ArticlePloS one2014
Genome-wide analysis of copy number variation identifies candidate gene loci associated with the progression of non-alcoholic fatty liver disease.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- Genetic Polymorphisms and Diversity in Nonalcoholic Fatty Liver Disease (NAFLD): A Mini Review.Biomedicines · 2022Review
- Update on genetics and epigenetics in metabolic associated fatty liver disease.Therapeutic advances in endocrinology and metabolism · 2022Review
- Hepatocellular Carcinoma in Non-Alcoholic Fatty Liver Disease: From Epidemiology to Diagnostic Approach.Cancers · 2021Review
- Nonalcoholic fatty liver disease and hepatocellular carcinoma: Distinct links.Journal of the Chinese Medical Association : JCMA · 2021Article
- Hepatocellular carcinoma in alcoholic and non-alcoholic fatty liver disease-one of a kind or two different enemies?Translational gastroenterology and hepatology · 2019Review
- Molecular Pathogenesis of Nonalcoholic Steatohepatitis- (NASH-) Related Hepatocellular Carcinoma.Canadian journal of gastroenterology & hepatology · 2018Review
- Prediction of early-stage hepatocellular carcinoma using OncoScan chromosomal copy number aberration data.World journal of gastroenterology · 2017Article
- Overactivation of intestinal sterol response element-binding protein 2 promotes diet-induced nonalcoholic steatohepatitis.American journal of physiology. Gastrointestinal and liver physiology · 2017Article
- Acyl-CoA Thioesterase 1 (ACOT1) Regulates PPARα to Couple Fatty Acid Flux With Oxidative Capacity During Fasting.Diabetes · 2017Article
- Type 2 diabetes mellitus and risk of hepatocellular carcinoma: spotlight on nonalcoholic fatty liver disease.Annals of translational medicine · 2017Review
- Type 2 Diabetes and Hepatocellular Carcinoma: Risk Factors and Pathogenesis.Current diabetes reports · 2017Review
- Development of an in vitro model to test antifibrotic drugs on primary human liver myofibroblasts.Laboratory investigation; a journal of technical methods and pathology · 2016Article
- Genetic and epigenetic mechanisms of NASH.Hepatology international · 2016Review
- Copy number variation in exportin-4 (XPO4) gene and its association with histological severity of non-alcoholic fatty liver disease.Scientific reports · 2015Article
- Multidisciplinary perspective of hepatocellular carcinoma: A Pacific Northwest experience.World journal of hepatology · 2015Review
- Chemokine ligand 2 and paraoxonase-1 in non-alcoholic fatty liver disease: The search for alternative causative factors.World journal of gastroenterology · 2015Review
- Living with Fibrosis: From Diagnosis to Future Hope.Frontiers in pharmacology · 2015Article
- DNA markers in molecular diagnostics for hepatocellular carcinoma.Expert review of molecular diagnostics · 2014Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Between 10 and 25% of individuals with non-alcoholic fatty liver disease (NAFLD) develop hepatic fibrosis leading to cirrhosis and hepatocellular carcinoma (HCC). To investigate the molecular basis of disease progression, we performed a genome-wide analysis of copy number variation (CNV) in a total of 49 patients with NAFLD [10 simple steatosis and 39 non-alcoholic steatohepatitis (NASH)] and 49 matched controls using high-density comparative genomic hybridization (CGH) microarrays. A total of 11 CNVs were found to be unique to individuals with simple steatosis, whilst 22 were common between simple steatosis and NASH, and 224 were unique to NASH. We postulated that these CNVs could be involved in the pathogenesis of NAFLD progression. After stringent filtering, we identified four rare and/or novel CNVs that may influence the pathogenesis of NASH. Two of these CNVs, located at 13q12.11 and 12q13.2 respectively, harbour the exportin 4 (XPO4) and phosphodiesterase 1B (PDE1B) genes which are already known to be involved in the etiology of liver cirrhosis and HCC. Cross-comparison of the genes located at these four CNV loci with genes already known to be associated with NAFLD yielded a set of genes associated with shared biological processes including cell death, the key process involved in 'second hit' hepatic injury. To our knowledge, this pilot study is the first to provide CNV information of potential relevance to the NAFLD spectrum. These data could prove invaluable in predicting patients at risk of developing NAFLD and more importantly, those who will subsequently progress to NASH.
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