Within the CNS, Hedgehog (HH)-GLI signaling is implicated in modulating
precursor proliferation in the late embryonic and postnatal brain,
including in the cerebellum (Dahmane and Ruiz i Altaba, 1999), tectum
and cortex (Dahmane et al., 2001), as well as in the control of brain
stem cell behavior in stem cell niches (Palma and Ruiz i Altaba, 2004;
Palma et al., 2005).  In addition, abnormally sustained HH-GLI signaling
can induce tumor formation (Dahmane et al., 1997; 2001) and is essential
for the sustained growth of a large variety of human tumors (Dahmane et
al., 2001; Sanchez et al., 2004; Sanchez and Ruiz i Altaba, 2005).  How
HH signaling interacts with other pathways involved in stem cell
behavior and cancer remains unclear. I will present recent work
addressing the role of the GLI code (Ruiz i Altaba et al., 2007)  in
cancer, specifically focusing on its role in glioblastoma cancer stem
cells (Clement et al., 2007) and  melanomas (Stecca et al., 2007), and
in its integrations with oncogenic RAS/AKT signaling.