The experimental approach used here provides new ways to systematically explore the higher-order chromatin structure of any chromosomal region. In summary, classical pull-down Nilotinib (monohydrochloride monohydrate) assays involve the elution and gel-separation of the isolated protein complexes, whereas SINBAD directly visualizes protein-protein interactions on a single bead. These aberrations frequently are associated with a particular disease phenotype, such as widespread metastasis or early relapse, and are therefore clinically important. Allelic imbalance in solid tumors can be detected by a variety of methods, including sequence-specific hybridization of tumor cell DNA at polymorphic loci across the human genome. In this analysis, LOH was accompanied by copy number loss, normal copy number, and copy number gain. Further studies will be needed to determine whether chromosome 17q LOH in fact accompanies 17q gain in some cases of neuroblastoma or whether this phenomenon is merely an indication of allelic imbalance. The association of gain of chromosome arm 11p with 11q loss was seen in this analysis and has been reported in up to 55% of neuroblastomas with 11q loss, suggesting cooperation between tumor suppressors and oncogenes within these regions. Chromosome 17q gain was observed in all but 1 of the 22 tumors, and thus was the most prevalent abnormality in our series. Gain of either the entire chromosome 7 or its long arm has been detected in 40% of neuroblastomas by CGH; in our study, 7q gain was documented in 10/22 of tumors. In addition, chromosome 7q gain has been significantly correlated with lack of MYCN amplification, which was also the case in our series. Chromosome 7q gain has also been shown to occur through an unbalanced t translocation with loss of 3p material. In our series, 50% of tumor samples with 7q gain had concomitant loss of 3p, suggesting Gemifloxacin mesylate synergistic tumor suppressor pathways. We identified another area of amplification in our series, at chromosome 2p23, the locus of the ALK gene. ALK encodes a tyrosine kinase receptor and was first identified as a component of the NPM-ALK fusion gene in anaplastic large cell lymphoma.