Ontology highlight
ABSTRACT:
PROVIDER: PRJNA976509 | ENA |
REPOSITORIES: ENA
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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:Pancreatic cancer is the 3rd most prevalent cause of cancer related deaths in United states alone, with over 55000 patients being diagnosed in 2019 alone and nearly as many succumbing to it. Late detection, lack of effective therapy and poor understanding of pancreatic cancer systemically contributes to its poor survival statistics. Obesity and high caloric intake linked co-morbidities like type 2 diabetes (T2D) have been attributed as being risk factors for a number of cancers including pancreatic cancer. Studies on gut microbiome has shown that lifestyle factors as well as diet has a huge effect on the microbial flora of the gut. Further, modulation of gut microbiome has been seen to contribute to effects of intensive insulin therapy in mice on high fat diet. In another study, abnormal gut microbiota was reported to contribute to development of diabetes in Db/Db mice. Recent studies indicate that microbiome and microbial dysbiosis plays a role in not only the onset of disease but also in its outcome. In colorectal cancer, Fusobacterium has been reported to promote therapy resistance. Certain intra-tumoral bacteria have also been shown to elicit chemo-resistance by metabolizing anti-cancerous agents. In pancreatic cancer, studies on altered gut microbiome have been relatively recent. Microbial dysbiosis has been observed to be associated with pancreatic tumor progression. Modulation of microbiome has been shown to affect response to anti-PD1 therapy in this disease as well. However, most of the studies in pancreatic cancer and microbiome have remained focused om immune modulation. In the current study, we observed that in a T2D mouse model, the microbiome changed significantly as the hyperglycemia developed in these animals. Our results further showed that, tumors implanted in the T2D mice responded poorly to Gemcitabine/Paclitaxel (Gem/Pac) standard of care compared to those in the control group. A metabolomic reconstruction of the WGS of the gut microbiota further revealed that an enrichment of bacterial population involved in drug metabolism in the T2D group.
2020-11-30 | E-MTAB-8739 | biostudies-arrayexpress
Project description:<p>Background: The gut microbiota is a key hallmark of tumor and plays a central role in colorectal cancer (CRC). However, the contribution of gut fungi, an important community of gut microbes, remains substantially understudied in CRC.</p><p>Objective: To characterize the gut fungal landscape in CRC and elucidate its associations with bacterial communities, metabolites, and trace elements.</p><p>Methods: We conducted metagenomic sequencing on fecal samples from three cohorts: healthy controls (n = 401), colorectal polyp patients (n = 162), and CRC patients (n = 253). The fungal genomic data from NCBI database (PRJNA833221) was served as the reference for annotating gut fungi. Metabolites and trace elements were quantified via liquid chromatography and inductively Coupled Plasma Mass Spectrometry (ICP-MS), respectively. Fungal diversity and compositional differences were analyzed across groups. A random forest model was trained to discriminate healthy controls from intestinal disease groups (polyps and CRC) based on microbial biomarkers, with an ablation study optimizing co-marker selection. Structural equation modeling (SEM) was employed to dissect interactions among fungi, bacteria, metabolites, and trace elements.</p><p>Results: CRC patients exhibited increased fungal diversity at the genus level. Seven fungal genera displayed differential abundance across three groups: Rhizopus was specifically enriched in CRC, whereas Sporisorium, Cladosporium, Aureobasidium, Zygoascus, and Meyerozyma were enriched in polyps. Ablation study identified an optimal 31-microbial-marker panel (28 bacterial and 3 fungal species) that effectively distinguished intestinal disease groups (AUC = 0.89). SEM analysis identified three fungal markers—Penicillium citrinum, Penicillium sp. PG10607D, and Rhizopus stolonifera—that influence bacterial-metabolite-trace element networks through distinct correlations.</p><p>Conclusion: This study plots the first gut fungal atlas for CRC and reveals complex cross-kingdom interactions involving fungi, bacteria, metabolites, and trace elements, providing new insights into CRC research.</p>
2025-07-26 | MTBLS12776 | MetaboLights
Project description:We report the association between CpG islander methylator phenotype (CIMP) and the gut microbiome in human colorectal cancer tumor and adjacent normal tissue.
2024-06-12 | GSE237522 | GEO
Project description:We report the association between CpG islander methylator phenotype (CIMP) and the gut microbiome in human colorectal cancer tumor and adjacent normal tissue.
2024-06-12 | GSE237523 | GEO
Project description:Gut microbial dysbiosis can play a causal role of in colorectal cancer. Gut microbiota chnages with age and becomes moer pro-inflammatory. We sought to determine whether microbiota from Old donors promotes more tumor formation in recipients than meterial from young donors.
2023-11-30 | GSE237335 | GEO
Project description:Gut microbial dysbiosis can play a causal role of in colorectal cancer. Gut microbiota chnages with age and becomes moer pro-inflammatory. We sought to determine whether microbiota from Old donors promotes more tumor formation in recipients than meterial from young donors.
2023-11-30 | GSE237336 | GEO