作者: Renee D. Read
DOI: 10.1002/GLIA.21148
关键词:
摘要: Glioblastomas (GBM), the most common primary brain tumors, infiltrate brain, grow rapidly, and are refractory to current therapies. Signature genetic lesions in glioblastomas include mutation of epidermal growth factor receptor tyrosine kinase (EGFR) activating mutations components PI-3 (PI3K) pathway. Despite years study, how these pathways specifically regulate glial pathogenesis is unclear. To address cellular origins this disease, a novel Drosophila GBM model has been developed which progenitor cells give rise proliferative invasive neoplastic that create transplantable tumors response constitutive co-activation EGFR-Ras PI3K pathways. Standing with rich literature demonstrating direct relevance studies on human cancer, neurological neurodevelopment, represents robust cell-type specific disease malignant created by thought be driving forces homologous disease. Using lineage analysis markers, were found originate from committed cells, rather than multipotent neuroblasts. Genetic analyses demonstrated induce fly neoplasia through activation combinatorial network composed, part, other also commonly mutated glioblastomas. In future, large-scale forward screens may reveal new insights into treatments glioblastoma. © 2011 Wiley-Liss, Inc.