Cancer growth depends to a large extent on a continuous supply of nutrients by new blood vessels that grow into the tumour. This process is called ”tumour angiogenesis”, and is regulated by an interaction between cancer cells and normal cells.
A strong focus in the scientific community has been on identifying and validating novel therapeutic targets that regulate tumour angiogenesis. A high number of therapeutic compounds have been developed that inhibit the growth of tumour blood vessels where the most prominent has been the monoclonal antibody bevacizumab that inhibit the vascular endothelial growth factor VEGF. Yet, clinical studies have shown that many tumor types, including glioblastomas, develop escape mechanisms towards anti-angiogenic therapy. Although several mechanisms have been proposed, the exact mechanism by which GBMs escape bevacizumab treatment remains enigmatic.
We have developed animal glioblastoma models where we study the mechanisms leading to angiogenesis independent growth. By the identification of such mechanisms, our aim is to develop novel combinatorial treatment strategies targeting the adaptive response to anti-angiogenic therapy.