GEO accession GSE278879 is currently private and is scheduled to be released on Jun 01, 2026.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1169347 | ENA |
REPOSITORIES: ENA
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Project description:Endometrial cancer (EC) is the sixth most prevalent malignancy affecting women worldwide, with an increasing incidence that poses a substantial public health challenge. This study investigates the tumor microenvironment (TME) of EC, particularly high grade endometrioid endometrial cancer (HEEC), utilizing single nucleus RNA sequencing (snRNA-seq). The analysis encompassed normal endometrium (NE), HEEC, middle grade endometrioid endometrial cancer (MEEC), and low grade endometrioid endometrial cancer (LEEC). Significant cellular heterogeneity was identified within the TME, including immune cells, fibroblasts, and epithelial cells. Notably, SULF1+ NREP+ fibroblasts were significantly enriched in HEEC and associated with aggressive tumor behavior. Additionally, the study highlighted the overexpression of metabolic pathways and immune checkpoint molecules in HEEC epithelial cells, including Human Leukocyte Antigen E (HLA-E) and Killer Cell Lectin Like Receptor C1 (KLRC1), which may contribute to immune evasion and enhanced tumor aggressiveness. Identifying the EYA transcriptional coactivator and phosphatase 1 (EYA1) gene as a prospective biomarker in HEEC due to its association with poor prognosis and the enhanced proliferative and migratory capabilities of EC cells. Furthermore, analyses of cell-cell interactions revealed critical signaling pathways, such as the Leucocyte Associated Immunoglobulin Like Receptor-1 (LAIR1)- Leukocyte Immunoglobulin-like Receptor B4 (LILRB4) axis in macrophages, which may play a role in immune suppression and EEC progression. A comprehensive single-cell level characterization of the TME in EEC offers critical insights into the molecular mechanisms driving EEC progression, while identifying potential therapeutic targets. These discoveries advance our understanding of EEC pathophysiology and hold promise for the development of targeted therapies, particularly in HEEC
2026-06-01 | GSE278879 | GEO
Project description:Purpose: Increasing genomics-based evidence suggests that synchronous endometrial and ovarian cancer (SEOC) represents clonally related primary and metastatic tumors. A systematic analysis of the global protein landscape of SEOCs, heretofore lacking, could reveal functional and disease-specific consequences of known genetic alterations, the directionality of metastasis, and accurate histological markers to distinguish SEOCs from single-site tumors. Experimental Design: We performed a systematic proteogenomic analysis of 29 patients diagnosed with SEOC at three international gynecologic oncology treatment centers (Chicago, Vancouver, Tübingen). For direct comparison to single-site tumors, we included 9 patients with single-site endometrioid ovarian and 26 patients with single-site endometrial endometrioid cancer. For all 64 patients, we performed sequencing of a 275-gene cancer panel combined with compartment-resolved mass spectrometry (MS) based proteomics of consecutive tissue sections to compare global (6,000+ proteins), tumor, and stromal proteomes. Results: DNA-based panel sequencing confirmed that most SEOCs are clonally related, suggesting primary and metastatic disease. These findings were further substantiated on the global proteome level, uncovering pronounced differences between SEOCs and single tumors and underscoring the importance of the stromal proteome in defining and identifying SEOCs. Our integrated proteogenomic approach confirmed that SEOCs more closely resemble endometrial endometrioid than endometrioid ovarian cancers. Conclusions: The integrated proteogenomic data show that SEOCs are distinguishable from endometrial endometrioid or endometrioid ovarian cancers. Based on their proteogenomic similarity to endometrial endometrioid cancers, we conclude that most synchronous endometrial and ovarian cancers represent primary endometrial endometrioid cancers that have metastasized to the ovary.
2025-03-11 | PXD059172 | Pride
Project description:For normal endometrium, middle/low/high grade endometrioid endometrial cancer proteomic and lactylome sequencing were performed to find the key proteins and lactyl site affecting the progression of endometrioid endometrial cancer
2025-07-06 | PXD065831 |
Project description:We performed genome-wide DNA methylation profiling of endometrial endometrioid adenocarcinoma tissues derived from patients in the Cancer Institute Hospital of Japanese Foundation for Cancer Research.
