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These data indicate that clinical use of VEGFR inhibitors, when delivered in combination with myelosuppressive agents, could result in lifethreatening complications.Suppression of angiogenesis through VEGFR inhibition might block tumour angiogenesis and growth, but, conversely, it could cause lifethreatening bonemarrow toxicity.Haematopoietic progenitor cells that were stably transfectedwith thymidine kinase gene were shown to localize to the tumour vasculature and impair the growth of xenotransplanted tumours. Recent developments in obtaining human and mouse endothelial cells from embryonic stem cells have opened up new avenues to study the role of these cells in therapeutic angiogenesis.Human and mouse embryonic stem cells can be induced to differentiate into pr imitive endothelial cells, which express the cellsurface markers CD, VEGFR, VEGFR and platelet endothelialcell adhesion molecule. PECAM is expressed on both endothelial cells and a subset of myelomonocy tic cells.Immunostainingwith antibodies to this antigen allows identification and quantification of tumour vessels.Tumours produce angiogenic factors, such as vascular endothelial growth factor, and possibly angiopoietin.These activate matrix metalloproteinase within the bonemarrow microenvironment, which then results in cleavage of membrane KIT ligand within the bone marrow promote cellcycle entry and motility of stem and progenitor cells, including circulating endothelial progenitor cells and haematopoietic stem cells.These cells then translocate from an osteoblastic zone to a vascular zone, where they proliferate, differentiate and are launched to the peripheral circulation.These are referred to as colonyforming units of endothelial cells. Extensive incorporation of vessels, identified by the expression of PECAM, was detected in the tumour mass and localized to the tumour periphery.Intravenous injection of these cells into tumourbearing mice resulted in incorporation of genetically marked cells into the tumour vasculature. Identification of molecular pathways that selectively guide the homing of these bonemarrowderived cells to the tumour vasculature will lay the foundation to develop strategies to block tumour angiogenesis.We are, however, a long way off from being able to target these cells in patients with malignancies.Further understanding of the biology of these cells is required.Based on mouse tumour models, it seems that these ce lls are most likely to contr ibute to the early R E V I E W S stages of tumour growth, but are only involved in the angiogenic phase.Lymphatic vessels exist predominantly in the periphery of the tumour vasculature.This information might help us understand why certain tumours only par tially respond to Pentoxifylline therapy.Identification of such unique ECM and chemocy tokines will provide new targets to tailor the treatment of each specific malignancy.A recent study Ciclopirox showed that fibronectin can bind VEGFA.Whether such combined molecular cues are expressed by the tumour microenvironment and are the determinants of CEP differentiation in vivo is not known and is the subject of ongoing studies.Shows the role of vessel cooption in supporting tumour angiogenesis.Defines the mechanism by which angiogenic factors, including placentalderived growth factor, recruit haematopoietic cells from bone marrow to the tumour vasculature.NATU R E R EV I EW S C A N C E R Nature Publishing Group VO LUM E NOV EM B E R In the adult, neovascularization is now known to occur by both angiogenesis and vasculogenesis.

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