Another cooperating mutation is the activation of β-catenin. This co-occurrence is common in medulloblastomas (98). β-catenin binds Brg and regulates its ability to activate genes (99). Hence, one could propose a transcriptional mechanism for this cooperation. On the other hand, as with activation of PI3K, activation of β-catenin would increase the number of cell divisions at risk for TopoII dysfunction during anaphase, thereby generating more mutations and moving the cell further along on the pathway to cancer. Future studies will be necessary to resolve these questions.
