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CXCL12 alone is insufficient for gliomagenesis in Nf1 mutant mice.

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.

journal_name

J Neuroimmunol

journal_title

Journal of neuroimmunology

authors

Sun T,Gianino SM,Jackson E,Piwnica-Worms D,Gutmann DH,Rubin JB

doi

10.1016/j.jneuroim.2010.05.002

subject

Has Abstract

pub_date

2010-07-27 00:00:00

pages

108-13

issue

1-2

eissn

0165-5728

issn

1872-8421

pii

S0165-5728(10)00186-4

journal_volume

224

pub_type

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