Transmissible inflammation-induced colorectal cancer in inflammasome-deficient mice

Bo Hu; Gil Friedman; Eran Elinav; Richard A. Flavell

doi:https://doi.org/10.4161/2162402X.2014.981995

Transmissible inflammation-induced colorectal cancer in inflammasome-deficient mice

Bo Hu, Gil Friedman, Eran Elinav, Richard A. Flavell

Weizmann Institute of Science

Research output: Contribution to journal › Article › peer-review

Abstract

The microbiota is pivotal in orchestrating the pathogenesis of IBD-associated colorectal cancer (CRC). We recently demonstrated that altered elements in the microbiota of inflammasome-deficient mice drive transmissible inflammation-induced CRC. This microbiota-mediated effect is dependent upon microbiome-induced CCL5-driven inflammation, which, in turn, promotes epithelial cell proliferation through local activation of the IL-6 pathway, leading to cancer development.

Original language	English
Article number	981995
Number of pages	3
Journal	OncoImmunology
Volume	8
Issue number	10
Early online date	7 May 2018
DOIs	https://doi.org/10.4161/2162402X.2014.981995
State	Published - 3 Oct 2019

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title = "Transmissible inflammation-induced colorectal cancer in inflammasome-deficient mice",

abstract = "The microbiota is pivotal in orchestrating the pathogenesis of IBD-associated colorectal cancer (CRC). We recently demonstrated that altered elements in the microbiota of inflammasome-deficient mice drive transmissible inflammation-induced CRC. This microbiota-mediated effect is dependent upon microbiome-induced CCL5-driven inflammation, which, in turn, promotes epithelial cell proliferation through local activation of the IL-6 pathway, leading to cancer development.",

author = "Bo Hu and Gil Friedman and Eran Elinav and Flavell, {Richard A.}",

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Y1 - 2019/10/3

N2 - The microbiota is pivotal in orchestrating the pathogenesis of IBD-associated colorectal cancer (CRC). We recently demonstrated that altered elements in the microbiota of inflammasome-deficient mice drive transmissible inflammation-induced CRC. This microbiota-mediated effect is dependent upon microbiome-induced CCL5-driven inflammation, which, in turn, promotes epithelial cell proliferation through local activation of the IL-6 pathway, leading to cancer development.

AB - The microbiota is pivotal in orchestrating the pathogenesis of IBD-associated colorectal cancer (CRC). We recently demonstrated that altered elements in the microbiota of inflammasome-deficient mice drive transmissible inflammation-induced CRC. This microbiota-mediated effect is dependent upon microbiome-induced CCL5-driven inflammation, which, in turn, promotes epithelial cell proliferation through local activation of the IL-6 pathway, leading to cancer development.

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JF - OncoImmunology

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Transmissible inflammation-induced colorectal cancer in inflammasome-deficient mice

Abstract

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