# Inflammation & NF-κB

Source: https://onco.cc/pathways/inflammation-nfkb/  
OnCo record `inflammation-nfkb` (Pathway). Data CC BY-NC 4.0, attribute "Data from OnCo (onco.cc)"; commercial use needs a licence.

## TL;DR

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.

## Summary

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.

## Fields

- Kind: Pathway
- Last checked: 2026-09-08
- Tags: mechanism
- Analogy: 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.
- Interventions: 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

- Leading programmes: Karin (UCSD) on NF-κB and inflammation-driven cancer; Coussens (OHSU) on inflammation and TME; Greten (Frankfurt); CAPP2 (Burn, Newcastle).

## Sources

- Wikipedia: https://en.wikipedia.org/wiki/NF-κB
- Greten & Grivennikov, Inflammation and cancer: triggers, mechanisms, and consequences (Immunity 2019): https://doi.org/10.1016/j.immuni.2019.06.025

## Connected records

- cancers: [Craniopharyngioma](https://onco.cc/cancers/craniopharyngioma/), [Diffuse large B-cell lymphoma](https://onco.cc/cancers/dlbcl/), [Ependymoma](https://onco.cc/cancers/ependymoma/), [Extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma)](https://onco.cc/cancers/malt-lymphoma/), [Gallbladder cancer](https://onco.cc/cancers/gallbladder/), [Marginal zone lymphoma](https://onco.cc/cancers/marginal-zone-lymphoma/), [Non-Hodgkin lymphoma (all types)](https://onco.cc/cancers/non-hodgkin-lymphoma/), [Peripheral T-cell lymphomas (including cutaneous T-cell lymphoma)](https://onco.cc/cancers/peripheral-t-cell-lymphoma/), [Primary CNS lymphoma](https://onco.cc/cancers/primary-cns-lymphoma/), [Waldenström macroglobulinaemia](https://onco.cc/cancers/waldenstrom/)
- technologies: [Chemoprevention & risk-reducing surgery](https://onco.cc/technologies/chemoprevention/), [HPV & HBV vaccination](https://onco.cc/technologies/hpv-vaccine/)
- targets: [BCL10](https://onco.cc/targets/bcl10/), [BIRC3](https://onco.cc/targets/birc3/), [BTK (Bruton tyrosine kinase)](https://onco.cc/targets/btk/), [CARD11](https://onco.cc/targets/card11/), [CCR4](https://onco.cc/targets/ccr4/), [CD30](https://onco.cc/targets/cd30/), [CD79b](https://onco.cc/targets/cd79b/), [IRF4](https://onco.cc/targets/irf4/), [MALT1](https://onco.cc/targets/malt1/), [MYC](https://onco.cc/targets/myc-gene/), [MYD88](https://onco.cc/targets/myd88/), [PLCG1](https://onco.cc/targets/plcg1/), [PLCG2](https://onco.cc/targets/plcg2/), [PRKCB](https://onco.cc/targets/prkcb/), [STAT3](https://onco.cc/targets/stat3/), [SYK](https://onco.cc/targets/syk/), [TNFAIP3](https://onco.cc/targets/tnfaip3/), [VAV1](https://onco.cc/targets/vav1/)
- drugs: [Ibrutinib](https://onco.cc/drugs/ibrutinib/), [Zanubrutinib](https://onco.cc/drugs/zanubrutinib/)
- institutions: [German Cancer Research Center (DKFZ)](https://onco.cc/institutions/dkfz/), [Memorial Sloan Kettering Cancer Center](https://onco.cc/institutions/mskcc/), [UCSF Helen Diller Family Comprehensive Cancer Center](https://onco.cc/institutions/ucsf/)
- pathways: [B-cell receptor / BTK signalling (to NF-κB)](https://onco.cc/pathways/bcr-signalling/), [Cancer cachexia](https://onco.cc/pathways/cachexia-biology/), [Cellular senescence](https://onco.cc/pathways/senescence/), [Clonal haematopoiesis (CHIP)](https://onco.cc/pathways/clonal-haematopoiesis/), [Complement in cancer](https://onco.cc/pathways/complement-in-cancer/), [JAK-STAT signalling](https://onco.cc/pathways/jak-stat/), [Microbiome-tumour interactions](https://onco.cc/pathways/microbiome-tumour/), [Oncogenic viruses](https://onco.cc/pathways/oncogenic-viruses/), [Tumour microenvironment (TME)](https://onco.cc/pathways/tumor-microenvironment/), [Ubiquitin-proteasome system & protein homeostasis](https://onco.cc/pathways/ubiquitin-proteasome-system/)
- terms: [Cytokine release syndrome (CRS)](https://onco.cc/terms/crs/), [Enabling characteristic: tumour-promoting inflammation](https://onco.cc/terms/tumor-promoting-inflammation/), [Epstein-Barr virus latency programmes, and why they decide which lymphoma](https://onco.cc/terms/lymphoma-bio-ebv-latency/), [HTLV-1, Tax and HBZ in adult T-cell leukaemia/lymphoma](https://onco.cc/terms/lymphoma-bio-htlv1/), [Inflammation](https://onco.cc/terms/inflammation/), [LymphGen and the genetic clusters of large B-cell lymphoma](https://onco.cc/terms/lymphoma-bio-lymphgen/), [Microenvironment and inflammation: tumours as wounds that do not heal](https://onco.cc/terms/microenvironment-inflammation-theory/), [MYD88 L265P and CXCR4 mutations](https://onco.cc/terms/myd88-l265p/), [Salmonella Typhi carriage and gallbladder cancer](https://onco.cc/terms/salmonella-typhi-gallbladder-cancer/)
- key papers: [Balkwill and Mantovani 2001: inflammation and cancer, back to Virchow?](https://onco.cc/key-papers/paper-balkwill-mantovani-inflammation-virchow-lancet-2001/), [Grivennikov, Greten and Karin 2010: immunity, inflammation and cancer](https://onco.cc/key-papers/paper-grivennikov-immunity-inflammation-cancer-cell-2010/), [Inflammation and Cancer: Triggers, Mechanisms, and Consequences](https://onco.cc/key-papers/paper-greten-immunity/), [TRACERx 421: the full-cohort picture of how lung cancer evolves and which subclones drive relapse](https://onco.cc/key-papers/paper-tracerx-evolution-nature-2023/)
- biomarkers: [CD79B ITAM mutation](https://onco.cc/biomarkers/cd79b-itam-mutation/)

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