Abstract
Glioblastoma multiforme (GBM) is the most common primary brain malignancy and is often resistant to conventional treatments due to its extensive cellular heterogeneity. Thus, the overall survival of GBM patients remains extremely poor. Insulin-like growth factor (IGF) signaling entails a complex system that is a key regulator of cell transformation, growth and cell-cycle progression. Hence, its deregulation is frequently involved in the development of several cancers, including brain malignancies. In GBM, differential expression of several IGF system components and alterations of this signaling axis are linked to significantly worse prognosis and reduced responsiveness to temozolomide, the most commonly used pharmacological agent for the treatment of the disease. In the present review we summarize the biological role of the IGF system in the pathogenesis of GBM and comprehensively discuss its clinical significance and contribution to the development of resistance to standard chemotherapy and experimental treatments.
Highlights
Malignant gliomas represent 30% of all intracranial tumors and include a heterogeneous group of neoplasms that arise from multiple cell types with neural stem cell-like properties [1]
receptor tyrosine kinases (RTK) are a family of cell surface receptors, comprising the epidermal growth factor receptor (EGFR), the fibroblast growth factor receptor (FGFR), the hepatocyte growth factor receptor (HGFR/c-MET), the platelet-derived growth factor receptor (PDGFR), the vascular endothelial growth factor receptor (VEGFR) and the insulin-like growth factor 1 receptor (IGF1R)
In the present review we summarize current research on the role of the Insulin-like growth factor (IGF) system in the pathogenesis of glioblastoma multiforme (GBM) and discuss the clinical significance and therapeutic implications of this pathway in the development of resistance to both currently approved and experimental treatments
Summary
Malignant gliomas represent 30% of all intracranial tumors and include a heterogeneous group of neoplasms that arise from multiple cell types with neural stem cell-like properties [1]. In the US, the annual incidence of gliomas is 3.2 cases for every 100,000 individuals and about half of them are classified as glioblastoma or glioblastoma multiforme (GBM) [2]. Several small molecules have been tested in the last few years [6, 7]. None of these strategies represent an effective cure for GBM, as this malignancy displays extensive intra-tumoral heterogeneity that favors disease recurrence [8, 9].
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