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Epigenome analysis of precursor lesions of endometrial endometrioid carcinoma.

ABSTRACT: Epigenome analysis of precursor lesions of endometrial endometrioid carcinoma.

PROVIDER: PRJNA1017682 | ENA |

REPOSITORIES: ENA

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Epigenome analysis of precursor lesions of endometrial endometrioid carcinoma

Project description:Epigenome analysis of precursor lesions of endometrial endometrioid carcinoma

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Epigenome analysis of precursor lesions of endometrial endometrioid carcinoma.

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

Epigenome analysis of endometrial endometrioid adenocarcinoma tissues

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Project description:We performed genome-wide DNA methylation profiling on 126 samples from 59 cases with atypical endometrial hyperplasia, atypical polypoid adenomyoma, and endometrial carcinoma, all of whom had received oral MPA treatment at the Cancer Institute Hospital of Japanese Foundation for Cancer Research.

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Epigenome analysis of endometrial endometrioid adenocarcinoma tissues

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.

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A Proteogenomic View of Synchronous Endometrioid Endometrial and Ovarian Cancer

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

lactylome and proteome of endometrioid endometrial cancer

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

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Charachterizing the Discordance Between ARID1A Protein and Genotype in Endometrioid Type Endometrial Tumors

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.

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