UC San Diego

Vestibular schwannomas (VS) are known to carry mutations on the neurofibromatosis type 2 (NF2) tumor suppressor gene. However, the mechanism by which vestibular schwannomas occur is not well understood. The gene expression of several growth factors and receptors implicated in oncogenesis were evaluated in greater auricular nerve control tissue and vestibular schwannoma tissue taken from patients with sporadic VS and those with NF2-related VS using quantitative real-time polymerase chain reaction and normalized with standardization to a single constitutively expressed control gene, human cyclophylin. Result demonstrated significant upregulation of fibroblast growth factor receptor 1(FGFR-1), glial cell line derived growth factor receptor alpha 1(GFRA-1), insulin-like growth factor 1(IGF-1), vascular endothelial growth factor (VEGF), transforming growth factor beta 1(TGFB-1), nerve growth factor receptor(NGFR), and downregulation of platelet derived growth factor beta (PDGFR-B) in sporadic VS. Significant differences in fibroblast growth factor receptor 1(FGFR-1), glial cell line derived growth factor receptor alpha 1(GFRA-1), and vascular endothelia growth factor(VEGF) gene expression was found between sporadic and NF2-related VS. Also the proportion of VS samples that exhibited upregulation of gene expression of FGRA-1 and VEGF were significantly greater in sporadic VS than in NF2-related VS