{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Laskowski J"],"funding":["NCATS NIH HHS","NIDDK NIH HHS","NCI NIH HHS","National Institutes of Health","Wellcome Trust","NIH HHS"],"pagination":["4039-4054"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7410061"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["130(8)"],"pubmed_abstract":["Hepatocellular carcinoma (HCC) is difficult to detect, carries a poor prognosis, and is one of few cancers with an increasing yearly incidence. Molecular defects in complement factor H (CFH), a critical regulatory protein of the complement alternative pathway (AP), are typically associated with inflammatory diseases of the eye and kidney. Little is known regarding the role of CFH in controlling complement activation within the liver. While studying aging CFH-deficient (fH-/-) mice, we observed spontaneous hepatic tumor formation in more than 50% of aged fH-/- males. Examination of fH-/- livers (3-24 months) for evidence of complement-mediated inflammation revealed widespread deposition of complement-activation fragments throughout the sinusoids, elevated transaminase levels, increased hepa"],"journal":["The Journal of clinical investigation"],"pubmed_title":["Complement factor H-deficient mice develop spontaneous hepatic tumors."],"pmcid":["PMC7410061"],"funding_grant_id":["P30 CA046934","CA225840","R01 DK076690","R01 DK113586","S10 OD023485","DK076690","R01 CA236222","DK113586","212252/Z/18/Z","UL1 TR001082"],"pubmed_authors":["Smith-Jones PM","Thurman JM","Serkova NJ","Laskowski J","Renner B","Nemenoff RA","Pickering MC","Clambey ET"],"additional_accession":[]},"is_claimable":false,"name":"Complement factor H-deficient mice develop spontaneous hepatic tumors.","description":"Hepatocellular carcinoma (HCC) is difficult to detect, carries a poor prognosis, and is one of few cancers with an increasing yearly incidence. Molecular defects in complement factor H (CFH), a critical regulatory protein of the complement alternative pathway (AP), are typically associated with inflammatory diseases of the eye and kidney. Little is known regarding the role of CFH in controlling complement activation within the liver. While studying aging CFH-deficient (fH-/-) mice, we observed spontaneous hepatic tumor formation in more than 50% of aged fH-/- males. Examination of fH-/- livers (3-24 months) for evidence of complement-mediated inflammation revealed widespread deposition of complement-activation fragments throughout the sinusoids, elevated transaminase levels, increased hepa","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Aug","modification":"2026-05-03T22:15:30.423Z","creation":"2025-02-19T01:01:13.951Z"},"accession":"S-EPMC7410061","cross_references":{"pubmed":["32369457"],"doi":["10.1172/JCI135105","10.1172/jci135105"]}}