Anticancer Agents: VTA or VDA
Paul R. Sebahar,
J. Adam Willardsen,
Mark B. Anderson.
The tumor vasculature is quite an attractive target for anti-cancer/anti-tumor therapy because the blood vessels provide the route for nutrient/waste and oxygen/carbon dioxide exchanges as well as a convenient route for tumor metastatic spread. The complex interplay of the tumor with the local blood vasculature is intriguing. Targeting the vasculature in an effort to control the tumor life cycle is therefore very complex yet enticing as a treatment option. In reviewing the literature discussing vascular targeting/disrupting agents, it is sometimes less than clear as to what exactly defines or differentiates a vascular targeting agent (VTA; antiangiogenic or stopping tumors from producing new blood vessels) from a vascular disrupting agent (VDA; disrupting the "established" tumor vasculature). Although, there appears to be differences between these two strategies of modifying the tumor vasculature including differences in the administration schedules. The use of the VTA/VDA terms in scientific reports is not always clear since some agents may also exhibit activities attributed to a VTA and/or a VDA. However these agents are defined, the important goal is to severely cripple and/or “shut-down” the tumors ability to maintain viability and to subsequently become metastatic and hence are important in the armamentarium of anti-tumor/anti-cancer treatment strategies. This brief review of selected literature reports attempts to summarize some of the chemical structural elements associated with these types of agents and asks the question “Are there common chemical structural features emerging that may assist in a differentiating theme?”
Keywords: Vascular disrupting, vascular targeting, tubulin, oncology, angiogenesis, inhibitor
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