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.
Highlights
Glioblastoma is the most common intracranial malignancy and constitutes about 50% of all gliomas
Additional glioblastoma cell lines were later established by other centers, yielding the Duke (D-) [4], Lausanne (LN-) [5], and University of California, San Francisco (SF-) [6] series of cell lines, in addition to the Uppsala (U-) series
In 1976, during my visit to Stanley Cohen’s laboratory at Vanderbilt University, we showed that human glioma cell lines were endowed with epidermal growth factor (EGF) receptors in relatively high numbers (Westermark B, Carpenter G, and Cohen S, unpublished)
Summary
Glioblastoma is the most common intracranial malignancy and constitutes about 50% of all gliomas. Additional glioblastoma cell lines were later established by other centers, yielding the Duke (D-) [4], Lausanne (LN-) [5], and University of California, San Francisco (SF-) [6] series of cell lines, in addition to the Uppsala (U-) series. Together, these ‘classical’ cell lines have contributed to our understanding of glioblastoma cell biology and, importantly, fueled our enthusiasm in molecular and cellular neuro-oncology.
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