Vascular Targeting Agents as Cancer Therapeutics

Ultrasonically targeted delivery into endothelial and smooth muscle cells in ex vivo arteries

“…A targeted loss of viability or denuding may not be desirable for drug or gene delivery applications but may be beneficial for other therapeutic applications. A number of vascular targeting agents, such as combretastatins, are currently being studied to cause EC death for anti-vascular targeting [39]. This therapy aims to selectively destroy endothelium of tumor blood vessels and subsequently cause vascular shutdown, which limits sustaining nutrients and waste removal required by the tumor [5].…”

Effects of androgen suppression and radiation on prostate cancer suggest a role for angiogenesis blockade

“…16 Newly formed tumour blood vessels differ substantially from normal capillaries in several ways that make them accessible targets for antiangiogenic therapy. [17][18][19][20] Some tumour vessels have a defective cellular lining composed of disorganised, loosely connected, branched, overlapping or sprouting endothelial cells. 21 Tumour-induced neovasculature exhibits increased expression of receptors for angiogenic factors, and angiogenic endothelial cells proliferate up to 50 times more than normal endothelial cells.…”

Regulation of VEGF-expression by patupilone and ionizing radiation in lung adenocarcinoma cells

“…The accumulation of tumor cells in the most radiosensitive G2-M phase of the cell cycle represents the major rationale for the sensitization to IR [6][7][8][9], though other Sphase progression-related mechanisms have been observed as well [4]. Additional anti-vascular and anti-angiogenic effects might contribute to the supra-additive tumor growth delay observed in vivo, and indeed, direct targeting of endothelial cells [10][11][12] and indirect, anti-angiogenic interference with the secretion of pro-angiogenic factors from tumor cells have been proposed [2,13]. Microtubule stabilizing and destabilizing agents block the nuclear translocation and correct assembly of the hypoxia inducible factor (HIF) by disrupting the structural organization of the microtubule cytoskeleton.…”