Glioblastoma Models in Drosophila Melanogaster

Abstract

Abstract Gliomas comprise the most common and most malignant intrinsic human brain tumours, with a very poor prognosis. Despite some recent therapeutic progress, there is still a large demand for novel drug targets to cope with the high recurrence rate. In the present article, we introduce the Drosophila model as a new tool in deciphering the mechanisms underlying the generation and progression of glial tumours. Despite the fact that Drosophila has only few glial cells and no vascular system with patrolling lymphocytes, the basic principles underlying glioblastoma biology appear very well conserved. The role of epidermal growth factor (EGF) receptor pathways, PVR (PDGF‐ and VEGF‐receptor related) and phophatidylinositol 3‐kinase (PI3K) signalling in Drosophila glioma models is discussed. Key Concepts: Gliomas are the most common and most malignant intrinsic human brain tumours, with a very poor prognosis. In majority of the glioblastoma, the molecular cause of malignancy is due to an amplification of receptor tyrosine kinase genes. The role of EGF‐receptor pathways, PVR and PI3K signalling in Drosophila glioma models is introduced in the text. Glial cell proliferation and glial cell migration is controlled by evolutionary conserved mechanisms. The insect Drosophila melanogaster has a very simple structured nervous and glial cells perform similar tasks as their vertebrate counterparts. The model organism Drosophila provides a rich source to decipher the mechanisms underlying the biology of human glioma and can be used to define novel drug targets.