Reduced microglial CX3CR1 expression delays neurofibromatosis‐1 glioma formation. Issue 2 (19th February 2013)

• Record Type: Journal Article
• Authors: Pong, Winnie W.; Higer, Samantha B.; Gianino, Scott M.; Emnett, Ryan J.; Gutmann, David H.
• Is Part Of: Annals of neurology. Volume 73:Issue 2(2013:Feb.)
• Page Start: 303
• Page End: 308
• Publication Date: 2013-02-19
• Subjects: Neurology -- Periodicals; Pediatric neurology -- Periodicals; Nervous system -- Surgery -- Periodicals; 616.8
• DOI: 10.1002/ana.23813
• Languages: English
• ISSNs: 0364-5134

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <p>Although traditional models of carcinogenesis have largely focused on neoplastic cells, converging data have revealed the importance of non‐neoplastic stromal cells in influencing tumor growth and progression. Leveraging a genetically engineered mouse model of neurofibromatosis type 1 (NF1)‐associated optic glioma, we now demonstrate that stromal microglia express the CX3CR1 chemokine receptor, such that reduced CX3CR1 expression decreases optic nerve microglia. Moreover, genetic reduction of <italic>Cx3cr1</italic> expression in <italic>Nf1</italic> optic glioma mice delays optic glioma formation. Coupled with previous findings demonstrating that microglia maintain optic glioma growth, these new findings provide a strong preclinical rationale for the development of future stroma‐directed glioma therapies in children. ANN NEUROL 2013;73:303–308</p> </abstract>