The most striking characteristic about solid tumors when compared to normal tissues is the vascular architecture. In normal tissues, the vasculature is well organized to provide ideal conditions for each cell. In contrast, the growing tumor vasculature is abnormal, chaotic, and inadequate in both structure and function. This vasculature relies on tubulin alone as the cytoskeleton support, whereas the cytoskeleton of normal tissue is composed of both tubulin and actin. Tumor vasculature also expresses distinct antigens on its cell surface. Common features of these vessels include dilatation, elongated shapes, blind ends, bulges, leaky sprouts, abrupt changes in diameters, and evidence of vascular compression. Blood flow in these vessels is sluggish and irregular and may even be via arteriovenous shunts, all of which provide a much poorer nutrient environment than normal cells. This irregularity of vessel density and blood flow leads to altered cellular and biochemical microenvironments resulting in hypoxic areas which are very characteristic of solid tumors.  Chemotherapeutic drug resistance can also be caused by tumor cell hypoxia. Some agents, such as bleomycin, require oxygen for free radical production in their mechanism of tumor cell killing. 
Agents which target cell cycle products and require proliferating cells are also inhibited in hypoxic conditions as proliferation is decreased. As a result of the tumor vasculature being so distorted and limited, the effective delivered dose of a chemotherapeutic to hypoxic areas of tumor may be much less than to more oxygenated areas, thus sparing tumor cells that exist away from the blood vessels. Increasing knowledge of the molecular mechanisms of angiogenesis has stimulated the development of a variety of antiangiogenic agents to target tumor growth at each step of the process in blood vessel formation. Although vascular disrupting agents (VDAs), formerly known as vascular targeting agents, have often been grouped with the antiangiogenic agents, the rationale behind this therapy is quite different. VDAs, in contrast to antiangiogenic compounds, are cytotoxic rather than cytostatic. Rather than inhibiting the development of new blood vessels, these agents target the already formed neo-vasculature of actively growing tumors, producing a rapid shutdown of tumor blood vessels. The resulting ischemia can lead to extensive tumor cell death.

References

1.Pilat MJ, Lorusso PM. J Cell Biochem. 2006;99(4):1021–1039.