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 journalArticle

5 Citations (Scopus)

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 languageEnglish (US)
Article numbere24184
JournalOncoImmunology
Volume2
Issue number5
DOIs
StatePublished - May 1 2013
Externally publishedYes

Fingerprint

Carcinogenesis
Macrophages
Advanced Glycosylation End Product-Specific Receptor
Myeloid-Derived Suppressor Cells
Neoplasms

Keywords

  • DAMPs
  • MDSCs
  • Pancreatic carcinogenesis
  • RAGE

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Oncology

Cite this

The myeloid response to pancreatic carcinogenesis is regulated by the receptor for advanced glycation end-products. / Vernon, Philip J.; Zeh, Herbert J.; Lotze, Michael T.

In: OncoImmunology, Vol. 2, No. 5, e24184, 01.05.2013.

Research output: Contribution to journalArticle

@article{0c04cd196709481a952533e1b7ab4168,
title = "The myeloid response to pancreatic carcinogenesis is regulated by the receptor for advanced glycation end-products",
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.",
keywords = "DAMPs, MDSCs, Pancreatic carcinogenesis, RAGE",
author = "Vernon, {Philip J.} and Zeh, {Herbert J.} and Lotze, {Michael T.}",
year = "2013",
month = "5",
day = "1",
doi = "10.4161/onci.24184",
language = "English (US)",
volume = "2",
journal = "OncoImmunology",
issn = "2162-4011",
publisher = "Landes Bioscience",
number = "5",

}

TY - JOUR

T1 - The myeloid response to pancreatic carcinogenesis is regulated by the receptor for advanced glycation end-products

AU - Vernon, Philip J.

AU - Zeh, Herbert J.

AU - Lotze, Michael T.

PY - 2013/5/1

Y1 - 2013/5/1

N2 - 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.

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.

KW - DAMPs

KW - MDSCs

KW - Pancreatic carcinogenesis

KW - RAGE

UR - http://www.scopus.com/inward/record.url?scp=84886945422&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84886945422&partnerID=8YFLogxK

U2 - 10.4161/onci.24184

DO - 10.4161/onci.24184

M3 - Article

C2 - 23762800

AN - SCOPUS:84886945422

VL - 2

JO - OncoImmunology

JF - OncoImmunology

SN - 2162-4011

IS - 5

M1 - e24184

ER -