Hypoxia induced migration in patient-derived glioma stem cell lines

OLIVIA MORRIS HANON; MARIANA BELÉN VERA; GUSTAVO E. SEVLEVER; MARÍA E. SCASSA; GUILLERMO A. VIDELA RICHARDSON

Congreso; Society for Neuro-Oncology Annual Meeting; 2019

The ability of tumor cells to invade surrounding tissues is one of their most damaging characteristics. The acquisition of an invasive phenotype defines the malignancy of a tumor. In fact, in most cases the death of cancer patients is due to the spread of cancer (1). High-grade gliomas are highly aggressive and invasive tumors. In their progression they produce great neurological damage and are among the most deadly tumors that exist. The effectiveness of treatments for glioblastoma multiforme (GBM) remains a challenge in the field of oncology. GBMs are characterized by exhibiting high expression of vascular endothelial growth factor (VEGF), which results in highly angiogenic tumors. Therefore, the prevention of the formation of new blood vessels in the GBM could theoretically limit tumor growth. At present, various anti-angiogenic molecules have been studied in numerous clinical trials (Bevacizumab, antibody against VEGF; Cediranib and Vatalanib, VEGF receptor inhibitors) (2); however, their therapeutic efficacy is not entirely encouraging. It has been postulated that this type of treatments cause hypoxia and thus trigger a response called "angiogenic/invasion shift" that allows tumor progression with a marked increase in cell invasiveness.