American Gastroenterological Association

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PD-1 Signaling Promotes Tumor-Infiltrating Myeloid-Derived Suppressor Cells and Gastric Tumorigenesis in Mice

Immune checkpoint inhibitors have limited efficacy in many tumors. We investigated mechanisms of tumor resistance to inhibitors of programmed cell death 1 (PDCD1, also called PD1) in mice with gastric cancer, and the role of its ligand, PDL1.

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Regeneration Defects in Yap and Taz Mutant Mouse Livers are Caused by Bile Duct Disruption and Cholestasis

The Hippo pathway and its downstream effectors YAP and TAZ (YAP/TAZ) are heralded as important regulators of organ growth and regeneration. However, different studies provided contradictory conclusions about their role during regeneration of different organs ranging from promoting proliferation to inhibiting it. Here, we resolve the function of YAP/TAZ during regeneration of the liver, where Hippo’s role in growth control has been studied most intensely.

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Destroying visceral sensory nerves impacts pancreatic islet function, glucose metabolism and diabetes onset, but how islet endocrine cells interact with sensory neurons has not been studied.

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Epithelial TLR4 signaling activates DUOX2 to induce microbiota-driven tumorigenesis

Chronic colonic inflammation leads to dysplasia and cancer in patients with inflammatory bowel disease (IBD). We have described the critical role of innate immune signaling via toll-like receptor 4 (TLR4) in the pathogenesis of dysplasia and cancer. In the current study, we interrogate the intersection of TLR4 signaling, epithelial redox activity, and the microbiota in colitis-associated neoplasia.

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Central reading of ulcerative colitis clinical trial videos using neural networks

Machine reading of endoscopic videos in an ulcerative colitis clinical trial shows promise in replacing central readers with excellent machine-to-human interobserver agreement for UCEIS and endoscopic Mayo score

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Prevalence and Effect of Genetic Risk of Thrombo-embolic Disease in Inflammatory Bowel Disease.

The largest cause of mortality in patients with inflammatory bowel disease (IBD) remains thrombo-embolic disease (TED). Recent reports have demonstrated that both monogenic and polygenic factors contribute to TED and 10% of ‘healthy’ subjects are genetically at high risk for TED. Our aim was to utilize whole exome sequencing (WES) and genome-wide genotyping to determine the proportion of IBD patients genetically at risk for TED and investigate the effect of genetic risk of TED in IBD.

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