High fat diet contributed to the acceleration of the disease state in a mouse model of inflammation-based Barrett Esophagus and Esophageal Adenocarcinoma (EAC). We suggest that diet, along with bile acids and the microbiome create a dysbiosis, altering the immune microenvironment and stem cell niche through increased expression of pro-inflammatory cytokines, such as IL-8, accelerating proliferation and stem cell expansion into the esophagus. Continued exposure to these factors can lead to genetic alterations within stem cells and malignant transformations that result in EAC.
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High fat diet contributed to the acceleration of the disease state in a mouse model of inflammation-based Barrett Esophagus and Esophageal Adenocarcinoma (EAC). We suggest that diet, along with bile acids and the microbiome create a dysbiosis, altering the immune microenvironment and stem cell niche through increased expression of pro-inflammatory cytokines, such as IL-8, accelerating proliferation and stem cell expansion into the esophagus. Continued exposure to these factors can lead to geneti...
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