Cyclic AMP suppression is sufficient to induce gliomagenesis in a mouse model of neurofibromatosis-1.

ABSTRACT: Current models of oncogenesis incorporate the contributions of chronic inflammation and aging to the patterns of tumor formation. These oncogenic pathways, involving leukocytes and fibroblasts, are not readily applicable to brain tumors (glioma), and other mechanisms must account for microenvironmental influences on central nervous system tumorigenesis. Previous studies from our laboratories have used neurofibromatosis-1 (NF1) genetically engineered mouse (GEM) models to understand the spatial restriction of glioma formation to the optic pathway of young children. Based on our initial findings, we hypothesize that brain region-specific differences in cAMP levels account for the pattern of NF1 gliomagenesis. To provide evidence that low levels of cAMP promote glioma formation in NF1, we gen

SUBMITTER: Warrington NM 

PROVIDER: S-EPMC2905483 | biostudies-literature | 2010 Jul

REPOSITORIES: biostudies-literature