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Anti-angiogenic effect of metformin in human liver carcinogenesis related to metabolic syndrome
  1. François Cauchy1,2,
  2. Mouniya Mebarki1,
  3. Miguel Albuquerque3,
  4. Samira Laouirem1,
  5. Pierre Emmanuel Rautou4,
  6. Olivier Soubrane2,
  7. Eric Raymond5,
  8. Pierre Bedossa1,3,
  9. Valérie Paradis1,3
  1. 1 INSERM UMR1149, Inflammation Research Center, Paris-Diderot University, Paris, France
  2. 2 Hepatobiliary Surgery and Liver Transplantation Department, Beaujon Hospital, APHP, Clichy, France
  3. 3 Pathology Department, Beaujon Hospital, APHP, Clichy, France
  4. 4 Hepatology Department, Beaujon Hospital, APHP, Clichy, France
  5. 5 Oncology Department, Beaujon Hospital, APHP, Clichy, France
  1. Correspondence to Professor Valérie Paradis, Department of Pathology, Beaujon Hospital, Assistance Publique-Hôpitaux de Paris, 100 Boulevard du Général Leclerc, Clichy 92110, France; vparadis{at}

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Dear Editor,

We read with interest the work by Chen et al 1 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 al 1 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 …

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