The long-term survival of high-risk neuroblastoma patients has not improved substantially in recent decades and thus remains the leading cause of death by cancer in the age group 1-4 years.
Moreover, current treatment is very harsh and toxic, causing severe short and long term side effects. Therefore, the search for more effective and less toxic targeted drugs remains at the forefront of neuroblastoma research. In the era of emerging personalized medicine, identification of the molecular drivers of oncogenesis is a key towards development of such targeted therapies. ALK mutations constitute an excellent druggable target in NB, and similarly, targeting oncogenic RET in different tumor types is widely explored in the clinic. Preliminary data in our lab pointing at a crosstalk between ALK and RET signaling in neuroblastoma offers us an excellent opportunity to
further explore these signaling nodes in neuroblastoma and establish a basis for new
complementary or synergistic ALK downstream oriented targeted therapies.