Marli E. Ebus

TL;DR: The genomic landscape of neuroblastoma reveals two novel molecular defects, chromothripsis and neuritogenesis gene alterations, which frequently occur in high-risk tumours.

TL;DR: It is shown that RAS-MAPK pathway mutations may function as a biomarker for new therapeutic approaches to refractory disease and provide a rationale for genetic characterization of relapse neuroblastomas.

TL;DR: It is reported that LIN28B showed genomic aberrations and extensive overexpression in high-risk neuroblastoma compared to several other tumor entities and normal tissues and was an independent risk factor for adverse outcome in neuroblastomas.

TL;DR: It is shown that most neuroblastomas include two types of tumor cells with divergent gene expression profiles, and two super-enhancer-associated TF networks thus dominate epigenetic control of neuroblastoma and shape intratumoral heterogeneity.

TL;DR: It is reported that analysis of Affymetrix expression data of primary neuroblastic tumors shows an extensive overexpression of Cyclin D1, which correlates with histologic subgroups and concludes that neuroblastoma functionally depend on overeexpression of G(1)-regulating genes to maintain their undifferentiated phenotype.