TI - Sporadic medulloblastomas contain oncogenic beta-catenin mutations . AB - The beta-catenin , glycogen synthase kinase 3beta ( GSK-3beta ) , and adenomatous polyposis coli ( APC ) gene products interact to form a network that influences the rate of cell proliferation . Medulloblastoma occurs as part of Turcot's syndrome , and patients with Turcot's who develop medulloblastomas have been shown to harbor germ - line APC mutations . Although APC mutations have been investigated and not identified in sporadic medulloblastomas , the status of the beta-catenin and GSK-3beta genes has not been evaluated in this tumor . Here we show that 3 of 67 medulloblastomas harbor beta-catenin mutations , each of which converts a GSK-3beta phosphorylation site from serine to cysteine . The beta-catenin mutation seen in the tumors was not present in matched constitutional DNA in the two cases where matched DNA was available . A loss of heterozygosity analysis of 32 medulloblastomas with paired normal DNA samples was performed with four microsatellite markers flanking the GSK-3beta locus ; loss of heterozygosity with atleast one marker was identified in 7 tumors . Sequencing of the remaining GSK-3beta allele in these cases failed to identify any mutations . Taken together , these data suggest that activating mutations in the beta-catenin gene may be involved in the development of a subset of medulloblastomas . The GSK-3beta gene does not appear to be a target for inactivation in this tumor .