Genome-Wide Analysis of DNA Copy Number Changes in Liver Steatosis
Félix Royo, Amaia Zabala, Nerea Paz, Francesco Acquadro, José J. Echevarria, Iñaki Zabalza, Juan C. Cigudosa, José L. Zugaza, Luis A. Parada
Journal of Advances in Medicine and Medical Research · pp. 1773–1785 · Published 5 Jun 2013
10.9734/BJMMR/2013/2543Abstract
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.
Cited by 3
Ana F. Vega-Benedetti, Cinthia N. Saucedo, Patrizia Zavattari · Oncotarget · 2018
Shamsul Mohd Zain, Zahurin Mohamed, Munir Pirmohamed · Scientific Reports · 2015
Shamsul Mohd Zain, Rosmawati Mohamed, David N. Cooper · PLoS ONE · 2014
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