ScienceVEGF

Versatility to address changing tumour biology

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The current understanding of tumour biology, based primarily on preclinical observations, suggests that antitumour strategies must be made versatile over time in order to remain effective.¹⁸ In particular, while multiple angiogenic factors may be activated over the course of a tumour life cycle, continuously expressed VEGF is the only one known to be critical throughout.²⁰ Therefore, the strategy of maintaining direct inhibition of VEGF – supplemented by selective targeting of secondary pathways as they emerge – continues to be explored in both the laboratory and the clinic.^21,22

 

As observed in preclinical models, the ability to maintain precise VEGF inhibition as part of an overall antitumour strategy may be a function of the specificity of direct VEGF inhibitors. This specificity may facilitate combination with approaches that target other mechanisms of tumour proliferation.^2,6

 

Indeed, the anti-angiogenic effects of precise VEGF inhibition have been observed in a wide range of preclinical settings. In addition to antitumour activity demonstrated in single-agent experiments, precise VEGF inhibition has been shown to be active in combination with a range of modalities that target other mechanisms of tumour proliferation.¹⁹ This ability to apply precise and continuous VEGF inhibition, either alone or with other modalities, may add versatility to an overall antitumour approach.¹⁸ Further preclinical investigation is ongoing to further evaluate the versatility of precise VEGF inhibition.