High <i>ALK</i> Receptor Tyrosine Kinase Expression Supersedes <i>ALK</i> Mutation as a Determining Factor of an Unfavorable Phenotype in Primary Neuroblastoma

Abstract

Primary neuroblastomas with mutated ALK exhibit high ALK expression levels and strongly resemble neuroblastomas with elevated WT ALK expression levels in both their clinical and molecular phenotypes. These data suggest that high levels of mutated and WT ALK mediate similar molecular functions that may contribute to a malignant phenotype in primary neuroblastoma.