Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA288277 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Identification of DNA methylation-independent epigenetic events underlying clear cell renal cell carcinoma
| PRJNA304737 | ENA
Project description:Aberrant DNA methylation is common in cancer. To associate DNA methylation with gene function, we performed RNAseq upon tumor tissue and matched normal tissues of two ccRCC (clear cell renal cell carcinoma) patients. To quantify 5mC and 5hmC level in each CG site at genome-wide level, we performed BS-seq and TAB-seq upon tumor tissue and matched normal tissues of two ccRCC (clear cell renal cell carcinoma) patients, respectively. mRNA profiles of tumor and matched normal tissues from two ccRCC patients were generated by deep sequencing, using Hiseq 2000. Single-nucleotide-resolution, whole-genome, 5mC and 5hmC profiles of tumor and matched normal tissues from two ccRCC (clear cell renal cell carcinoma) patients were generated by deep sequencing, using Hiseq 2000.
2016-02-29 | E-GEOD-63183 | biostudies-arrayexpress
Project description:Alterations in chromatin accessibility independent of DNA methylation can affect cancer-related gene expression, but are often overlooked in conventional epigenomic profiling approaches. In this study, we describe a cost-effective and computationally simple assay called AcceSssIble to simultaneously interrogate DNA methylation and chromatin accessibility alterations in primary human clear cell renal cell carcinomas (ccRCC). Our study revealed significant perturbations to the ccRCC epigenome, and identified gene expression changes that were specifically attributed to the chromatin accessibility status whether or not DNA methylation was involved. Compared to commonly mutated genes in ccRCC, such as the von Hippel-Lindau (VHL) tumor suppressor, the genes identified by AcceSssIble comprised distinct pathways and more frequently underwent epigenetic changes, suggesting that genetic and epigenetic alterations could be independent events in ccRCC. Specifically, we found unique DNA methylation-independent promoter accessibility alterations in pathways mimicking VHL deficiency. Overall, this study provides a novel approach for identifying new epigenetic-based therapeutic targets, previously undetectable by DNA methylation studies alone, that may complement current genetic-based treatment strategies. Examination of 3 different histone modifications in 2 patient tumor and adjacent normal samples.
2016-03-15 | E-GEOD-75597 | biostudies-arrayexpress
Project description:Multi-Omics analysis to gain novel insights into clear cell renal carcinoma aetiology and progression. The DNA methylation data of 121 clear clear renal carcinoma (ccRCC) were integrated with WGS and transcriptomic data using Multi-Omics Factor Analysis (MOFA) to detect the inter-patient variations related to aetiological and disease progression related factors.
2024-06-07 | GSE269180 | GEO
Project description:Aberrant DNA methylation is common in cancer. To associate DNA methylation with gene function, we performed RNAseq upon tumor tissue and matched normal tissues of two ccRCC (clear cell renal cell carcinoma) patients. To quantify 5mC and 5hmC level in each CG site at genome-wide level, we performed BS-seq and TAB-seq upon tumor tissue and matched normal tissues of two ccRCC (clear cell renal cell carcinoma) patients, respectively.
2016-02-29 | GSE63183 | GEO
Project description:Background The kidney's tubular system, composed of nephrons and collecting ducts, relies on cellular planar polarity and tight junctions to maintain structure and function. Disruptions in this polarity contribute to diseases like cystic kidney disease and cancer. Tight junctions, such as those formed by Claudin proteins, are critical for cellular polarity and tissue organization. Therefore, epigenetically inactivated Claudins can actively contribute to tumorigenesis.
Results In this study, we identified the epigenetic silencing of Claudin 10B (CLDN10B) through DNA hypermethylation in renal cancers, including clear cell renal carcinoma (ccRCC) and post-transplantation malignancies (PT-RCC). Hypermethylation selectively affected CLDN10B, while the related isoform, CLDN10A, was hypomethylated in clear cell and papillary RCC. Differential methylation of the Isoforms can serve as a discriminator of RCC from other malignancies. The epigenetic alteration of CLDN10B significantly correlated with reduced patient survival and advanced tumor staging. CLDN10B overexpression and CLDN10B induction via an inducible cell line significantly inhibited migration, cell cycle progression, and cellular growth. We further investigated CLDN10B using CRISPR-based epigenetic editing to reactivate CLDN10B to its endogenous level. Targeting the CLDN10B promoter with VP160 and TET1 in a dCas9-system effectively demethylated, significantly restored its expression and demonstrated its tumor-suppressive effects in 2D and 3D cell models.
Conclusion Our findings suggest that CLDN10B acts as a tumor suppressor, and its epigenetic regulation may represent a therapeutic target. Ultimately, understanding CLDN10Bs regulation and function could provide new insights into renal cancer treatment.
2024-10-01 | MSV000095998 | MassIVE
Project description:Methylation microarray data of human clear cell renal cell carcinoma
| PRJNA352797 | ENA
Project description:Alterations in chromatin accessibility independent of DNA methylation can affect cancer-related gene expression, but are often overlooked in conventional epigenomic profiling approaches. In this study, we describe a cost-effective and computationally simple assay called AcceSssIble to simultaneously interrogate DNA methylation and chromatin accessibility alterations in primary human clear cell renal cell carcinomas (ccRCC). Our study revealed significant perturbations to the ccRCC epigenome, and identified gene expression changes that were specifically attributed to the chromatin accessibility status whether or not DNA methylation was involved. Compared to commonly mutated genes in ccRCC, such as the von Hippel-Lindau (VHL) tumor suppressor, the genes identified by AcceSssIble comprised distinct pathways and more frequently underwent epigenetic changes, suggesting that genetic and epigenetic alterations could be independent events in ccRCC. Specifically, we found unique DNA methylation-independent promoter accessibility alterations in pathways mimicking VHL deficiency. Overall, this study provides a novel approach for identifying new epigenetic-based therapeutic targets, previously undetectable by DNA methylation studies alone, that may complement current genetic-based treatment strategies.
2016-03-15 | GSE75597 | GEO
Project description:We performed a transcriptomic analysis in a cohort of 6 Collecting Duct Carcinoma, 5 Clear Cell Renal Cell Carcinoma and 4 non-matched normal renal tissues to unravel the underlying biological and molecular determinants and to identifiy specific genes and pathways of this rare tumor type.
2021-07-13 | GSE153965 | GEO
Project description:We applied Illumina’s 317K high-density SNP-arrays to profile chromosomal aberrations in clear cell renal cell carcinoma (ccRCC) from 80 patients and analyzed the association of LOH/amplification events with clinicopathological characteristics
2009-05-09 | GSE16019 | GEO