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

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

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10.1016/j.ccell.2016.04.008

Cite this

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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",

month = may,

day = "9",

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

language = "English",

volume = "29",

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journal = "Cancer Cell",

issn = "1535-6108",

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number = "5",

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TY - JOUR

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.

UR - https://www.scopus.com/pages/publications/84975297356

U2 - 10.1016/j.ccell.2016.04.008

DO - 10.1016/j.ccell.2016.04.008

M3 - Short Survey

C2 - 27165738

AN - SCOPUS:84975297356

SN - 1535-6108

VL - 29

SP - 615

EP - 617

JO - Cancer Cell

JF - Cancer Cell

IS - 5

ER -

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

Abstract

UN SDGs

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