CXCL12 alone is insufficient for gliomagenesis in Nf1 mutant mice

Tao Sun, Scott M. Gianino, Erin Jackson, David Piwnica-Worms, David H. Gutmann, Joshua B. Rubin

Research output: Contribution to journalArticle

9 Scopus citations

Abstract

Tumorigenesis requires interactions between tumor progenitors and their microenvironment. We found that low cAMP levels were sufficient for tumorigenesis in a mouse model of Neurofibromatosis-1 (NF1)-associated optic pathway glioma (OPG). We hypothesized that the distinct pattern of glioma in NF1 reflected spatiotemporal differences in CXCL12 effects on cAMP levels. Thus, we sought to alter the pattern of gliomagenesis through manipulation of CXCL12-CXCR4 pathway activation in Nf1 OPG mice. Forced CXCL12 expression induced glioma at a low frequency. Further, treatment of Nf1 OPG mice with AMD3100, a CXCR4 antagonist, did not attenuate glioma growth. Thus, it appears, CXCL12 alone cannot promote gliomagenesis in NF1 mice.

Original languageEnglish
Pages (from-to)108-113
Number of pages6
JournalJournal of Neuroimmunology
Volume224
Issue number1-2
DOIs
StatePublished - Jul 1 2010

Keywords

  • AMD3100
  • CAMP
  • CXCL12
  • Glioma
  • NF1

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