Multifaceted Role of IRAK-M in the Promotion of Colon Carcinogenesis via Barrier Dysfunction and STAT3 Oncoprotein Stabilization in Tumors

Brendan J. Jenkins

doi:10.1016/j.ccell.2016.04.008

Multifaceted Role of IRAK-M in the Promotion of Colon Carcinogenesis via Barrier Dysfunction and STAT3 Oncoprotein Stabilization in Tumors

Brendan J. Jenkins

Hudson Institute - Department of Molecular and Translational Science

Research output: Contribution to journal › Short Survey › Other › peer-review

3 Citations (Scopus)

Abstract

Dysregulated interactions between the host immune system and gut microbiota can underpin inflammation, leading to colorectal cancer (CRC). In this issue of Cancer Cell, Kesselring et al. reveal a bimodal role of the TLR/IL-1R-signaling negative regulator, IRAK-M, in promoting tumoral microbial colonization and STAT3 oncoprotein stabilization during CRC.

Original language	English
Pages (from-to)	615-617
Number of pages	3
Journal	Cancer Cell
Volume	29
Issue number	5
DOIs	https://doi.org/10.1016/j.ccell.2016.04.008
Publication status	Published - 9 May 2016

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10.1016/j.ccell.2016.04.008

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title = "Multifaceted Role of IRAK-M in the Promotion of Colon Carcinogenesis via Barrier Dysfunction and STAT3 Oncoprotein Stabilization in Tumors",

abstract = "Dysregulated interactions between the host immune system and gut microbiota can underpin inflammation, leading to colorectal cancer (CRC). In this issue of Cancer Cell, Kesselring et al. reveal a bimodal role of the TLR/IL-1R-signaling negative regulator, IRAK-M, in promoting tumoral microbial colonization and STAT3 oncoprotein stabilization during CRC.",

author = "Jenkins, {Brendan J.}",

year = "2016",

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doi = "10.1016/j.ccell.2016.04.008",

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journal = "Cancer Cell",

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T1 - Multifaceted Role of IRAK-M in the Promotion of Colon Carcinogenesis via Barrier Dysfunction and STAT3 Oncoprotein Stabilization in Tumors

AU - Jenkins, Brendan J.

PY - 2016/5/9

Y1 - 2016/5/9

N2 - Dysregulated interactions between the host immune system and gut microbiota can underpin inflammation, leading to colorectal cancer (CRC). In this issue of Cancer Cell, Kesselring et al. reveal a bimodal role of the TLR/IL-1R-signaling negative regulator, IRAK-M, in promoting tumoral microbial colonization and STAT3 oncoprotein stabilization during CRC.

AB - Dysregulated interactions between the host immune system and gut microbiota can underpin inflammation, leading to colorectal cancer (CRC). In this issue of Cancer Cell, Kesselring et al. reveal a bimodal role of the TLR/IL-1R-signaling negative regulator, IRAK-M, in promoting tumoral microbial colonization and STAT3 oncoprotein stabilization during CRC.

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U2 - 10.1016/j.ccell.2016.04.008

DO - 10.1016/j.ccell.2016.04.008

M3 - Short Survey

C2 - 27165738

AN - SCOPUS:84975297356

VL - 29

SP - 615

EP - 617

JO - Cancer Cell

JF - Cancer Cell

SN - 1535-6108

IS - 5

ER -

Multifaceted Role of IRAK-M in the Promotion of Colon Carcinogenesis via Barrier Dysfunction and STAT3 Oncoprotein Stabilization in Tumors

Abstract

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