Garrett M. Brodeur, MD, Children's Hospital of Philadelphia

Garrett M. Brodeur, MD
Garrett M. Brodeur, MD

The Brodeur lab focuses on understanding the molecular pathogenesis of neuroblastoma, a common childhood tumor, and utilizing this information for better patient management. One focus is on the role of receptor tyrosine kinases (RTKs) that are involved in neuroblastoma pathogenesis. The lab was the first to demonstrate that high TrkA (NTRK1) expression was associated with younger age, lower stage and favorable outcome. Indeed, the expression of and dependence on TrkA may explain why some neuroblastomas differentiate (into ganglioneuromas) and others spontaneously regress, based on the presence or absence of the TrkA ligand, NGF, in the tumor microenvironment. Conversely, unfavorable neuroblastomas, especially those with MYCN amplification, frequently express TrkB and its ligand, BDNF. This represents an autocrine survival pathway for these tumors. However, in contrast to TrkA, where ligand exposure causes terminal differentiation, the TrkB/BDNF pathway causes neuroblastomas to be more invasive, metastatic, angiogenic and drug resistant.



  1. Iyer R, Wehrmann L, Golden RL, Naraparaju K, Croucher JL, MacFarland SP, Guan P, Kolla V, Wei G, Cam N, Li G, Hornby Z, Brodeur GM. Entrectinib is a potent inhibitor of Trk-driven neuroblastomas in a xenograft mouse model. Cancer Lett. 2016 Mar 28;372(2):179-86.
  2. Iyer R, Croucher JL, Chorny M, Mangino JL, Alferiev IS, Levy RJ, Kolla V, Brodeur GM. Nanoparticle delivery of an SN38 conjugate is more effective than irinotecan in a mouse model of neuroblastoma. Cancer Lett. 2015 May 1;360(2):205-12.