2019-09-13 | GSE136791 | GEO
Project description:Endometrial cancer (EC) is the most common female genital malignancy and the fourth most common cancer in women in the developing world1. EC has been traditionally classified into two main groups with different clinical, pathological and molecular features2,3. Type I or endometrioid endometrial carcinomas (EECs) account for about 75% of the cases and are typically estrogen-related and low-grade tumors with good prognosis that coexist or are preceded by endometrial hyperplasia, mainly diagnosed in perimenopausal women. In contrast, type II or non-endometrioid endometrial carcinomas (NEECs) are high-grade aggressive tumors associated with endometrial atrophy and poor prognosis, unrelated to estrogen and diagnosed in older women. These comprise several histological subtypes, being the most common the serous carcinomas (SEC)4. In recent years numerous large-scale studies of primary endometrioid and serous tumors have been performed5, revealing new mutated genes and establishing a new molecular subclassification based on the results obtained by The Cancer Genome Atlas (TCGA) consortium6, which implies different clinical outcomes. More recently, the genomic evolution of EC has been analyzed through a comparative study of samples from endometrial atypical hyperplasia, primary tumors and paired metastases7, revealing the presence of intratumor heterogeneity as previously described in primary EC and other tumor types8,9. However an in-depth study considering multiple regions from primary tumor and paired metastases has not been performed up to now to our knowledge. Here we analyze by whole-exome sequencing (WES), massive parallel targeted sequencing and array comparative genomic hybridization (aCGH) the clonal evolution and intratumor heterogeneity of 7 endometrioid and 3 serous metastatic endometrial carcinomas. Different locations from the primary tumor as well as from their paired metastases were included in the study, allowing the reconstruction of the spatial and temporal phylogenetic evolution of the tumor. Different phylogenetic evolution patterns were identified, independently of the classical histological or molecular classification of the tumor, although similar patterns were found in ovarian metastasis and recurrent disease.
2022-02-14 | GSE101447 | GEO
Project description:We performed genome-wide DNA methylation profiling of precursor lesions of endometrial endometrioid carcinoma tissues derived from patients in the Cancer Institute Hospital of Japanese Foundation for Cancer Research.
2024-02-26 | GSE243303 | GEO
Project description:ARID1A is one of the most frequently mutated genes in endometrial cancer, with approximately 40% of patients harboring an ARID1A mutation. However, relatively little is known about how ARID1A protein loss shapes endometrial cancer pathogenesis. Mounting evidence from other malignancies suggests that ARID1A protein can be regulated post-translationally, independent of genotype. However, most studies in endometrial cancer evaluate genotype alone, overlooking the potential for alternative mechanisms of ARID1A loss. To address this gap, ARID1A protein expression and genotype were examined in endometrioid tumors and associated transcriptional changes were characterized. Evaluation of ARID1A protein in 71 human endometrioid tumors demonstrates that protein loss can occur regardless of ARID1A genotype. Retention or deficiency of ARID1A protein was not significantly related to variant allele frequency or location of mutation in human tumors with mutant ARID1A. A human endometrial cancer cell model suggests that ARID1A protein loss can occur through proteasomal degradation. Furthermore, ARID1A protein expression was found to be a predictor of worse overall survival in a TCGA cohort of ARID1A wild-type endometrioid tumors. Spatial transcriptomics of 16 human endometrioid tumors revealed that both genotype and protein expression of ARID1A play a role in shaping unique transcriptional signatures in endometrial cancer and can be used to predict patient prognosis. Suggesting evaluation of ARID1A should not be done solely by sequencing techniques.
2026-04-22 | GSE327714 | GEO
Project description:To determine the expression profiles of microRNAs (miRNAs) and to examine specific miRNA expression in endometrial serous adenocarcinoma in comparison with normal endometrial tissue and endometrial endometrioid adenocarcinoma. Twenty-one serous adenocarcinoma tissues, 20 endometrioid adenocarcinoma tissues, and 7 normal endometrial tissues were enrolled. miRNA expression profiles were examined using miRNA microarray.
2018-11-01 | GSE25405 | GEO
Project description:Epigenome analysis of endometrial endometrioid adenocarcinoma tissues
| PRJNA563677 | ENA
Project description:Genome-wide DNA methylation screening was performed using the Infinium MethylationEPIC BeadChip in 49 fresh-frozen tissue samples and 31 formalin-fixed paraffin-embedded tissue samples obtained from surgically resected materials of patients with endometrioid endometrial cancer.
2022-11-09 | GSE178610 | GEO