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Leukocytes found within the HCC microenvironment are implicated as regulators of tumour growth. We show that diethylnitrosamine (DEN)-induced murine HCC is attenuated by antibody-mediated depletion of hepatic neutrophils, the latter stimulating hepatocellular ROS and telomere DNA damage. We additionally report a previously unappreciated tumour suppressor function for hepatocellular\n                    <jats:italic>nfkb1<\/jats:italic>\n                    operating via p50:p50 dimers and the co-repressor HDAC1. These anti-inflammatory proteins combine to transcriptionally repress hepatic expression of a S100A8\/9, CXCL1 and CXCL2 neutrophil chemokine network. Loss of\n                    <jats:italic>nfkb1<\/jats:italic>\n                    promotes ageing-associated chronic liver disease (CLD), characterized by steatosis, neutrophillia, fibrosis, hepatocyte telomere damage and HCC.\n                    <jats:italic>Nfkb1<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>S340A\/S340A<\/jats:italic>\n                    <\/jats:sup>\n                    mice carrying a mutation designed to selectively disrupt p50:p50:HDAC1 complexes are more susceptible to HCC; by contrast, mice lacking S100A9 express reduced neutrophil chemokines and are protected from HCC. Inhibiting neutrophil accumulation in CLD or targeting their tumour-promoting activities may offer therapeutic opportunities in HCC.\n                  <\/jats:p>","DOI":"10.1038\/ncomms7818","type":"journal-article","created":{"date-parts":[[2015,4,16]],"date-time":"2015-04-16T09:02:49Z","timestamp":1429174969000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":141,"title":["NF\u03baB1 is a suppressor of neutrophil-driven hepatocellular carcinoma"],"prefix":"10.1038","volume":"6","author":[{"given":"C. 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