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Glioblastoma is the most common malignant brain tumor and has an extremely lethal course (Clark et al., 2010). Although genetic abnormalities in p53, Akt, phosphatase and tensin homolog deleted from chromosome 10 (PTEN), and epidermal growth factor receptor that are common to various cancers are also found in glioblastoma, the prime cause of glioblastoma’s malignant features and conclusive treatment targets have yet to be determined. Better understanding of non-major signal pathways involved in glioblastoma could thus provide breakthroughs in treatment strategies. Insulin-like growth factor binding protein-2 (IGFBP2) was originally reported to be a modulator of the action of insulin-like growth factors (IGFs), but IGF-independent effects of IGFBP2 on cellular proliferation, apoptosis, metabolism, and mobility have since been reported in pathological conditions, including cancers. Recent studies of gene expression microarray revealed that elevated expression of IGFBP2 occurs in gliomas, and is associated with increasing grades of malignancy with significant overexpression in glioblastomas (Fuller et al., 1999; Sallinen et al., 2000). Subsequent studies have suggested that IGFBP2 may be one of the proteins that play an important role in malignant phenotypes of glioblastoma cells (Fukushima & Kataoka, 2007). This chapter highlights key examples of recent biological and epidemiological research focusing on IGFBP2 in brain tumors and reviews more specialized studies on the fundamental role of IGFBP2 in glioma progression.

Insulin-Like Growth Factor Binding Protein-2: A Possible Regulator of Invasive Growth in Glioblastoma