Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA355242 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Tumor-host interactions play an important role in cancer initiation and progression. To investigate changes in local host factors associated with proximity to the tumor, the global gene expression profiles of cancer tissues and histologically normal tissues taken at various distances from the tumor (1 cm, 5 cm and the proximal end of the resected sample) from 32 rectal cancer patients were used to establish a distance-related model. Two distance-related expression patterns were considered, one with a trend toward gradual down-regulation and one with a trend toward gradual up-regulation as the distance from the tumor decreased. Gene Ontology (GO) analysis highlighted 7 genes enriched in the endosomal sorting complex required for transport (ESCRT) machinery in the group with a pattern of gradual down-regulation. Survival analysis of patients in the TCGA colorectal cancer (CRC) dataset revealed that higher expression of two of these genes (PDCD6IP and CHMP2B) was associated with a better prognosis (p = 0.021, p = 0.031). A tissue array confirmed that patients with up-regulated PDCD6IP expression in cancer tissue compared with normal tissue had better prognoses (p = 0.04). In conclusion, we built a distance-related model to study the local tumor-host interactions and identified PDCD6IP as a local host protective factor in CRC.
2017-11-01 | GSE90627 | GEO
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: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:We sequenced cell-free RNA (cfRNA) for five cancer types (colorectal cancer, stomach cancer, liver cancer, lung cancer and esophageal cancer) and healthy individuals in 230 plasma samples collected from 6 clinical centers in China. Cancer related signaling pathway and microbial genus were identified. Cancer detection and specific classification were achieved through combining both host and microbial cfRNA reads.
2022-07-12 | GSE174302 | GEO
Project description:Background: Colorectal adenoma is the primary precursor in colorectal cancer development, partially driven by epigenetic alteration occurring at a very early stage. While aberrant DNA-methylations have been observed in mucosa adjacent to primary tumors, this study aimed to investigate whether such alterations exist in distant background mucosa as global defect rather than local transition, and identify adenoma-related CpG sites which may serve as potential targets for early intervention. Methods: DNA methylation in normal rectal mucosal biopsies from 24 individuals with colorectal adenoma and 20 normal controls were profiled utilizing the Illumina Infinium MethylationEPIC v2.0 BeadChip (935K). Linear regression model was employed to investigate the relationship between adenoma incidence and DNA methylation at each CpG site, adjusted for demographic characteristics. GO and KEGG enrichment analysis were conducted using genes containing CpG sites significantly associated with adenoma. A sensitivity analysis was conducted with individuals who had one or more known risk factors for colorectal adenoma. Results: Twenty-seven CpG sites with aberrant DNA-methylation were significantly correlated with the incidence of adenoma (P<1×10-5, |Δβ|≧0.2). Through GO and KEGG enrichment analysis and lookups in EWAS atlas, a group of CpG sites and genes were identified as potential intervention targets. Conclusions: A group of adenoma-related CpG sites and genes with aberrant DNA-methylation was identified in normal-appearing rectal mucosa. Further extensive validation of the adenoma-related loci as targets for molecular intervention could pave the way for colorectal cancer prevention.
2025-12-31 | GSE284238 | GEO
Project description:Rectal cancer (RC) accounts for one-third of colorectal cancer (CRC), and 40% of these are locally advanced rectal cancer (LARC) at diagnosis. The use of neoadjuvant chemoradiotherapy (nCRT) significantly reduces the rate of local recurrence compared to adjuvant therapy or surgery alone. However, after nCRT, up to 40-60% of patients show a poor pathological response, while only about 20% achieve a pathological complete response. In this scenario, the identification of novel predictors of tumor response to nCRT are urgently needed to reduce LARC mortality, and to spare poorly responding patients from unnecessary treatments. Therefore, by combining gene and microRNA expression datasets with proteomic data from LARC patients, we developed an integrated network centered on seven hub-genes putatively involved in the response to nCRT. In an independent validation cohort of LARC patients, we confirmed the differential expression of NFKB1, TRAF6 and STAT3 depending on a response to nCRT. In addition, the functional enrichment analysis also revealed that these genes are strongly related to hallmarks of cancer and inflammation, whose dysfunction may causatively affect LARC patient’s response to nCRT. Furthermore, by constructing the transcription factor-module network, we hypothesized a protective role of POU2F3 gene, which could be used as a new drug target in LARC patients. Finally, we identified and in vitro tested entinostat, a histone deacetylase (HDAC) inhibitor, as a chemical compound that could be combined with classical therapeutic regimen in order to design more efficient therapeutic strategies in LARC.
2023-01-05 | PXD035408 | Pride
Project description:The objective of the experiment was to compare serum fatty acid metabolite abundance between individuals with varying clinical stages of colorectal cancer (stage I-IV) and age-and-gender matched disease-free controls. Fatty acid metabolite abundance was compared between locoregional (stage I-III) and liver metastatic (stage IV) cancer, as well as between all stages of colorectal cancer (stage I-IV) and disease-free controls. Reprogrammed energy metabolism is now listed as one of the central hallmarks of cancer cells. Aberrant fatty acid metabolism contributes to tumourigenesis through provision of substrates for membrane synthesis, signalling molecules, and synthesis of complex lipids. In this thesis, the role of fatty acid metabolism is explored in the context of colorectal cancer. Metabolomics techniques were employed to characterize fatty acid metabolites in serum, and lipogenic gene expression was quantified in tumour and normal tissues to investigate host response to cancer. Fatty acid metabolite abundance was increased in the serum of individuals with colorectal cancer, and a growth factor signalling axis and lipogenic transcription factor upstream of the endogenous fatty acid synthesis pathway were increased in colorectal liver metastases. It was concluded that liver metastases have an effect on growth factor production in the hepatic microenvironment, leading to increased signalling through a pathway that activates the lipogenic transcription factor that regulates fatty acid synthesis.
2016-12-15 | MTBLS27 | MetaboLights
Project description:To identify the potential biomarkers related to the development of colorectal cancer.we established an inflammation-induced colorectal cancer disease model in mice.
2022-12-31 | GSE200076 | GEO
Project description:The objective of this study is to identify a gene set to predict recurrence of colorectal cancer (CRC) patients. We generated RNA-seq data of 110 primary CRC samples and identified significant genes associated with recurrence of CRC. Through diverse statistical methods including generalized linear model likelihood ratio test, significant 10 genes were identified. In the validation cohorts, a risk classifier consisting of the 10 genes was an independent risk factor in colorectal cancers.
2019-10-29 | GSE107422 | GEO
Project description:We have identified TEAD4 as a key prognosis factor in colorectal cancer. To elucidate the potentail mechanism and function of TEAD4 in colorectal caner, we generated two stable cell lines expressing different shRNA targeting TEAD4 in the mesenchymal-like LoVo cells and the differential genes were detected by microarray. LoVo colorectal cancer cells stably expressing pLKO.1 control shRNA or sh1_shTEAD4 or sh2_shTEAD4
2014-01-01 | E-GEOD-53063 | biostudies-arrayexpress