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mri images of patients were spatially normalized into a standard stereotaxic space for quantitative comparison of tumor location ( spm5 ; www.fil.ion.ucl.ac.uk/spm ) .
radiologists masked to patient subtype determined the 3-dimensional location of the tumor or surgical cavity relative to predefined anatomical landmarks .
the expression of mouse orthologs of key signature genes of human wnt and shh - subtype medulloblastoma ( supplemental dataset 1 and supplemental table ) were mapped in the developing mouse hindbrain using four publically accessible datasets ( see supplemental methods ) .
blbp - cre , ctnnb1 , atoh1-cre and tp53 mice were bred to generate appropriate genotypes and subject to clinical surveillance for signs of tumor development .
atoh1-ctnnb1 transgenic mice were generated by pro - nuclear injection . in utero electroporation and cell tracking
the uterus was externalized and the dorsal brainstem of e12.5 embryos electroporated with cmv - egfp plasmid dna .
. 2  10 gfp cells / well were cultured in poly - d - lysine - coated 96-well plates and challenged with mutant - ctnnb1-gfp , control gfp virus , wnt1 protein ( 50ng / ml ) or shh supernatant ( 3ug / ml ) prior to pulsing with [ methyl-3h]thymidine and scintillation counting .
immunohistochemistry was performed using routine techniques and primary antibodies of the appropriate tissues as described ( supplemental methods ) .
mrna expression ( geo accession number gse24628 ) and dna copy number profiles ( available at http://stjuderesearch.org/site/authors/gilbertson ) were generated from mouse and human tissues using appropriate microarray platforms as detailed ( supplemental methods ) .
reverse transcriptase real time - pcr analysis and gene re - sequencing of human medulloblastomas were performed as described previously3 .
mrna expression and dna microarray profiles of human and mouse medulloblastomas were integrated using established and novel bioinformatic and statistical approaches .
mri images of patients were spatially normalized into a standard stereotaxic space for quantitative comparison of tumor location ( spm5 ; www.fil.ion.ucl.ac.uk/spm ) .
radiologists masked to patient subtype determined the 3-dimensional location of the tumor or surgical cavity relative to predefined anatomical landmarks .
the expression of mouse orthologs of key signature genes of human wnt and shh - subtype medulloblastoma ( supplemental dataset 1 and supplemental table ) were mapped in the developing mouse hindbrain using four publically accessible datasets ( see supplemental methods ) .
blbp - cre , ctnnb1 , atoh1-cre and tp53 mice were bred to generate appropriate genotypes and subject to clinical surveillance for signs of tumor development .
atoh1-ctnnb1 transgenic mice were generated by pro - nuclear injection . in utero electroporation and cell tracking were performed by anesthetizing pregnant mice of the appropriate genotype .
the uterus was externalized and the dorsal brainstem of e12.5 embryos electroporated with cmv - egfp plasmid dna .
. 2  10 gfp cells / well were cultured in poly - d - lysine - coated 96-well plates and challenged with mutant - ctnnb1-gfp , control gfp virus , wnt1 protein ( 50ng / ml ) or shh supernatant ( 3ug / ml ) prior to pulsing with [ methyl-3h]thymidine and scintillation counting .
immunohistochemistry was performed using routine techniques and primary antibodies of the appropriate tissues as described ( supplemental methods ) .
mrna expression ( geo accession number gse24628 ) and dna copy number profiles ( available at http://stjuderesearch.org/site/authors/gilbertson ) were generated from mouse and human tissues using appropriate microarray platforms as detailed ( supplemental methods ) .
reverse transcriptase real time - pcr analysis and gene re - sequencing of human medulloblastomas were performed as described previously3 .
mrna expression and dna microarray profiles of human and mouse medulloblastomas were integrated using established and novel bioinformatic and statistical approaches .
medulloblastoma encompasses a collection of clinically and molecularly diverse tumor subtypes that together comprise the most common malignant childhood brain tumor14 . 
 these tumors are thought to arise within the cerebellum , with approximately 25% originating from granule neuron precursor cells ( gnpcs ) following aberrant activation of the sonic hedgehog pathway ( hereafter , shh - subtype)38 . 
 the pathological processes that drive heterogeneity among the other medulloblastoma subtypes are not known , hindering the development of much needed new therapies . here 
 , we provide evidence that a discrete subtype of medulloblastoma that contains activating mutations in the wnt pathway effector ctnnb1 ( hereafter , wnt - subtype)1,3,4 , arises outside the cerebellum from cells of the dorsal brainstem . 
 we found that genes marking human wnt - subtype medulloblastomas are more frequently expressed in the lower rhombic lip ( lrl ) and embryonic dorsal brainstem than in the upper rhombic lip ( url ) and developing cerebellum . 
 magnetic resonance imaging ( mri ) and intra - operative reports showed that human wnt - subtype tumors infiltrate the dorsal brainstem , while shh - subtype tumors are located within the cerebellar hemispheres . activating mutations in ctnnb1 had little impact on progenitor cell populations in the cerebellum , but caused the abnormal accumulation of cells on the embryonic dorsal brainstem that included aberrantly proliferating zic1 + precursor cells . 
 these lesions persisted in all mutant adult mice and in 15% of cases in which tp53 was concurrently deleted , progressed to form medulloblastomas that recapitulated the anatomy and gene expression profiles of human wnt - subtype medulloblastoma . 
 we provide the first evidence that subtypes of medulloblastoma have distinct cellular origins . 
 our data provide an explanation for the marked molecular and clinical differences between shh and wnt - subtype medulloblastomas and have profound implications for future research and treatment of this important childhood cancer .