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New data, published in Science, show that adrenergic nerves can activate an angiometabolic switch in prostate cancer. Activation of this switch promotes tumour growth via altered endothelial
cell metabolism; thus, crosstalk between nerves and endothelial cells, affecting metabolism, could be a target for anticancer therapy.
In wild-type mice, orthotopically implanted prostate cancer xenografts grew exponentially after day 18; however in mice deficient in Adrb2 and Adrb3, no substantial tumour growth was
observed after this time point. These knockout mice did initially develop tumours, and no difference in tumour size, vascular permeability, or hypoxic area was seen in wild-type and knockout
mice before day 18. Further analysis revealed that tumours from knockout mice had a lower density of tumour vessels than their wild-type counterparts, caused by considerable alterations in
vascular patterns (such as reduced length and branching) in the prostate. Orthotopically transplanting cell-free collagen I (an angiogenic superpolymer) matrix into the prostate capsule
resulted in reduced vessel migration, density, and branching in chemically sympathectomized mice.
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