Neuroblastoma (NB) is one of the leading causes of pediatric cancer mortality. Despite advances in therapy, the survival rate for relapsed NB patients is dismal. MYCN is a major genetic driver for NB disease progression and relapse. However, targeting MYCN directly remains challenging, and novel therapeutic approaches against MYCN warrant in-depth investigations. Our lab has shown that MYCN profoundly rewires the way NB utilizes nutrients--specifically lipids--to drive oncogenesis. This function is effectively opposed by a core component of the circadian clock called BMAL1.
