Abstract
A subset of glioblastomas (GBM) has high levels of TGFβ signaling, and anti-TGFβ therapies are being pursued as treatments for GBM. The work presented here identifies CREB1 as a potential biomarker for TGFβ-dependent GBM. CREB1 integrates signaling from TGFβ and the PI3K pathway and nucleates a self-sustaining signaling loop that maintains TGFβ2 expression in GBM with high CREB1 levels.
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