NF-κB signaling pathway and cancer related mutations. Only canonical (classical) pathway is shown. Extracellular stimuli transmitted though receptor complexes activate IKK via phosphorylation. Consequently, IKK phosphorylates IκB, leading to its dissociation from inactive NF-κB complex and ubiquitin-mediated proteasomal degradation. Freed from IκB, active NF-κB dimer translocates into the nucleus and induces the transcription of various target genes involved in multiple cellular pathways. Cancer-relevant mutations, indicated in orange boxes, can occur in all steps of NF-κB signaling cascade.|@|~(^,^)~|@|A model of how oncogenic network influences cancer treatment outcome. How two oncogenic moieties (NF-κB and bcl2) are connected in a network at diagnosis - a linear pathway in which NF-κB drives bcl2 expression reminiscent of ABC DLBCL, or in independent parallel pathways reminiscent of GCB DLBCL - influences the cellular outcome and sensitivity to treatment using conventional chemotherapy and/or novel NF-κB inhibitor.

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