Inflammation & NF-κB
Chronic inflammation is soil for cancer: it feeds growth signals, DNA damage, and immune suppression. The NF-κB switch inside cells is the master relay, and colitis, hepatitis, and H. pylori gastritis are the clinical proof.
Tumour-promoting inflammation (a hallmark enabling characteristic) acts through IL-6/STAT3, TNF/NF-κB, IL-1β, COX-2/PGE2, and inflammasome signalling. NF-κB (canonical IKK/IκB and non-canonical NIK/RelB) drives survival, cytokine production, and the SASP; it is constitutively active in many lymphomas (ABC-DLBCL via MYD88/CD79B, BTK-dependent) and myeloma. Aspirin reduces colorectal cancer in Lynch syndrome (CAPP2) and canakinumab reduced lung cancer incidence in CANTOS (secondary analysis), though as treatment it failed. Anti-inflammatory chemoprevention is one of the few validated mechanism-based preventions.
In one picture
A wound that never heals: the repair crews keep pouring in growth signals and clearing away rubble, and a wound that is always being rebuilt is a wound where mistakes accumulate.
Diagram
top- Aspirin chemoprevention in Lynch syndrome (CAPP2); NSAIDs in FAP
- BTK inhibitors (ibrutinib, zanubrutinib) shut NF-κB in CLL/lymphoma
- IL-6/STAT3 blockade in cachexia and CRS (tocilizumab)
- Anti-H. pylori therapy prevents gastric cancer; HBV/HCV treatment prevents HCC
Notes
top- Leading programmes: Karin (UCSD) on NF-κB and inflammation-driven cancer; Coussens (OHSU) on inflammation and TME; Greten (Frankfurt); CAPP2 (Burn, Newcastle).
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