Toll-like receptor-4 promotes the development of colitis-associated colorectal tumors.

By M. Fukata, Anli Chen, Arunan S. Vamadevan, J. Cohen, Keith J. Breglio, S. Krishnareddy, David S. Hsu, Ruliang Xu, N. Harpaz, A. Dannenberg and 4 more. Gastroenterology, 2007

639 citations recorded by the source corpus.

Subfields: Genetics, Immunology, Pharmacology

View Paper: https://www.semanticscholar.org/paper/773249e8ee2be05b2285f96752013049c5aa21da

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In Genetics

1. Y. Belkaid
2. T. Hand
3. J. Tschopp
4. Robert F. Schwabe
5. M. Abreu
6. R. Sartor
7. J. Turner

In Immunology

1. E. Latz
2. Katherine A. Fitzgerald
3. J. Tschopp
4. Robert F. Schwabe
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In Pharmacology

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Citations in the corpus

• Colitis induced in mice with dextran sulfate sodium (DSS) is mediated by the NLRP3 inflammasome (2010, background): “This ‘two-hit’ model of caspase-1 activation leading to the secretion of IL-1β and IL-18 in human IBD appears to be closely mirrored in the DSS colitis model in mice. Initially, DSS exerts a direct toxic effect on the epithelial barrier, hence allowing bacteria to stimulate lamina propria macrophage”
• Toll-like receptor signalling in the intestinal epithelium: how bacterial recognition shapes intestinal function (2010, background): “Blocking amphiregulin prevented LPS-mediated EGFR phosphorylation in IECs, suggesting that TLR4 signalling can activate a programme of proliferation through the induction of growth factor”
• 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).”
• Mechanisms and consequences of intestinal dysbiosis (2017, background): “In contrast to MyD88, TLR4 signaling showed consistent tumor-promoting effects in several cancer models [215].”
• 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).”
• The Gut Microbiota and Inflammation: An Overview (2020, background): “One inflammation-related mechanistic link between microbiota and cancer is the NF-κB pathway, as demonstrated by a study of mice deficient of TLR-4 (a receptor of LPS and an upstream regulator of NF-κB), whereby tumour development was reduced compared to wild type mice [149].”