Optic Nerve Glioma in Mice Requires Astrocyte Nf1 Gene Inactivation and Nf1 Brain Heterozygosity

M. Livia Bajenaru, M. Rosario Hernandez, Arie Perry, Yuan Zhu, Luis F. Parada, Joel R. Garbow, David H. Gutmann

Research output: Contribution to journalArticle

201 Scopus citations

Abstract

Whereas biallelic neurofibromatosis 1 (NF1) inactivation is observed in NF1-associated gliomas, astrocyte-restricted Nf1 conditional knockout mice do not develop gliomas. These observations suggest that NF1 glioma formation requires additional cellular or genetic conditions. To determine the effect of an Nf1 heterozygous brain environment on NF1 glioma formation, we generated Nf1+1- mice lacking Nf1 expression in astrocytes. In contrast to astrocyte-restricted Nf1 conditional knockout mice, Nf1+/- mice lacking Nf1 in astrocytes develop optic nerve gliomas. This mouse model demonstrates that Nf1+/- cells contribute to the pathogenesis of gliomas in NF1 and provides a tool for the preclinical evaluation of potential therapeutic interventions for these tumors.

Original languageEnglish
Pages (from-to)8573-8577
Number of pages5
JournalCancer research
Volume63
Issue number24
StatePublished - Dec 15 2003

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    Bajenaru, M. L., Hernandez, M. R., Perry, A., Zhu, Y., Parada, L. F., Garbow, J. R., & Gutmann, D. H. (2003). Optic Nerve Glioma in Mice Requires Astrocyte Nf1 Gene Inactivation and Nf1 Brain Heterozygosity. Cancer research, 63(24), 8573-8577.