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A novel genetic marker of liver disease aetiology in hepatocellular carcinoma: culling the metabolic syndrome
  1. Elizabeth M Brunt
  1. Correspondence to Dr Elizabeth M Brunt, Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA; ebrunt{at}

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Paradis et al 1 describe the work in which they identified CUL7 as a unique target gene in metabolic syndrome-related hepatocellular carcinoma (HCC). The increased worldwide prevalence and incidence of liver disease related to metabolic syndrome2 are noted as factors in the changing epidemiology and demographics of HCC, especially in otherwise ‘low-risk’ regions.3–5 Although this highly lethal malignancy remains most commonly associated with underlying cirrhosis secondary to viral hepatitis C or B,6 ,7 or alcohol,7 there is growing acceptance of the role of non-alcoholic steatohepatitis as another chronic liver disease that may predispose to the subsequent genetic and molecular aberrations that result in malignancy. Furthermore, investigators are showing the existence of an alarming trend in the evolution of HCC in the presence of metabolic syndrome before advanced fibrosis or cirrhosis.3 ,8 The implications for clinical management are apparent.

The group of Paradis et al,1 started with a comparative genomic hybridisation analysis that showed amplification in 6p21.1. Another gene that resides in the …

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  • Competing interest None.

  • Provenance and peer review Commissioned; externally peer reviewed.

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