E-PROT-138
Ontology highlight
ABSTRACT:
PROVIDER: E-PROT-138 | ExpressionAtlas | 2024-06-05
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-PROT-138-MappedToGeneID.txt | Txt | |||
| E-PROT-138-analysis-methods.tsv | Tabular | |||
| E-PROT-138-configuration.xml | Xml | |||
| E-PROT-138-factors.xml | Xml | |||
| E-PROT-138-pipeline.pdf |
Items per page: 5 1 - 5 of 11 |
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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.
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Project description:We showed that some microRNAs could be characteristic of the progression from adenoma to adenocarcinoma in colorectal cancer. 48 colorectal biopsy samples (28 adenomas, 15 adenocarcinomas and 5 normal mucosae) were analyzed. We generated three comparisons: adenomas versus. normal mucosae, adenocarcinomas versus. normal mucosae, and adenocarcinomas versus. adenomas.
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Project description:Colorectal tumorigenesis proceedes through well defined clinical stages assoicated with charateristic mutations. Besides genetic alterations, epi-driver genes that are aberrantly expressed in cancers in a fashion that confers a seletive growth advantage can also contribute to tumor evolution. To gain a global view of methylation patterns in normal and maliganant colorectal epithelia, we performed genome-wide DNA methylation analysis on DNAs from 48 fresh frozen CRC samples at different stages of CRC progression. We used IlluminaHumanMethylation450 Beadchip to get a broad view of genome-wide DNA methylationdata during CRC progression and identified significantly differentially methylated genes during CRC progression A total of 48 macro-dissected tissues including normal colon tissue, adenomas, carcinomas and metastases were collected by the Department of Pathology at the University of Virginia under the supervision of an experienced pathologist. DNA was extracted and run on IlluminaHumanMethylation450 Beadchip by Expression Analyisis.
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Project description:Background & aim: Flat adenomas form a specific phenotype of colorectal adenomas that has been associated with more severe molecular changes and consequently a more aggressive clinical behavior compared to their polypoid counterparts. In the present study we set out to compare one of the molecular changes most explicitly associated with adenoma to carcinoma progression, i.e. chromosomal instability, between flat and polypoid colorectal adenomas. Methods: Consecutive series of 83 flat and 35 polypoid adenomas were analyzed for DNA copy number changes using a high resolution arrayCGH platform as well as for mutations in the adenomatous polyposis coli (APC) gene. Gene ontology on the genes located on the significantly different regions was performed. Results: Overall, flat adenomas show similar DNA copy number changes as polypoid adenomas. Patterns of DNA copy number changes differed between the two phenotypes with significantly more frequently loss of 5q14.3 and 5q15-q23.3 in flat adenomas, while loss of 1p36.32-p35.3, 10q25.2-q25.3, 17p12 and chromosome 18 were more frequent in polypoid adenomas. The 5q15-q23.3 region harbors the APC locus, therefore mutation status of APC was investigated, showing significantly less mutations in flat adenomas. Pathway analysis and datamining linked the 5q region to inflammation. Conclusion: These results provide evidence that flat and polypoid adenomas have partly overlapping DNA copy number changes, while alterations more specific to flat adenomas have associations with inflammation. Loss of 5q has been associated with aggressive behavior and this could serve as an explanation for a more aggressive clinical behavior of flat lesions. FFPE colorectal tissue samples of 35 polypoid adenomas and 83 flat adenomas. Test samples were compared to an external pool of normal male/female reference DNA.
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Project description:Colorectal adenomas are benign precursor lesions of colorectal cancer (CRC) that arise from normal epithelium1. The prevalence of adenomas in the large intestine is much higher than the incidence of cancer implying that the majority of adenomas will never progress to CRC4. In clinical practice, adenomas detected during colonoscopy are completely removed, and consequently the natural history of disease disrupted. Based on the prevalence of focal cancer in endoscopically removed adenomas, it is estimated that only 5% of adenomas will eventually progress to CRC. The aim of the present study was to characterize adenomas at low and high risk of progressing to cancer by extensive molecular profiling at DNA, RNA, and protein level, allowing to examine the biological processes in which they differ and to discover putative drivers of early colorectal tumor development.
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