Tumor Growth in the High Frequency Medulloblastoma Mouse Model Ptch1^+/-/Tis21^KO Has a Specific Activation Signature of the PI3K/AKT/mTOR Pathway and Is Counteracted by the PI3K Inhibitor MEN1611.

ABSTRACT: We have previously generated a mouse model (Ptch1^+/-/Tis21^KO ), which displays high frequency spontaneous medulloblastoma, a pediatric tumor of the cerebellum. Early postnatal cerebellar granule cell precursors (GCPs) of this model show, in consequence of the deletion of Tis21, a defect of the Cxcl3-dependent migration. We asked whether this migration defect, which forces GCPs to remain in the proliferative area at the cerebellar surface, would be the only inducer of their high frequency transformation. In this report we show, by further bioinformatic analysis of our microarray data of Ptch1^+/-/Tis21^KO GCPs, that, in addition to the migration defect, they show activation of the PI3K/AKT/mTOR pathway, as the mRNA levels of sev

SUBMITTER: Ceccarelli M 

PROVIDER: S-EPMC8362831 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature