Abstract
Background: Disruption of transcriptional regulatory networks that drive normal cellular differentiation and development can result in oncogenic transformation and transcriptional addiction. Many pediatric sarcomas are defined by/harbor oncogenic fusion proteins, resulting from chromosomal translocations such as the EWSR1 gene fused to an ETS family transcription factor (TF) gene (FLI1 or ERG) in Ewing sarcoma (ES), or PAX3/PAX7 and FOXO1 translocations in alveolar rhabdomyosarcoma (ARMS). In neuroblastoma, MYCN, a member of the MYC family of TFs, is often amplified and localizes to super enhancer regions, where it rewires lineage-specific transcriptional programs driving oncogenesis.
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