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

Keywords

  • DAMPs
  • MDSCs
  • Pancreatic carcinogenesis
  • RAGE

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Oncology

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