Regulation of Spontaneous Intestinal Tumorigenesis Through the Adaptor Protein MyD88

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Promotion of Hepatocellular Carcinoma by the Intestinal Microbiota and TLR4 (2012, background): “These findings are similar to intestinal tumorigenesis in which TLR4 and MyD88 drive carcinogenesis (Fukata et al., 2007; Lee et al., 2010; Rakoff-Nahoum and Medzhitov, 2007).”
Paneth cells directly sense gut commensals and maintain homeostasis at the intestinal host-microbial interface (2008, background): “1 A), consistent with previous findings of MyD88-dependent RegIII expression in the small intestine (11, 12).”
Mechanisms and consequences of intestinal dysbiosis (2017, background): “In a mouse model of spontaneous intestinal tumorigenesis, signaling through MyD88 was necessary for extensive tumor growth [209].”
Role of the Microbiota in Immunity and inflammation (2014, result): “…immune receptors in the GI tract and disease in mouse models of colorectal cancer; however, the results have been disparate, perhaps due to the confounding factor of themicrobiota (Elinav et al., 2013; Fukata et al., 2007; Lowe et al., 2010; Rakoff-Nahoum and Medzhitov, 2007; Salcedo et al., 2010).”
Toll-like receptor signalling in the intestinal epithelium: how bacterial recognition shapes intestinal function (2010, background): “It was found that the overall incidence of intestinal tumours was similar in Apc Min/+ mice and MYD88-deficient × Apc Min/+ mice, but the tumours were significantly smaller in the absence of MYD88, with few macroscopically visible tumour”