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There is an ongoing debate on the therapeutic potential of vaso-modulatoryinterventions against glioma invasion. Prominent vasculature-targetingtherapies involve functional tumour-associated blood vessel deterioration andnormalisation. The former aims at tumour infarction and nutrient deprivationmedi- ated by vascular targeting agents that induce occlusion/collapse oftumour blood vessels. In contrast, the therapeutic intention of normalising theabnormal structure and function of tumour vascular net- works, e.g. viaalleviating stress-induced vaso-occlusion, is to improve chemo-, immuno- andradiation therapy efficacy. Although both strategies have shown therapeuticpotential, it remains unclear why they often fail to control glioma invasioninto the surrounding healthy brain tissue. To shed light on this issue, wepropose a mathematical model of glioma invasion focusing on the interplaybetween the mi- gration/proliferation dichotomy (Go-or-Grow) of glioma cellsand modulations of the functional tumour vasculature. Vaso-modulatoryinterventions are modelled by varying the degree of vaso-occlusion. Wediscovered the existence of a critical cell proliferation/diffusion ratio thatseparates glioma invasion re- sponses to vaso-modulatory interventions into twodistinct regimes. While for tumours, belonging to one regime, vascularmodulations reduce the tumour front speed and increase the infiltration width,for those in the other regime the invasion speed increases and infiltrationwidth decreases. We show how these in silico findings can be used to guideindividualised approaches of vaso-modulatory treatment strategies and therebyimprove success rates.

Why one-size-fits-all vaso-modulatory interventions fail to control glioma invasion: in silico insights