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In Gut, Longerich et al describe the identification of a new gene, RSPO2, involved in the pathogenesis of hepatocellular adenomas (HCA) and of a small fraction of hepatocellular carcinomas (HCC), through the activation of the Wnt/beta-catenin pathway, already known to be involved in the pathogenesis of a significant proportion of liver tumours.1 These results reduce the percentage of so-called ‘unclassified’ HCA, underline the tight relationship of some HCA with HCC and add another piece to the puzzle of the extraordinary clinical and biological diversity of HCA. This prompts several comments, mainly about the ‘HCA story’, but also about general tumour biology.
The ‘HCA story’ is a paradigm of how the better knowledge of a tumour group might form the basis of a better tumour classification and how a better tumour classification might result in an improved management of the patients. At the end of the previous century, HCA were viewed as rare benign liver tumours, occurring mainly in young females in the context of oral contraception.2 Their management was simple: when feasible, surgical resection was performed in all cases in order to prevent sometimes severe complications, such as rupture or bleeding. The risk of malignant transformation was a matter of debate. With the new millennium, started a series of in-depth molecular investigations which definitively changed our understanding of this tumour group, with major consequences on their clinical management and their understanding.3 From what was previously seen as a homogeneous entity, rapidly emerged a much …
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