EGFR phosphorylates tumor-derived EGFRvIII driving STAT3/5 and progression in glioblastoma.


EGFRvIII, a frequently occurring mutation in primary glioblastoma, results in a protein product that cannot bind ligand, but signals constitutively. Deducing how EGFRvIII causes transformation has been difficult because of autocrine and paracrine loops triggered by EGFRvIII alone or in heterodimers with wild-type EGFR. Here, we document coexpression of EGFR… (More)
DOI: 10.1016/j.ccr.2013.09.004

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