<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>22(1)</volume><submitter>Hymel E</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>Nonalcoholic fatty liver disease affects about 24% of the world's population and may progress to nonalcoholic steatohepatitis (NASH), cirrhosis, and hepatocellular carcinoma (HCC). While more common in those that are obese, NASH-HCC can develop in lean individuals. The mechanisms by which HCC develops and the role of epigenetic changes in the context of obesity and normal weight are not well understood.&lt;h4>Methods&lt;/h4>In this study, we used previously generated mouse models of lean and obese HCC using a choline deficient/high trans-fat/fructose/cholesterol diet and a choline supplemented/high trans-fat/fructose/cholesterol diet, respectively, to evaluate methylation differences in HCC progression in lean versus obese mice. Differentially methylated regions were determine</pubmed_abstract><journal>BMC cancer</journal><pagination>1276</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9727966</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Differential methylation patterns in lean and obese non-alcoholic steatohepatitis-associated hepatocellular carcinoma.</pubmed_title><pmcid>PMC9727966</pmcid><pubmed_authors>Hymel E</pubmed_authors><pubmed_authors>Farazi PA</pubmed_authors><pubmed_authors>Fisher KW</pubmed_authors></additional><is_claimable>false</is_claimable><name>Differential methylation patterns in lean and obese non-alcoholic steatohepatitis-associated hepatocellular carcinoma.</name><description>&lt;h4>Background&lt;/h4>Nonalcoholic fatty liver disease affects about 24% of the world's population and may progress to nonalcoholic steatohepatitis (NASH), cirrhosis, and hepatocellular carcinoma (HCC). While more common in those that are obese, NASH-HCC can develop in lean individuals. The mechanisms by which HCC develops and the role of epigenetic changes in the context of obesity and normal weight are not well understood.&lt;h4>Methods&lt;/h4>In this study, we used previously generated mouse models of lean and obese HCC using a choline deficient/high trans-fat/fructose/cholesterol diet and a choline supplemented/high trans-fat/fructose/cholesterol diet, respectively, to evaluate methylation differences in HCC progression in lean versus obese mice. Differentially methylated regions were determine</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Dec</publication><modification>2025-04-19T06:36:21.891Z</modification><creation>2025-04-19T06:36:21.891Z</creation></dates><accession>S-EPMC9727966</accession><cross_references><pubmed>36474183</pubmed><doi>10.1186/s12885-022-10389-7</doi></cross_references></HashMap>