KeywordsNF-κB; hypoxia; inflammation; κB Kinase (IKK); Prolyl Hydroxylases (PHDs); cancer; Transforming Growth Factor-β-Activated Kinase 1 (TAK1); Factor Inhibiting HIF (FIH); Cancer; NF-κB; Non-conventional pathways; IKKs; IκBs; NF-κB; leukemia; lymphoma; brain cancer; cancer stem-like cells; DNA damage repair; glioblastoma; mesenchymal glioblastoma subtype; NF-κB (nuclear factor-κB); Aspirin; non-steroidal anti-inflammatory drugs; nuclear factor kappaB; apoptosis; colon cancer; nucleolus; nucleolar; nucleoli; sequestration; stress; RelA; p65; nuclear factor κB; NF-κB inhibitors; cancer; IκB kinase; Gadd45β; ubiquitin; NFκB; BET inhibition; transcription; chromatin looping; acetylation B cell non-Hodgkin lymphoma; NF-κB; transcription; cancer; NF-κB; lymphoma; leukemia; CARMA1; CARD11; CD79; MyD88; miRNAs; NF-κB; transcriptional regulatory networks; oncogenic and tumor suppressor pathways; cancer; inflammation; nuclear factor κB; signal transduction; ubiquitin; ubiquitination/deubiquitination; NF-κB; RELA; cREL; RELB; tumor; cancer; transformation; inflammation; gene expression; tumor necrosis factor; Treg; NF-κB; dynamics; live cell imaging; microfluidics; cancer; transcription; n/a; ER stress; cancer; infection; inflammation; unfolded protein response; NF-κB; IκBα; thapsigargin; NF-κB; multiple myeloma; canonical; non-canonical; mutations; microenvironment; cytokines; crosstalk; gene-expressions; deubiquitinylases; NF-κB signaling; apoptotic cell death; gastric carcinoma; therapeutic targets; chemoresistance; ubiquitin-specific proteases; noncanonical NF-κB; cancer; cellular signaling; inflammation; tumor initiating cells; NIK; RelB; p52
