Focal nodular hyperplasia and hepatocellular adenomas are benign solitary or multiple hepatocellular tumors with different outcomes. It is, therefore, important to differentiate these two types of tumors. So far the risk of HCA bleeding and malignant transformation into hepatocellular carcinoma is based only on size. Molecular signature of HCA subtypes has permitted to better divide FNH from HCA and HCA from HCC and to identify HCA subtypes with different risks of HCC transformation. These advances have allowed to individualize HCA subtypes by immunohistochemistry on liver biopsy and to recognize the 2 major subtypes by imaging. HCA and FNH are thought to occur on the same background, but this is much too restrictive. Due to the rarity of HCA, it has not been possible to set up a consensus regarding treatment and followup of patients with benign hepatocellular tumors.

We invite investigators to contribute original research as well as review articles that will take into account the identification of FNH and HCA subtypes particularly those at risk of bleeding and malignant transformation, the circumstances and mechanisms leading to the formation of FNH and HCC, and the rational therapeutic and follow-up modalities . Potential topics include, but are not limited to:

• Molecular biology of FNH and HCA
• Identification of FNH and HCA by modern imaging technics
• Identification and management of HCA (solitary and multiple) at risk of bleeding and bleeding
• Identification and management of HCA (solitary and multiple) at risk of malignancy and with malignant transformation
• Radiological followup of unresected FNH and HCA
• Vascular involvement in the genesis of FNH and HCA
• Genetic (constitutional) diseases leading to HCA
• HCA and pregnancy

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