Abstract
The MET oncogene, a crucial regulator of the genetic program known as "invasive growth" or "epithelial-mesenchymal transition," has recently emerged as a functional marker of glioblastoma stem cells. Here, we review findings that associate MET expression and activity with a specific, genetically defined glioblastoma stem cell subtype, and data showing how MET sustains the stem cell phenotype in glioblastoma and other tumors. Finally, we discuss issues related to identification of tumorigenic clones driven by MET in the context of genetically heterogeneous tumors and strategies aimed at eradicating cancer stem cells.
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