<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Nardo AD</submitter><funding>Austrian Science Fund FWF</funding><pagination>1620-1633</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7384114</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>40(7)</volume><pubmed_abstract>&lt;h4>Background &amp; aims&lt;/h4>Osteopontin, a multifunctional protein and inflammatory cytokine, is overexpressed in adipose tissue and liver in obesity and contributes to the induction of adipose tissue inflammation and non-alcoholic fatty liver (NAFL). Studies performed in both mice and humans also point to a potential role for OPN in malignant transformation and tumour growth. To fully understand the role of OPN on the development of NAFL-derived hepatocellular carcinoma (HCC), we applied a non-alcoholic steatohepatitis (NASH)-HCC mouse model on osteopontin-deficient (Spp1&lt;sup>-/-&lt;/sup> ) mice analysing time points of NASH, fibrosis and HCC compared to wild-type mice.&lt;h4>Methods&lt;/h4>Two-day-old wild-type and Spp1&lt;sup>-/-&lt;/sup> mice received a low-dose streptozotocin injection in order to ind</pubmed_abstract><journal>Liver international : official journal of the International Association for the Study of the Liver</journal><pubmed_title>Impact of osteopontin on the development of non-alcoholic liver disease and related hepatocellular carcinoma.</pubmed_title><pmcid>PMC7384114</pmcid><funding_grant_id>W1205‐B09</funding_grant_id><pubmed_authors>Oberhuber G</pubmed_authors><pubmed_authors>Helbich TH</pubmed_authors><pubmed_authors>Markgraf DF</pubmed_authors><pubmed_authors>Grun NG</pubmed_authors><pubmed_authors>Dumanic M</pubmed_authors><pubmed_authors>Roden M</pubmed_authors><pubmed_authors>Zeyda M</pubmed_authors><pubmed_authors>Nardo AD</pubmed_authors><pubmed_authors>Rivelles E</pubmed_authors><pubmed_authors>Trauner M</pubmed_authors><pubmed_authors>Stulnig TM</pubmed_authors><pubmed_authors>Claudel T</pubmed_authors></additional><is_claimable>false</is_claimable><name>Impact of osteopontin on the development of non-alcoholic liver disease and related hepatocellular carcinoma.</name><description>&lt;h4>Background &amp; aims&lt;/h4>Osteopontin, a multifunctional protein and inflammatory cytokine, is overexpressed in adipose tissue and liver in obesity and contributes to the induction of adipose tissue inflammation and non-alcoholic fatty liver (NAFL). Studies performed in both mice and humans also point to a potential role for OPN in malignant transformation and tumour growth. To fully understand the role of OPN on the development of NAFL-derived hepatocellular carcinoma (HCC), we applied a non-alcoholic steatohepatitis (NASH)-HCC mouse model on osteopontin-deficient (Spp1&lt;sup>-/-&lt;/sup> ) mice analysing time points of NASH, fibrosis and HCC compared to wild-type mice.&lt;h4>Methods&lt;/h4>Two-day-old wild-type and Spp1&lt;sup>-/-&lt;/sup> mice received a low-dose streptozotocin injection in order to ind</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Jul</publication><modification>2025-04-19T23:02:54.917Z</modification><creation>2025-04-19T23:02:54.917Z</creation></dates><accession>S-EPMC7384114</accession><cross_references><pubmed>32281248</pubmed><doi>10.1111/liv.14464</doi></cross_references></HashMap>