Human gut metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1091934 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28483904_1.fastq.gz | Fastqsanger.gz | |||
| SRR28483904_2.fastq.gz | Fastqsanger.gz | |||
| SRR28483905_1.fastq.gz | Fastqsanger.gz | |||
| SRR28483905_2.fastq.gz | Fastqsanger.gz | |||
| SRR28483906_1.fastq.gz | Fastqsanger.gz |
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Project description:Colorectal laterally spreading tumors (LSTs) are rare comparing to adenomas but are becoming more prevalent. Unlike many neoplasms in colons, LST grows to extremely large size, usually greater than 10mm in diameter while rarely invades deeply. Also, there is a low tendency for LSTs to become cancerous. The epigenetic landscape of LST has not been defined. In this study, we used a genome-wide methylation profiling technology, i.e. the Illumina Human Methylation 450K array, to query the main epigenetic difference between LST and para-cancerous samples. Our results suggest that LST displays significant decrease in DNA methylation, especially in some intergenic regions (IGR). By integration of public data for adenomas and colorectal cancers, we defined the commonality and specific epigenetic signatures for these three types of neoplasms in colon, in particular LST and adenomas which represent precancerous conditions. These three diseases shared little specific DNA methylation abnormalities. However, our pathway-level analysis revealed that certain pathways were common targets of epimutation. More interestingly, different diseases seem to employ distinct epigenetic insult to disturb these pathways. Between LST and adenoma, we found eight pathways were commonly targeted but the epi-mutation patterns were opposite between the two diseases. Comparison between precancerous conditions and invasive states revealed the key pathways governing the progression to malignancy, including CAMs and PI3K-Akt pathways.
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Project description:To investigate the role of RAD21 in the transcriptional regulation of global gene expression at early stage of colorectal cancer developments, we peformed the genome-wide analysis to map genomic regions bound by Rad21 in normal small testinal crypts and tumors (adenomas) harvested from Apc Min/+ mice using ChIP-seq. ChIP-seq naalysis identified high confidence RAD21 binding sites unique to normal crypts or adenomas, as well as those common to both tissues. We further performed RNA-seq to profile the changes in gene expression from normal WT crypts to adenomas at the very early stage of adenomagenesis in the context of Rad21 heterozygous loss. mRNA profiles of normal small intestinal crypts (WT) and adenomas from Apc Min/+ and Apc Min/+:Rad21+/- double mutant mouse; Mapping of Rad21 genomic binding sites in normal intestinal crypts (WT) and Apc Min/+ adenomas
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Project description:Colorectal adenomas are precursor lesions of colorectal cancers and represent clonal amplifications of single cells from colonic crypts. DNA methylation patterns specify cell-type identity during cellular differentiation and therefore provide novel opportunities for the molecular analysis of tumors. We have now analyzed DNA methylation patterns in colorectal adenomas and identified three biologically defined subclasses that describe different intestinal crypt differentiation stages. Importantly, colorectal carcinomas could be classified into the same methylation subtypes, reflecting their shared cell-types of origin with adenomas. Further data analysis also revealed significantly reduced overall survival for one of the subtypes. Our results establish a novel concept for understanding the methylation patterns observed in colorectal cancer and provide opportunities for tumor subclassification and patient stratification.
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Project description:Genetic and Epigenetic Landscapes of Laterally Spreading Tumors of the Colorectum
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Project description:To examine the role of Rb1 in gastrointestinal (GI) tumors we generated mice with an Apc1638N allele, Rbtm2brn floxed alleles, and a villlin-cre transgene (RBVCA). These mice had reduced median survival due to an increase in tumor incidence and multiplicity in the cecum and the proximal colon; they differed from murine intestinal tumors of the Apc1638N type which normally arise solely in the small intestine. We have examined by micro-array analysis three cecal tumors from these mice (probable adenomas), and compared them to three duodenal tumors (probable adenocarcinomas). Expression profiles of duodenal and cecal tumors relative to each other show unique gene subsets up and down regulated. The two tumor types were subsequently shown to differentially regulate distinct sets of genes over expressed in a majority of human colorectal carcinomas. Experiment Overall Design: We have compared 3 cecal tumors with 3 duodenal tumors from Rb1 deficient Apc1638N mice.
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