Primary brain tumors are classified and treated based on their histological features, however the factors which specify these tumor types remain largely unknown. We demonstrate that the over-expression of HRAS (V12) and MYC alone or in combination directs the development of glioma, CNS PNET, and atypical teratoid/rhabdoid (AT/RT)-like tumors from postnatal murine p53-deficient neural stem/progenitor cells.
Definition of genetic events directing the development of distinct types of brain tumors from postnatal neural stem/progenitor cells.
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View SamplesNeural stem/progenitor cells were isolated from the lateral ventricle wall of 4-6 week-old CD1 mice and grown as neurospheres under low density culture conditions. Test cells were transduced with bicistronic retroviral constructs for the over-expression of Bmi1 together with eGFP, and control cells were transduced with an empty vector construct expressing eGFP only. To identify genes, which are regulated by BMI1 in neural stem/progenitor cells, the gene expression profiles of neurosphere cells over-expressing Bmi1 were compared empty vector control cells using Affymetrix Gene mouse ST1.0 arrays
The putative tumor suppressor gene EphA7 is a novel BMI-1 target.
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