Glioblastoma—a moving target

Abstract

The slow development of effective treatment of glioblastoma is contrasted by the rapidly advancing research on the molecular mechanisms underlying the disease. Amplification and overexpression of receptor tyrosine kinases, particularly EGFR and PDGFRA, are complemented by mutations in the PI3K, RB1, and p53 signaling pathways. In addition to finding effective means to target these pathways, we may take advantage of the recent understanding of the hierarchical structure of tumor cell populations, where the progressive expansion of the tumor relies on a minor subpopulation of glioma stem cells, or glioma-initiating cells. Finding ways to reprogram these cells and block their self-renewal is one of the most important topics for future research.

Key words::

• Brain tumors
• molecular biology
• oncogenes
• pathogenesis
• suppressor genes
• tumor biology

Acknowledgements

I am most grateful to my mentor, the late Jan Pontén, who led me into cancer research and guided me during my first years in science with generosity and never-ending enthusiasm. I would also like to thank all my PhD students and collaborators during the years, some of whom have been mentioned in the text. I am especially grateful to my friend and colleague, Carl-Henrik Heldin, with whom I have shared many moments of joy and despair. My own work has been supported by several funding organizations, e.g. the Swedish Research Council, the Children Cancer Foundation, National Institutes of Health, Ax:son Johnson Foundation, and Lundberg Foundation. Special thanks are conveyed to the Swedish Cancer Society, which has supported me throughout the years with generous grants, including an endowment for my position as a professor of tumor biology at Uppsala University from 1986 to 2012.

Declaration of interest: The author reports no conflicts of interest. The author alone is responsible for the content and writing of the paper.