# Grivennikov, Greten and Karin 2010: immunity, inflammation and cancer

Source: https://onco.cc/key-papers/paper-grivennikov-immunity-inflammation-cancer-cell-2010/  
OnCo record `paper-grivennikov-immunity-inflammation-cancer-cell-2010` (Key paper). Data CC BY-NC 4.0, attribute "Data from OnCo (onco.cc)"; commercial use needs a licence.

## TL;DR

The review that laid out how inflammation contributes at every stage of cancer, from the DNA damage that starts it to the signals that help it grow and spread, and named the molecular switches, such as NF-kB and STAT3, that connect immune cells to tumour cells.

## Summary

Grivennikov, Greten and Karin reviewed the roles of inflammation in tumour initiation, promotion, progression and metastasis. Chronic inflammation from infection, autoimmunity or environmental irritants produces reactive oxygen species and cytokines that damage DNA and stimulate proliferation; tumour-promoting inflammation acts through transcription factors NF-kB and STAT3 and cytokines such as IL-6, TNF and IL-1; and inflammation also supports angiogenesis and metastasis while suppressing anti-tumour immunity. They noted that a substantial share of cancers, on some estimates up to a fifth, is linked to chronic infection or inflammation.

## Fields

- Kind: Key paper
- Last checked: 2026-09-08
- Journal: Cell
- Year: 2010
- DOI: 10.1016/j.cell.2010.01.025
- Authors: Grivennikov SI, Greten FR, Karin M.
- Findings: Inflammation contributes to initiation through DNA damage and to promotion through NF-kB and STAT3 signalling driven by cytokines such as IL-6 and TNF.; Tumour-associated inflammation also supports angiogenesis and metastasis and dampens adaptive anti-tumour immunity.; Chronic infection and inflammation are estimated to underlie up to about a fifth of cancers.
- What it means: This paper is the molecular sequel to the 2002 inflammation and cancer review and the basis for IL-6, JAK-STAT and NF-kB directed strategies in cancer as well as for aspirin and other anti-inflammatory prevention trials.
- Caveats: A review synthesising mostly mouse genetic evidence.; Anti-inflammatory approaches have shown clearer benefit in prevention than in treating established cancers.

## Sources

- Full text (DOI): https://doi.org/10.1016/j.cell.2010.01.025

## Connected records

- key papers: [Balkwill and Mantovani 2001: inflammation and cancer, back to Virchow?](https://onco.cc/key-papers/paper-balkwill-mantovani-inflammation-virchow-lancet-2001/), [Coussens and Werb 2002: inflammation and cancer](https://onco.cc/key-papers/paper-coussens-werb-inflammation-cancer-nature-2002/), [Darnell, Kerr and Stark 1994: JAK-STAT pathways and transcriptional activation by interferons](https://onco.cc/key-papers/paper-darnell-jak-stat-science-1994/)
- technologies: [Aspirin for cancer prevention and adjuvant therapy](https://onco.cc/technologies/aspirin-cancer-prevention/)
- targets: [Interleukin-6 and IL-6 receptor](https://onco.cc/targets/il6/)
- institutions: [UC San Diego Moores Cancer Center](https://onco.cc/institutions/ucsd-moores/), [University Cancer Center Frankfurt (UCT)](https://onco.cc/institutions/uct-frankfurt/)
- pathways: [Inflammation & NF-κB](https://onco.cc/pathways/inflammation-nfkb/), [JAK-STAT signalling](https://onco.cc/pathways/jak-stat/)
- terms: [Enabling characteristic: tumour-promoting inflammation](https://onco.cc/terms/tumor-promoting-inflammation/), [Inflammation](https://onco.cc/terms/inflammation/)
- people: [Florian R. Greten](https://onco.cc/people/florian-greten/)

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