{"entity":{"id":"tumor-promoting-inflammation","kind":"term","name":"Enabling characteristic: tumour-promoting inflammation","aka":[],"tldr":"Chronic inflammation supplies growth factors, survival signals, and mutagens that help cancers start and grow.","summary":"Tumour-promoting inflammation is the enabling characteristic by which chronic inflammation supplies growth factors, survival signals and mutagens that help cancers start and grow. The signalling runs through IL-6/STAT3, TNF/NF-κB, COX-2/PGE2 and inflammasomes, described in the Inflammation & NF-κB, JAK-STAT signalling and Microbiome-tumour interactions pathways, and infection-driven cancers (HPV, HBV, Helicobacter pylori) are the clearest examples, as the Oncogenic viruses pathway explains. Prevention rests on HPV & HBV vaccination, anti-infectives and aspirin, covered under Chemoprevention & risk-reducing surgery, while BTK inhibitors shut down NF-κB in B-cell cancers. Readers meet this characteristic from the Hallmarks of Cancer overview and from the Inflammation entry.","asOf":"2026-09-08","wikipedia":"https://en.wikipedia.org/wiki/The_Hallmarks_of_Cancer","links":[{"label":"Hanahan, Hallmarks of Cancer: New Dimensions (Cancer Discovery 2022)","url":"https://doi.org/10.1158/2159-8290.CD-21-1059"}],"tags":["hallmark"],"related":[],"cancers":[],"sections":[],"technologies":["chemoprevention","hpv-vaccine"],"targets":[],"drugs":[],"companies":[],"institutions":[],"pathways":["inflammation-nfkb","jak-stat","microbiome-tumour"],"terms":[],"trials":[],"people":[],"bottlenecks":[],"keyPapers":[],"journals":[],"dependsOn":[],"notes":[],"category":"Cancer biology"},"route":"/terms/tumor-promoting-inflammation/","neighbours":{"technology":[{"id":"chemoprevention","kind":"technology","name":"Chemoprevention & risk-reducing surgery","route":"/technologies/chemoprevention/"},{"id":"hpv-vaccine","kind":"technology","name":"HPV & HBV vaccination","route":"/technologies/hpv-vaccine/"}],"pathway":[{"id":"inflammation-nfkb","kind":"pathway","name":"Inflammation & NF-κB","route":"/pathways/inflammation-nfkb/"},{"id":"jak-stat","kind":"pathway","name":"JAK-STAT signalling","route":"/pathways/jak-stat/"},{"id":"microbiome-tumour","kind":"pathway","name":"Microbiome-tumour interactions","route":"/pathways/microbiome-tumour/"},{"id":"oncogenic-viruses","kind":"pathway","name":"Oncogenic viruses","route":"/pathways/oncogenic-viruses/"}],"target":[{"id":"cox2","kind":"target","name":"COX-2 (PTGS2)","route":"/targets/cox2/"}],"term":[{"id":"hallmarks-of-cancer","kind":"term","name":"Hallmarks of Cancer","route":"/terms/hallmarks-of-cancer/"},{"id":"hallmarks-synthesis","kind":"term","name":"Hallmarks of cancer as a synthesis of the theories","route":"/terms/hallmarks-synthesis/"},{"id":"inflammation","kind":"term","name":"Inflammation","route":"/terms/inflammation/"},{"id":"microenvironment-inflammation-theory","kind":"term","name":"Microenvironment and inflammation: tumours as wounds that do not heal","route":"/terms/microenvironment-inflammation-theory/"}],"paper":[{"id":"paper-grivennikov-immunity-inflammation-cancer-cell-2010","kind":"paper","name":"Grivennikov, Greten and Karin 2010: immunity, inflammation and cancer","route":"/key-papers/paper-grivennikov-immunity-inflammation-cancer-cell-2010/"}]}}