Conclusions

Investigations of angiogenesis in neuroblastoma to date reflect the complexity that results from the combined influences of genetic and epigenetic factors on tumor vessel formation. Tumors that are clinically aggressive may express higher levels of proangiogenic cytokines, while concurrently expressing decreased levels of factors that function to restrain new blood vessel growth (Fig. 16.1). Conversely, the more benign nature of ganglioneuroblastomas and other relatively indolent, differentiated tumors may reflect the influence of secreted angiogenesis inhibitors. Such factors may be elaborated by Schwann cells in the tumor stroma, or possibly by tumor cells that have undergone further differentiation.

Preclinical studies suggest that neuroblastoma may be susceptible to certain anti-angiogenic strategies. For example, blockade of VEGF in neuroblas-toma has shown consistent effectiveness between experimental models and investigators. In addition, this approach has recently been shown to have efficacy in clinical trials of adult human cancers (Glade-Bender et al. 2003); however,even the most promising reports suggest that neuroblastoma may be able to partially evade anti-VEGF agents by co-opting host vessels (Kim et al. 2002a). Understanding such events will require further dissection of the unique interactions between neuroblastoma cells and developing vasculature. Such studies are essential if patients with advanced neuroblastoma are to benefit from this area of investigation.

Acknowledgements. The authors thank J. Kandel and J. Glade-Bender for reviewing the chapter. This work was supported in part by NCI grant number CA088951 (D.J.Y.), the Neuroblastoma Children's Cancer Society (S.L.C.), Friends for Steven Pediatric Cancer Research Fund (S.L.C.), and the Elise Anderson Neuroblastoma Research Fund (S.L.C.)

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