Epigenomic profile of diverse cancer
Ontology highlight
ABSTRACT:
PROVIDER: EGAS00001004352 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:Epigenetic dysregulation is a universal feature of cancer that results in altered patterns of gene expression that drive malignancy. Brain tumors exhibit subtype-specific epigenetic alterations, however the molecular mechanisms responsible for these diverse epigenetic states remain unclear. Here we show that the developmental transcription factor Sox9 differentially regulates epigenomic states in high-grade glioma (HGG) and ependymoma (EPN). These contrasting roles for Sox9 correspond with protein interactions with histone deacetylating complexes in HGG, and association with the Rela oncofusion in EPN. Together, our studies demonstrate how epigenomic states are differentially regulated in distinct subtypes of brain tumors, while revealing divergent roles for Sox9 in HGG and EPN tumorigenesis.
2022-07-13 | PXD033863 | Pride
Project description:Cancer-specific changes in DNA methylation can alter genetic stability, genomic structure, and gene expression. Promoter CpG island methylation can result in transcriptional silencing and plays an important role in the oncogenic process. We used genome-wide analysis to characterize the methylomes of breast cancers with diverse metastatic behavior. Here, we describe the identification of novel groups of breast tumors characterized by the presence or absence of coordinate hypermethylation at a large number of genes, demonstrating the existence of a breast-CpG island methylator phenotype (B-CIMP). B-CIMP imparts a distinct epigenomic profile and is a strong determinant of metastatic potential. Gene Expression Samples (GSM647057-GSM647077): Twenty-one breast cancer primary samples were analyzed. There are 10 CIMP positive and 11 CIMP negative samples. Methylation Profiling Samples (GSM651372-GSM651410): Thirty-nine breast cancer primary samples were analyzed. There are 17 CIMP positive and 22 CIMP negative samples.
2011-03-31 | E-GEOD-26349 | biostudies-arrayexpress
Project description:Epigenomic profile of bladder cancer cell line HT1376 treated with CPI-0209
| PRJNA736422 | ENA
Project description:Cancer-specific changes in DNA methylation can alter genetic stability, genomic structure, and gene expression. Promoter CpG island methylation can result in transcriptional silencing and plays an important role in the oncogenic process. We used genome-wide analysis to characterize the methylomes of breast cancers with diverse metastatic behavior. Here, we describe the identification of novel groups of breast tumors characterized by the presence or absence of coordinate hypermethylation at a large number of genes, demonstrating the existence of a breast-CpG island methylator phenotype (B-CIMP). B-CIMP imparts a distinct epigenomic profile and is a strong determinant of metastatic potential.
2011-03-31 | GSE26349 | GEO
Project description:Epigenetic mechanisms contribute to the initiation and development of cancer, and epigenetic variation promotes dynamic gene expression patterns that facilitate tumor evolution and adaptation. While the NCI-60 panel represents a diverse set of human cancer cell lines that has been used to screen chemical compounds, a comprehensive epigenomic atlas of these cells has been lacking. Here, we report an integrative analysis of 60 human cancer epigenomes, representing a catalog of activating and repressive histone modifications. We identify genome-wide maps of canonical sharp and broad H3K4me3 domains at promoter regions of tumor suppressors, H3K27ac-marked conventional enhancers and super enhancers, and widespread inter-cancer and intra-cancer specific variability in H3K9me3 and H4K20me3-marked heterochromatin domains. Furthermore, we identify features of chromatin states, including chromatin state switching along chromosomes, correlation of histone modification density with genetic mutations, DNA methylation, enrichment of DNA binding motifs in regulatory regions, and gene activity and inactivity. These findings underscore the importance of integrating epigenomic maps with gene expression and genetic variation data to understand the molecular basis of human cancer. Our findings provide a resource for mining epigenomic maps of human cancer cells and for identifying epigenetic therapeutic targets.
2021-01-21 | GSE143653 | GEO
Project description:Altering cancer transcriptomes using epigenomic inhibitors
| PRJNA269931 | ENA
Project description:Pathogenic gene dysregulation can be attributed to chromatin state change that pre-transcriptionally regulates expression. Recent breakthroughs elucidating the rules governing this DNA control layer, an epigenetic code, unlock a new modality in precision medicine to target gene dysregulation across myriad diseases. Leveraging these natural mechanisms, we developed a modular platform to design programmable mRNA therapeutics, Epigenomic Controllers (EC), that control gene expression through directed epigenetic change. ECs tune expression levels of one or multiple genes with durable effect of weeks-to-months in vivo following a single dose. We characterized ECs across multiple targets and designed an EC effectively inhibiting the cancer- and inflammatory-disorder-associated multi-gene cluster CXCL1-8. With precision targeting of NF-kB signaling and novel identification of homologous murine surrogates, ECs significantly reduced neutrophil migration in vivo during acute lung inflammation. A platform approach to EC design for epigenomic modulation opens new treatment frontiers for diverse gene targets, including those considered "undruggable."
2025-03-04 | GSE290866 | GEO
Project description:Histone variant H2A.Z has multiple roles in regulating gene transcription and its overexpression has been observed in various cancer types. However, the epigenomic characterization of H2A.Z in cancer is unclear. Combining the pool-and-split strategy with sequencing, we developed mChIP-seq, a multiplexed chromatin immunoprecipitation followed by sequencing method to efficiently profile multifactorial epigenetic landscapes of histone marks for multiple samples in parallel. mChIP-seq generates high-quality profiles comparable to standard ChIP-seq but with merits of high efficiency, low cost, and low-input requirement. Using mChIP-seq to profile H2A.Z and 10 H3 histone modifications for 24 cancer cell lines spanning 9 cancer types, we generated 528 epigenomic profiles from two workflows, comprehensively characterized genomic distribution of H2A.Z, and revealed its associations with main histone modifications and gene expression. Moreover, compared with normal cells by integration analysis of public data, we found a decoupling of H2A.Z and H3K4me3 at promoter sites in cancer cells, where the signal intensity of H2A.Z is not in line with the signal intensity of H3K4me3, which further dysregulates gene expression. Altogether, our results demonstrate that mChIP-seq is a powerful technology for epigenomic profiling and reveal abnormal regulatory features of H2A.Z in cancer.
2026-08-05 | GSE280574 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE36204: Epigenomic enhancer profiling defines a signature of colon cancer [ChIP-seq] GSE36400: All exon array expression data in normal colon and primary colon cancer lines [expression] Refer to individual Series
2012-04-15 | E-GEOD-36401 | biostudies-arrayexpress
Project description:The architecture of chromatin specifies eukaryotic cell identity by controlling transcription factor access to sites of gene regulation. Here we describe a dual transposase/peroxidase approach, integrative DNA And Protein Tagging (iDAPT), which detects both DNA (iDAPT-seq) and protein (iDAPT-MS) associated with accessible regions of chromatin. In addition to direct identification of bound transcription factors, iDAPT enables the inference of their gene regulatory networks, protein interactors, and regulation of chromatin accessibility. We applied iDAPT to profile the epigenomic consequences of granulocytic differentiation of acute promyelocytic leukemia, yielding previously undescribed mechanistic insights with potential therapeutic implications. Our findings demonstrate the power of iDAPT as a discovery platform for both the dynamic epigenomic landscapes and their transcription factor components associated with biological phenomena and disease.
2020-11-02 | PXD022252 | Pride