Journal
JOURNAL OF NEUROIMMUNOLOGY
Volume 224, Issue 1-2, Pages 108-113Publisher
ELSEVIER
DOI: 10.1016/j.jneuroim.2010.05.002
Keywords
CXCL12; NF1; Glioma; cAMP; AMD3100
Categories
Funding
- NCI NIH HHS [R01 CA136573-02, R01 CA118389, R01 CA136573, P50 CA094056, U01CA84314, R01CA118389, P50 CA94056, U01 CA084314] Funding Source: Medline
- NINDS NIH HHS [P30 NS057105] Funding Source: Medline
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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. (C) 2010 Elsevier B.V. All rights reserved.
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