SHORT REPORT
Rare allelic imbalances, but no mutations of the PRDX1 gene in human hepatocellular carcinomas
Department of Pathology, University of Zürich, Schmelzbergstrasse 12, CH-8091 Zürich, Switzerland
Correspondence to:
Correspondence to:
Dr W Jochum
Institute of Clinical Pathology, Department of Pathology, University Zürich, Schmelzbergstrasse 18, CH-8091 Zürich, Switzerland; wolfram.jochum{at}usz.ch
Allelic losses on chromosome 1p are frequent in hepatocellular carcinoma (HCC), suggesting the presence of a tumour suppressor gene in this region. The gene for peroxiredoxin 1 (PRDX1), an antioxidant enzyme, has been mapped to 1p34.1. Mice lacking PRDX1 develop HCC with high frequency. Because oxidative stress has been implicated in the pathogenesis of HCC, this study was designed to determine whether the PRDX1 gene is mutated in human HCC using loss of heterozygosity (LOH) analysis, polymerase chain reaction/denaturing gradient gel electrophoresis, and DNA sequencing. LOH of at least one of four microsatellite markers within 0.8 Mb of the PRDX1 gene was seen in three of 34 informative HCCs, but no mutations or polymorphisms in the translated exons 2–6 of the PRDX1 gene were found. These results suggest that genetic alterations of the PRDX1 locus are rare events in human HCC, indicating that other genes on chromosome 1p contribute to liver carcinogenesis.
Abbreviations: LOH, loss of heterozygosity; PCR, polymerase chain reaction; PRDX1, peroxiredoxin 1; ROS, reactive oxygen species
Keywords: hepatocellular carcinoma; PRDX1; peroxiredoxin; chromosome 1p34; oxidative damage
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