Abstract
When experimental tumours are inoculated into a host animal, the tumour growth depends, among other things, on its vascular supply. This vascular supply has been shown to be initiated by substances released by the tumour tissue, and vascular sprouting towards implanted tumour substances has been extensively demonstrated in nonvascular tissue. Most tissues, however, already contain a vascular supply sufficient for their own needs. In such conditions, the host vascular system is probably incorporated into the tumour without much vascular sprouting. It is well known that, as a tumour grows larger, the center tends to become ischaemic and necrotic. It is not clear why the tumour vascularity does not respond to this development with reactive vascular proliferation, but increased interstitial tissue pressure and impaired fluid transport may be implicated.
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