In the United States alone, there are more than 1.8 million people diagnosed with cancer every year. This number increases exponentially as the scope is expanded to look at the number of people affected worldwide (National Cancer Institute, 2020). Given that a large number of genetic mutations have been identified, and there is a wide variety of cancers and cancer promoting networks. The current treatments have been extensively researched and explored, but there is ultimately no cure for this aggressive and unrelenting disease. One extremely invasive type of cancer is Glioblastoma Multiforme (GBM), which is a specific type of brain cancer. The exact growth patterns of these tumors are unknown, but it is known that GBM is formed from excess glial stem cells, which are produced by neuroblasts (neural stem cells). One understudied area is if glioma tumors arise from neuroblasts already present in the brain, or in response to tumor promoting signals new neuroblasts are created to induce and promote GBM tumor metastasis. These aggressive tumors grow rapidly and aggressively, which makes their origins and pathways of growth extremely difficult to locate and track. Drosophila melanogaster, or the common fruit fly, is the model organism for this study. The power of Drosophila lies in the multiple genetic tools available for experimental design, and the conservation of genes and cell-biological processes between flies and humans, which means that findings from Drosophila studies can be easily verified in mammalian models and human patients. We have developed a GBM model in flies using the GAL4-UAS system, where two genotypically different flies will be crossed to induce these tumors in developing Drosophila larval brains. This study will explore the origins of GBM tumors and the nature of cell-biological and growth promoting pathways that promote uncontrolled growth of glial cells and neuroblasts within the brain.
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Salamone, Sadie, "Investigating the Role of Neural Stem Cells in Aggressive Gliomas" (2023). Honors Theses. 422.