The epigenetic landscape of human colorectal cancer - 10x dataset
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ABSTRACT:
PROVIDER: PRJEB40272 | ENA |
REPOSITORIES: ENA
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Project description:We characterized the epigenetic landscape of human colorectal cancer (CRC). To this extent, we performed gene expression profiling using high throughput sequencing (RNA-seq) and genome wide binding/occupancy profiling (ChIP-seq) for histone modifications correlated to transcriptional activity, enhancers, elongation and repression (H3K4me3, H3K4me1, H3K27Ac, H3K36me3, H3K27me3) in patient-derived organoids (PDOs), and in normal and tumoral primary colon tissues. We also generated ChIP-seq data for transcription factors YAP/TAZ in human CRC PDOs.
2021-02-23 | E-MTAB-8416 | biostudies-arrayexpress
Project description:We characterized the epigenetic landscape of human colorectal cancer (CRC). To this extent, we performed gene expression profiling using high throughput sequencing (RNA-seq) and genome wide binding/occupancy profiling (ChIP-seq) for histone modifications correlated to transcriptional activity, enhancers, elongation and repression (H3K4me3, H3K4me1, H3K27Ac, H3K36me3, H3K27me3) in patient-derived organoids (PDOs), and in normal and tumoral primary colon tissues. We also generated ChIP-seq data for transcription factors YAP/TAZ in human CRC PDOs.
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Project description:Cancer cells utilize genetic and epigenetic aberrations for their excessive growth. Although we have sufficient understanding of the genomic alterations in colorectal cancer, we have incomplete knowledge of epigenomic aberrations and their impact on tumor growth. In order to comprehensively define the epigenetic patterns specific to colorectal cancer, we generated profiles for 6 histone modification marks, including H3K4me1 (enhancer), H3K27Ac (active enhancer), H3K9me3 (heterochromatin), H3K27me3 (polycomb repression), H3K79me2 (transcription) and H3K4me3 (promoter), using a high-throughput ChIP-Seq methodology developed in house applicable to frozen tumors. Chromatin state transitions specifically pointed to drastic changes in enhancer patterns, consistent with some prior studies. Furthermore, we identified the best combinatorial chromatin states that could most efficiently distinguish and predict CRC from normal colon. In a more detailed investigation into patterns of active enhancers using normal colon, adenomas and colorectal cancers, we identified specific changes in enhancers from normal tissue to these neoplastic lesions. Importantly, we noted gains of enhancers in a large number of genomic loci in colon cancer compared to adjacent normal tissues. In summary, we have identified aberrant enhancer gains as a major feature of colorectal cancer and propose this to be utilized as a therapeutic approach.
2021-05-22 | GSE136888 | GEO
Project description:Enhancer aberrations are beginning to emerge as a key feature of colorectal cancers, however, we have limited understanding of epigenomic patterns that distinguish tumors and underlying heterogeneity between tumors. Here, using epigenomic profiling of colorectal tumors, adenomas and normal colon tissues, we identify unique pattern of regulatory elements in colorectal cancer, which could reliably distinguish tumors from normal colon specimens. We define shared and unique enhancer elements during colorectal cancer progression using normal adjacent colon, adenomas and adenocarcinomas. We validate the functional nature of tumor-specific enhancers for important oncogenes such as ASCL2 and Fzd10. NMF clustering identified 4 epigenetic (EPIC) subtypes in colorectal cancer, which mimics consensus molecular subtypes (CMS)1, with an advantage of introducing a novel epigenetically-identifiable subtype with poor prognosis and survival. Based on this correlation, we defined and validated a combination therapeutic strategy of enhancer-blocking BETi with pathway specific inhibitor for 3 CMS subtypes. In conclusion, by comprehensive characterization of chromatin state patterns in colorectal tumors, we define epigenomic patterns during tumor evolution, heterogeneity of enhancers among patients and a combination therapy strategy for CMS-subgroups.
2021-05-22 | GSE136629 | GEO
Project description:Enhancer aberrations are beginning to emerge as a key feature of colorectal cancers, however, we have limited understanding of epigenomic patterns that distinguish tumors and underlying heterogeneity between tumors. Here, using epigenomic profiling of colorectal tumors, adenomas and normal colon tissues, we identify unique pattern of regulatory elements in colorectal cancer, which could reliably distinguish tumors from normal colon specimens. We define shared and unique enhancer elements during colorectal cancer progression using normal adjacent colon, adenomas and adenocarcinomas. We validate the functional nature of tumor-specific enhancers for important oncogenes such as ASCL2 and Fzd10. NMF clustering identified 4 epigenetic (EPIC) subtypes in colorectal cancer, which mimics consensus molecular subtypes (CMS)1, with an advantage of introducing a novel epigenetically-identifiable subtype with poor prognosis and survival. Based on this correlation, we defined and validated a combination therapeutic strategy of enhancer-blocking BETi with pathway specific inhibitor for 3 CMS subtypes. In conclusion, by comprehensive characterization of chromatin state patterns in colorectal tumors, we define epigenomic patterns during tumor evolution, heterogeneity of enhancers among patients and a combination therapy strategy for CMS-subgroups.
2021-05-22 | GSE136630 | GEO