Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1171107 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Colorectal cancer is a leading cause of cancer-related deaths. Mutations in the innate immune receptor AIM2 are frequently identified in patients with colorectal cancer, but how AIM2 modulates colonic tumorigenesis is unknown. Here, we found that Aim2-deficient mice were hypersusceptible to colonic tumor development. Production of inflammasome-associated cytokines and other inflammatory mediators were largely intact in Aim2-deficient mice, however, intestinal stem cells were prone to uncontrolled proliferation. Aberrant Wnt signaling expanded a population of tumor-initiating stem cells in the absence of AIM2. Susceptibility of Aim2-deficient mice to colorectal tumorigenesis was enhanced by a dysbiotic gut microbiota, which was reduced by reciprocal exchange of gut microbiota with wild-type healthy mice. These findings uncover a synergy between a specific host genetic factor and gut microbiota in determining the susceptibility to colorectal cancer. Therapeutic modulation of AIM2 expression and microbiota has the potential to prevent colorectal cancer. We used microarrays to compare the transcriptome Aim2 deficent mice to wild type mice in colon tumor and colitis samples. Here were 12 mice in total, 3 for each genotype and tissue combination.
2015-07-15 | E-GEOD-69436 | biostudies-arrayexpress
Project description:In this study our aim was to document recurrent DNA copy number aberration associated breakpoints in primary tumors of colorectal cancer patients that ultimately received systemic treatment in the context of metastatic disease. Such data can be used to catalogue copy number aberration associated breakpoints and thereby affected genes. To this end, high quality arrayCGH data set of clinically well annotated colorectal cancer specimens was generated using FFPE tumor samples from patients from two phase III clinical trials, namely CAIRO and CAIRO2. arrayCGH data of colorectal cancers of patients from 2 clinical trials. 108 patients were treated with capecitabine first line, 110 patients were treated with capecitabine and irinotecan first line and 134 patients were treated with capecitabine, oxaliplatin and bevacizumab.
2014-11-14 | E-GEOD-63216 | biostudies-arrayexpress
Project description:Colorectal cancer is a leading cause of cancer-related deaths. Mutations in the innate immune receptor AIM2 are frequently identified in patients with colorectal cancer, but how AIM2 modulates colonic tumorigenesis is unknown. Here, we found that Aim2-deficient mice were hypersusceptible to colonic tumor development. Production of inflammasome-associated cytokines and other inflammatory mediators were largely intact in Aim2-deficient mice, however, intestinal stem cells were prone to uncontrolled proliferation. Aberrant Wnt signaling expanded a population of tumor-initiating stem cells in the absence of AIM2. Susceptibility of Aim2-deficient mice to colorectal tumorigenesis was enhanced by a dysbiotic gut microbiota, which was reduced by reciprocal exchange of gut microbiota with wild-type healthy mice. These findings uncover a synergy between a specific host genetic factor and gut microbiota in determining the susceptibility to colorectal cancer. Therapeutic modulation of AIM2 expression and microbiota has the potential to prevent colorectal cancer.
2015-07-15 | GSE69436 | GEO
Project description:Gut microbiota and gallstone formation - cohousing study
2020-01-10 | E-MTAB-8550 | ExpressionAtlas
Project description:Identificaiton of novel single-nucleotide polymorphism (SNP) candidates associated with chemo-responsiveness in colorectal cancers using microarray Response rates of 104 colorectal cancer patients to established regiments (FL, CAPE, FLOX, FLIRI) were evaluated by histoculture drug response assay. Affymetrix SNP 5.0 chips were used to determine genotypes of the same colorectal cancer patients. SNPs associated with chemosensitivity to standard regimens were identified by genome-wide association study. FL: 5-FU + Leucovorin; CA: Capecitabine, FLOX: 5-FU + Leucovorin + Oxaliplatin, FLIRI: 5-FU + Leucovorin + Irinotecan
2010-06-01 | GSE16718 | GEO
Project description:Response to drug therapy in individual colorectal cancer (CRC) patients is associated with tumor biology. Here we describe the genomic landscape of tumor samples of a homogeneous well-annotated series of patients with metastatic CRC of two phase III clinical trials, CAIRO and CAIRO2. DNA copy number aberrations of 349 patients are determined. Within three treatment arms, 194 chromosomal sub-regions are associated with progression free survival PFS (uncorrected single-test p-values < 0.005). These sub-regions are filtered for effect on mRNA expression, using an independent data set from The Cancer Genome Atlas (TCGA) which returned 171 genes. Three chromosomal regions are associated with a significant difference in PFS between treatment arms with or without irinotecan. One of these regions, 6q16.1-q21, correlates in vitro with sensitivity to SN-38, the active metabolite of irinotecan. This genomic landscape of metastatic CRC reveals a number of DNA copy number aberrations associated with response to drug therapy. aCGH data of colorectal cancers of patients from 2 clinical trials (CAIRO, CAIRO2). 105 patients were treated with capecitabine first line (CAIRO arm A), 111 patients were treated with capecitabine and irinotecan first line (CAIRO arm B), and 133 patients were treated with capecitabine, oxaliplatin and bevacizumab (CAIRO2 arm A).
2014-11-14 | E-GEOD-36864 | biostudies-arrayexpress
Project description:Transcription profiling by array of paired tumour and normal samples from colorectal cancer patients
2025-01-22 | E-MEXP-3715 | ExpressionAtlas
Project description:Chronic inflammation and gut microbiota dysbiosis are risk factors for colorectal cancer. In clinical practice, inflammatory bowel disease (IBD) patients have a greatly increased risk of developing colitis associated colorectal cancer (CAC). However, the basis underlying the initiation of CAC remains to be explored. Systematic filtration through existing genome-wide association study (GWAS) and conditional deletion of Zfp90 in CAC mice model indicated that Zfp90 was a putative oncogene in CAC development. Strikingly, depletion of gut microbiota eliminated the tumorigenic effect of Zfp90 in CAC mice model. Moreover, fecal microbiota transplantation demonstrated Zfp90 promoted CAC depending on gut microbiota. Combining 16s rDNA sequencing in feces specimens from CAC mice model, we speculated that Prevotella copri-defined microbiota might mediate the oncogenic role of Zfp90 in the development of CAC. Mechanistic studies revealed Zfp90 accelerated CAC development through Tlr4-Pi3k-Akt-Nf-κb pathway. Our findings elucidated the crucial role of Zfp90-microbiota-Nf-κb axis in creating a tumor-promoting environment and suggested therapeutic targets for CAC prevention and treatment.
2022-08-14 | GSE156241 | GEO
Project description:Triclosan (TCS), an antimicrobial agent in thousands of consumer products, is a risk factor for colitis and colitis-associated colorectal cancer. While the intestinal toxicities of TCS require the presence of gut microbiota, the molecular mechanisms involved have not been defined. Here we show that intestinal commensal microbes mediate metabolic activation of TCS in the colon and drive its gut toxicology. Using a range of in vitro, ex vivo, and in vivo approaches, we identify specific microbial β-glucuronidase (GUS) enzymes involved and pinpoint molecular motifs required to metabolically activate TCS in the gut. Finally, we show that targeted inhibition of bacterial GUS enzymes abolishes the colitis-promoting effects of TCS, supporting the essential roles of specific microbial proteins in TCS toxicity. Our results define a mechanism by which intestinal microbes cause the gut toxicity of environmental chemicals and suggest a therapeutic approach to alleviate colitis and associated diseases.
2021-11-04 | PXD025887 | Pride