a broad spectrum of transcriptional responses that underpin a diverse array of physiological and pathophysiological processes. Because of their potent coregulator properties, strict controls on SRC expression levels are required to maintain normal tissue functionality. Accordingly, an unwarranted increase in the cellular levels of SRC members has been causally linked to the initiation and/or progression of a number of clinical disorders. Although knockout mouse models have underscored the critical non-redundant roles for each SRC member in vivo, there are surprisingly few mouse models that have been engineered to overexpress SRCs. This deficiency is significant since SRC involvement in many of these disorders is based on unscheduled increases in the levels (rather than the absence) of SRC expression. To address this deficiency, we used recent mouse technology that allows for the targeted expression of human SRC-2 in cells which express the progesterone receptor. Through cre-loxP recombination driven by the endogenous progesterone receptor promoter, a marked elevation in expression levels of human SRC-2 was achieved in endometrial cells that are positive for the progesterone receptor. As a result of this increase in coregulator expression, female mice are severely subfertile due to a dysfunctional uterus, which exhibits a hypersensitivity to estrogen exposure. Our findings strongly support the proposal from clinical observations that increased levels of SRC-2 are causal for a number of endometrial disorders which compromise fertility. Future studies will use this mouse model to decipher the molecular mechanisms that underpin the endometrial defect. We believe such mechanistic insight may provide new molecular descriptors for diagnosis, prognosis, and/or therapy in the clinical management of female infertility.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.