Elevated expression of the neurotrophin-3 (NT-3) receptor TrkC by childhood 
medulloblastomas is associated with favorable clinical outcome. Here, we provide 
evidence that TrkC is more than simply a passive marker of prognosis. We 
demonstrate that: (a) medulloblastomas undergo apoptosis in vitro when grown in 
the presence of NT-3; (b) overexpression of TrkC inhibits the growth of 
intracerebral xenografts of a medulloblastoma cell line in nude mice; and (c) 
trkC expression by individual tumor cells is highly correlated with apoptosis 
within primary medulloblastoma biopsy specimens. TrkC-mediated NT-3 signaling 
promotes apoptosis by activating multiple parallel signaling pathways and by 
inducing immediate-early gene expression of both c-jun and c-fos. Considered 
collectively, these results support the conclusion that the biological actions 
of TrkC activation affect medulloblastoma outcome by inhibiting tumor growth 
through the promotion of apoptosis.