Genome-Wide Analysis of DNA Copy Number Changes in Liver Steatosis.
Br J Med Med Res
;
2013 Oct-Dec; 3(4): 1773-1785
Article
in English
| IMSEAR
| ID: sea-163056
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.
Full text:
Available
Index:
IMSEAR (South-East Asia)
Type of study:
Risk factors
Language:
English
Journal:
Br J Med Med Res
Year:
2013
Type:
Article
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