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

Philip J. Vernon; Herbert J. Zeh; Michael T. Lotze

doi:10.4161/onci.24184

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

Philip J. Vernon, Herbert J. Zeh, Michael T. Lotze

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

7 Scopus citations

Abstract

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.

Original language	English (US)
Article number	e24184
Journal	OncoImmunology
Volume	2
Issue number	5
DOIs	https://doi.org/10.4161/onci.24184
State	Published - May 2013
Externally published	Yes

Keywords

DAMPs
MDSCs
Pancreatic carcinogenesis
RAGE

ASJC Scopus subject areas

Immunology and Allergy
Immunology
Oncology

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10.4161/onci.24184

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

Abstract

Keywords

ASJC Scopus subject areas

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