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Anti-angiogenic therapy for uveal melanoma—more haste, less speed
  1. A W Stitt,
  2. T A Gardiner
  1. Department of Ophthalmology, Queen's University of Belfast
  1. Correspondence to: Alan W Stitt, McCauley Chair of Experimental Ophthalmology, Department of Ophthalmology, Queen's University of Belfast, Royal Victoria Hospital, Belfast BT12 6BA, Northern Ireland, UK; a.stitt{at}

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Vascularisation is critical for the support of substantial tumour growth. For a wide range of tumours, a complex microvasculature accompanies the transition from hyperplasia to neoplasia, a progression from low to high grade classification and enhanced metastatic capacity. The pioneering work of Folkman and Warren and Shubik outlined the critical importance of “tumour angiogenesis” to an initially sceptical field as far back as the late 1960s.1,2 Folkman's struggle to have this hypothesis supported has been recently portrayed in a fine biography by Robert Cooke.3 Thirty years on, it is now accepted that most tumours require a complex microvasculature in order to grow beyond approximately 1–2 mm in diameter. The belief that their essential, and potentially labile, vascular supply represents a chink in the tumour armour has precipitated an ever growing raft of research. Indeed, tumour angiogenesis is a key concept that supports investigations in a range of clinically relevant research areas such as the diagnosis and prognosis of cancers, discovery and molecular characterisation of new angiogenic factors, the identification and therapeutic potential of endogenous anti-angiogenic agents, and characterisation of tumour specific vascular markers.

Pathogenic angiogenesis is a well known phenomenon to ophthalmologists and vision scientists since it is the underlying basis of many important ocular diseases such as retinopathy of prematurity, proliferative diabetic retinopathy, and the wet form of age related macular degeneration. Not surprisingly, …

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