Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

High-fat diet-mediated dysbiosis cooperates with oncogenic K-Ras activation to promote intestinal carcinogenesis independently of obesity.


ABSTRACT: Several aspects of a Western lifestyle such as increased obesity and decreased physical activity are associated with increased risk for gastrointestinal cancers1. Although high-fat diet (HFD) induced low-grade inflammation has been closely linked to tumorigenesis2, however, the microbial shift that occurs due to diet and consequent alterations in host immunity have merely been considered to play a critical role during carcinogenesis. Here we show that HFD promotes tumor progression in the small intestine of genetically susceptible mice, however, independently of obesity and diet-induced chronic inflammation. HFD consumption cooperates with mutant K-Ras to mediate a shift in the composition of microbiota, which is associated with a decrease in Paneth cell antimicrobial host defense that com

ORGANISM(S): Mus musculus

SUBMITTER: Olivia Prazeres da Costa 

PROVIDER: E-GEOD-42840 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress