each of the following sequences: VRAAWRRL (ICAM-2 amino acids 241-248 to inhibit ICAM-2/a-actinin binding [30]); LARRRWAV (scrambled control); MTLGMIWTIILRFA (a- actinin amino acids 122–135 to inhibit a-actinin/actin binding [46]); WIRMIAFGLIMTLT (scrambled control). Oligopeptides were synthesized in the St. Jude Hartwell Center for Bioinfor- matics and were .99% pure. SK-N-ASpIRES.ICAM2 cells were incubated with 12.5 mM peptide for 4 hours, at which time cells were fixed with paraformaldehyde and the subcellular localization of actin fibers evaluated using FITC-conjugated phalloidan by standard methods. Distribution of F-actin Standard methods were used to fix cells using paraformaldehyde and incubate them for 30 minutes at room temperature with 10 mg fluorescein isothiocyanate (FITC)-conjugated phalloidan/ mL phosphate buffered saline. Actin fibers were visualized by confocal fluorescence microscopy, also by standard methods. Mouse Models of Neuroblastoma Subcutaneous xenografts: 16107 neuroblastoma cells transduced to express luciferin were injected subcutaneously in each hind flank of SCID mice (5 mice/group), and imaged noninvasively by standard methods. Disseminated neuroblastoma: 56105 neuroblas- toma cells injected intravenously into the tail veins of SCID mice produced disseminated tumors in 100% of mice [33]. In this model, there is no ‘‘primary tumor’’, but tumor development mimics that of clinical metastatic neuroblastoma in that tumors develop in multiple anatomic locations including supra-renal and bone marrow. Animal protocols were in accordance with the guidelines of the St. Jude Animal Care and Use Committee. 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