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We read with interest the work by Chen et al1 who reported the decreased risk for developing hepatocellular carcinoma (HCC) in patients treated with metformin in a dose-dependent and time-dependent manner. Indeed, the metabolic syndrome (MS) is becoming one of the leading risk factors for liver carcinogenesis, mainly through the presence of diabetes.2 ,3 In addition to clinical data confirming previous studies,4 Chen et al1 were the first to highlight experimental antitumoral effects of metformin both on hepatoma cell lines and on murine models through cell-cycle arrest via AMPK activation. However, whether these results are transposable in a clinical setting of HCC occurring in the specific context of MS has to date remained uncertain.
To address this issue, we analysed a series of eight surgically resected HCC samples obtained from diabetic patients with MS preoperatively receiving (n=4) or not metformin (n=4) for antidiabetic purpose. Their clinicopathological characteristics …