Abstract:
:We examined the genetic requirements for the Myc family of oncogenes in normal Sonic hedgehog (Shh)-mediated cerebellar granule neuronal precursor (GNP) expansion and in Shh pathway-induced medulloblastoma formation. In GNP-enriched cultures derived from N-myc(Fl/Fl) and c-myc(Fl/Fl) mice, disruption of N-myc, but not c-myc, inhibited the proliferative response to Shh. Conditional deletion of c-myc revealed that, although it is necessary for the general regulation of brain growth, it is less important for cerebellar development and GNP expansion than N-myc. In vivo analysis of compound mutants carrying the conditional N-myc null and the activated Smoothened (ND2:SmoA1) alleles showed, that although granule cells expressing the ND2:SmoA1 transgene are present in the N-myc null cerebellum, no hyperproliferation or tumor formation was detected. Taken together, these findings provide in vivo evidence that N-myc acts downstream of Shh/Smo signaling during GNP proliferation and that N-myc is required for medulloblastoma genesis even in the presence of constitutively active signaling from the Shh pathway.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Hatton BA,Knoepfler PS,Kenney AM,Rowitch DH,de Alborán IM,Olson JM,Eisenman RNdoi
10.1158/0008-5472.CAN-06-1621subject
Has Abstractpub_date
2006-09-01 00:00:00pages
8655-61issue
17eissn
0008-5472issn
1538-7445pii
66/17/8655journal_volume
66pub_type
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