The myeloid response to pancreatic carcinogenesis is regulated by the receptor for advanced glycation end-products

We identified a critical role for receptor for advanced glycation end products (RAGE) in the intratumoral accumulation of myeloid-derived suppressor cells (MDSCs) during pancreatic carcinogenesis. The absence of RAGE markedly delayed neoplasia and limited MDSC accumulation in mice expressing an onco...

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Autores principales: Vernon, Philip J., Zeh III, Herbert J., Lotze, Michael T.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Landes Bioscience 2013
Materias:
Author's View
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3667906/
https://www.ncbi.nlm.nih.gov/pubmed/23762800
http://dx.doi.org/10.4161/onci.24184
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author Vernon, Philip J.
Zeh III, Herbert J.
Lotze, Michael T.
author_facet Vernon, Philip J.
Zeh III, Herbert J.
Lotze, Michael T.
author_sort Vernon, Philip J.
collection PubMed
description We identified a critical role for receptor for advanced glycation end products (RAGE) in the intratumoral accumulation of myeloid-derived suppressor cells (MDSCs) during pancreatic carcinogenesis. The absence of RAGE markedly delayed neoplasia and limited MDSC accumulation in mice expressing an oncogenic variant of Kras. In spite of MDSCs, these mice accumulated non-immunosuppressive macrophages. Thus, RAGE regulates carcinogenesis and consequent myeloid responses.
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spelling pubmed-36679062013-06-12 The myeloid response to pancreatic carcinogenesis is regulated by the receptor for advanced glycation end-products Vernon, Philip J. Zeh III, Herbert J. Lotze, Michael T. Oncoimmunology Author's View We identified a critical role for receptor for advanced glycation end products (RAGE) in the intratumoral accumulation of myeloid-derived suppressor cells (MDSCs) during pancreatic carcinogenesis. The absence of RAGE markedly delayed neoplasia and limited MDSC accumulation in mice expressing an oncogenic variant of Kras. In spite of MDSCs, these mice accumulated non-immunosuppressive macrophages. Thus, RAGE regulates carcinogenesis and consequent myeloid responses. Landes Bioscience 2013-05-01 2013-05-01 /pmc/articles/PMC3667906/ /pubmed/23762800 http://dx.doi.org/10.4161/onci.24184 Text en Copyright © 2013 Landes Bioscience http://creativecommons.org/licenses/by-nc/3.0/ This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.
spellingShingle Author's View
Vernon, Philip J.
Zeh III, Herbert J.
Lotze, Michael T.
The myeloid response to pancreatic carcinogenesis is regulated by the receptor for advanced glycation end-products
title The myeloid response to pancreatic carcinogenesis is regulated by the receptor for advanced glycation end-products
title_full The myeloid response to pancreatic carcinogenesis is regulated by the receptor for advanced glycation end-products
title_fullStr The myeloid response to pancreatic carcinogenesis is regulated by the receptor for advanced glycation end-products
title_full_unstemmed The myeloid response to pancreatic carcinogenesis is regulated by the receptor for advanced glycation end-products
title_short The myeloid response to pancreatic carcinogenesis is regulated by the receptor for advanced glycation end-products
title_sort myeloid response to pancreatic carcinogenesis is regulated by the receptor for advanced glycation end-products
topic Author's View
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3667906/
https://www.ncbi.nlm.nih.gov/pubmed/23762800
http://dx.doi.org/10.4161/onci.24184
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