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Constitutive activation of NF-κB in glioblastoma multiforme (GBM). Heterozygous deletion of NFKBIA or HOTAIR-mediated phosphorylation of IκB leads to the constitutive activation of NF-κB, which in turn induces self-renewal, angiogenesis, and immune escape. NF-κB is also activated by constitutive activity of mutated EGFRvIII, which also confers self-renewal and invasion in GBM.
