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Rage signalling promotes intestinal tumourigenesis

Development of colon cancer is a multistep process that is regulated by intrinsic and extrinsic cellular signals. Extrinsic factors include molecular patterns that are derived from either pathogens (PAMPs) or cellular damage (DAMPs). These molecules can promote tumourigenesis by activation of the in...

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Main Authors: Heijmans, Jarom (Author) , Biemond, I. (Author) , Hardwick, J. C. H. (Author) , Hommes, D. W. (Author) , Muncan, V. (Author) , van den Brink, G. R. (Author) , Büller, N. V. J. A. (Author) , Hoff, E. (Author) , Dihal, A. A. (Author) , van der Poll, T. (Author) , van Zoelen, M. A. D. (Author) , Bierhaus, Angelika (Author)
Format: Article (Journal)
Language:English
Published: 2013
In: Oncogene
Year: 2013, Volume: 32, Issue: 9, Pages: 1202-1206
ISSN:1476-5594
DOI:10.1038/onc.2012.119
Online Access:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1038/onc.2012.119
Verlag, lizenzpflichtig, Volltext: https://www.nature.com/articles/onc2012119
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Author Notes:J. Heijmans, N.V.J.A. Büller, E. Hoff, A.A. Dihal, T. van der Poll, M.A.D. van Zoelen, A. Bierhaus, I. Biemond, J.C.H. Hardwick, D.W. Hommes, V. Muncan, and G.R. van den Brink
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Summary:Development of colon cancer is a multistep process that is regulated by intrinsic and extrinsic cellular signals. Extrinsic factors include molecular patterns that are derived from either pathogens (PAMPs) or cellular damage (DAMPs). These molecules can promote tumourigenesis by activation of the innate immune system, but the individual contribution of ligands and their receptors remains elusive. The receptor for advanced glycation end products (Rage) is a pattern recognition receptor that binds multiple ligands derived from a damaged cell environment such as Hmgb1 and S100 protein. Here we show that Rage signalling has a critical role in sporadic development of intestinal adenomas, as ApcMin/+ Rage−/− mice are protected against tumourigenesis.
Item Description:Published online 2 April 2012
Gesehen am 08.10.2021
Physical Description:Online Resource
ISSN:1476-5594
DOI:10.1038/onc.2012.119

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