Genome-Wide Analysis of DNA Copy Number Changes in Liver Steatosis
Félix Royo
CIC bioGUNE-CIBERehd, Par. Tec. Bizkaia, Derio, Spain.
Amaia Zabala
CIC bioGUNE, Par. Tec. Bizkaia, Derio, Spain.
Nerea Paz
Department of Genetics, Physic Anthropology and Animal Physiology, Faculty of Medicine and Dentistry, University of the Basque Country, Barrio Sarriena s/n, 48940 Leioa, Spain.
Francesco Acquadro
Molecular Cytogenetics Group, Spanish Nacional Cancer Research Centre (CNIO), Madrid, Spain.
José J. Echevarria
Department of Vascular and Interventional Radiology, Galdakao-Usansolo Hospital, Basque Country, Spain.
Iñaki Zabalza
Department of Pathology, Galdakao-Usansolo Hospital, Basque Country, Spain.
Juan C. Cigudosa
Molecular Cytogenetics Group, Spanish Nacional Cancer Research Centre (CNIO), Madrid, Spain.
José L. Zugaza
Department of Genetics, Physic Anthropology and Animal Physiology, Faculty of Medicine and Dentistry, University of the Basque Country, Barrio Sarriena s/n, 48940 Leioa, Spain and Achucarro Basque Center for Neuroscience, Bizkaia Science and Technology Park, Bg 205, Zamudio, Spain. IKERBASQUE, Basque Foundation for Science, Bilbao, Spain.
Luis A. Parada *
Institute of Experimental Pathology, Faculty of Health Sciences, National University of Salta, 4400-Salta, Argentina.
*Author to whom correspondence should be addressed.
Abstract
Aims: Liver steatosis is the most common benign form of non-alcoholic fatty liver disease. It might be a risk factor for hepatocellular carcinoma, either (i) by causing fibrosis, which highly predisposes to hepatoma, or (ii) by being an early precursor of carcinoma, although it is usually considered not to be pre-neoplastic. We investigated the genomic profile of liver samples from patients with fatty liver disease.
Study Design & Methodology: Copy number variation was investigated by array-CGH, using the Human Genome 244K catalogue array (Agilent Technologies), and changes validated by quantitative polymerase chain reaction analysis.
Results: The analysis of liver biopsies from 17 patients, 10 of whom had histological diagnosis of non-alcoholic fatty liver disease, showed differences in the type of variants in patients with steatosis compared to those without steatosis at several chromosome bands, including 3q29, 6p2, 11q11 and 22q11.
Conclusion: The genomic copy number changes we have demonstrated suggest that genomic structural variations may be associated with the pathogenesis or the evolution of steatosis.
Keywords: Array-CGH, chromosome, CNV, genomic profile, liver steatosis