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. Cancer Res; 73(11); 3193–9. ©2013 AACR.
- Received October 25, 2012.
- Revision received January 28, 2013.
- Accepted February 20, 2013.
- ©2013 American Association for Cancer Research.
June 2013
Volume 73, Issue 11
Volume 73, Issue 11
The MET Oncogene in Glioblastoma Stem Cells: Implications as a Diagnostic Marker and a Therapeutic Target
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- Article
- Abstract
- Glioblastoma: A Model for the Quest of Tumor Genetic Determinants and Tumorigenic Cell Hierarchies
- The MET Oncogene: A Marker of a Glioblastoma Stem Cell Subset
- MET Sustains the Stem, Tumorigenic, and Invasive Phenotype in Glioblastoma
- MET Expression and Function in Cancer Stem Cells: A Paradigm of “Inherence”
- Implications of MET Expression in Cancer Stem Cells for Diagnosis and Personalized Therapy of Glioblastoma (and Other Tumors)
- MET Inhibitors, Radiotherapy, and Antiangiogenesis
- Conclusions
- Disclosure of Potential Conflicts of Interests
- Authors' Contributions
- Grant Support
- Acknowledgments
- References
- Figures & Data
- Info & Metrics
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