On this latter array there were several intervening SNPs between the MYCN and ALK genes that did not show amplification, however this does not rule out ALK coamplification with MYCN, as discontinuous regions of amplification may have occurred. Nevertheless, the finding of ALK amplification in neuroblastoma may provide a novel therapeutic target that could be tested using available ALK inhibitor compounds. SNP arrays have many advantages over more conventional methods of cancer genome analysis in terms of efficiency, precision and minimal DNA requirements, and may well become the dominant technology for performing genome-wide tumor cell LOH and copy number measurements. This application seems especially relevant to large studies such as those of the Children��s Oncology Group, in which treatment for neuroblastoma patients is already based on genetic abnormalities and further stratifications are planned based on 1p and 11q LOH. Although the use of high-density SNP arrays to provide clinically relevant information has great appeal, this strategy must first be validated using newer generation SNP arrays containing probes for more SNP markers with higher informative rates. Ultimately, the results of cancer genome-wide allelotyping by SNP array analysis may predict responses to specific therapies, allowing more efficient modification of regimens for individual patients. Samples were identified from the Children��s Oncology Group Neuroblastoma Nucleic Acids Bank with the only inclusion criteria being 1) availability of matched constitutional DNA from peripheral blood mononuclear cells; 2) samples obtained at original diagnosis and immediately snap frozen; and 3) a tumor cell content of more than 90% based on differential count, clonal hyperdiploid percentage in some tumors, and direct examination of H&E-stained tumors in a subset of cases. Patients were staged according to the International Neuroblastoma Staging System and histology was analyzed by the Shimada Pathology Classification. MYCN gene amplification and DNA ploidy were determined as previously described. LOH and chromosome gain status were determined on chromosome arms 1p, 3p, 11q, and 17q using conventional microsatellite markers as previously described.