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  • RSPO2 abnormal transcripts result from read-through in liver tumours with high ß-catenin activation and CTNNB1 mutations

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RSPO2 abnormal transcripts result from read-through in liver tumours with high ß-catenin activation and CTNNB1 mutations
  1. Quentin Bayard1,2,
  2. Jean-Charles Nault1,2,3,
  3. Jessica Zucman-Rossi1,2,4
  1. 1 Centre de Recherche des Cordeliers, Inserm, Paris, France
  2. 2 Université de Paris, Sorbonne Université, Paris, France
  3. 3 Hepatology Department, Hopital Jean Verdier, APHP, Université Paris 13, Bondy, France
  4. 4 Oncology Department, Hopital Européen Georges Pompidou, APHP, Paris, France
  1. Correspondence to Professor Jessica Zucman-Rossi, Centre de Recherche des Cordeliers, Paris 75006, France; jessica.zucman-rossi{at}inserm.fr

http://dx.doi.org/10.1136/gutjnl-2019-319089

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    Thomas Longerich and collaborators1 recently published an intriguing observation in hepatocellular adenoma (HCA) showing an activation of the Wnt/ß-catenin signalling pathway without CTNNB1 or APC mutations. The authors identified a recurrent deletion leading to a fusion between a short interspersed nuclear element (SINE) sequence and RSPO2 gene in three HCAs and three hepatocellular carcinomas (HCCs) all activated for ß-catenin, including one tumour with CTNNB1 mutations and five tumours without APC or CTNNB1 mutations. The authors proposed RSPO2fusion as a recurrent mechanism of ß-catenin activation in liver tumourigenesis.

    Following this original observation, we analysed the expression and rearrangement of RSPO2 in a series of 10 HCAs and 163 HCCs analysed with RNAseq. We identified a correlation of RSPO2 mRNA expression with several genes known to be positively …

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    Footnotes

    • Contributors J-CN, QB and JZ-R: generation and analysis of data, and writing and approval of the manuscript.

    • Competing interests None declared.

    • Provenance and peer review Not commissioned; internally peer reviewed.

    • Patient consent for publication Not required.