The Trk proto-oncogene family contains four members, TrkA, TrkB, TrkC and TrkE, which are members of the neurotropic tyrosine kinase receptor family. They are variably expressed throughout the central and peripheral nervous systems. TrkA binds to nerve growth factor (NGF) and autophosphorylates to activate multiple downstream effector proteins (1-2). Phosphorylation of TrkA is required for Shc association and subsequent activation of the Ras-MAP kinase-signaling cascade, which leads to activation of Elk-1-dependent gene transcription and neurite growth (3). Also, phosphorylation is required for PI3-kinase association and activation of the Akt signaling cascade. The presence of TrkA leads to cell differentiation and may play a role in specifying sensory neuron subtypes. Mutations in this gene have been associated with congenital insensitivity to pain, anhidrosis, self-mutilating behavior, mental retardation and cancer. Expression of Trk receptors also plays an important role in the biology and clinical behavior of neuroblastomas. High expression of TrkA is present in neuroblastomas with favorable biological features and highly correlated with patient survival, whereas TrkB is mainly expressed on unfavorable, aggressive neuroblastomas (4).

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