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Genomic profiling of hepatocellular adenomas reveals recurrent FRK-activating mutations and the mechanisms of malignant transformation.

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Author information

Affiliations

  • 1. INSERM, UMR-1162, Génomique fonctionnelle des tumeurs solides, IUH, 75010 Paris, France; Labex Immuno-oncology, Université Paris Descartes, Sorbonne Paris Cité, Faculté de Médecine, 75006 Paris, France.
      Authors
    • Pilati C 1
    • Nault JC 1
    • Imbeaud S 1
    • Boulai A 1
    • Poussin K 1
    • Franconi A 1
    • Couchy G 1
    • Morcrette G 1
    • Mallet M 1
    (9 authors)
  • 2. Programme Cartes d'Identité des Tumeurs, Ligue Nationale Contre le Cancer, 75013 Paris, France.
      Authors
    • Letouzé E 2
    (1 author)
  • 3. INSERM, UMR-1162, Génomique fonctionnelle des tumeurs solides, IUH, 75010 Paris, France; Labex Immuno-oncology, Université Paris Descartes, Sorbonne Paris Cité, Faculté de Médecine, 75006 Paris, France; Department of Pathology, Assistance Publique-Hôpitaux de Paris, CHU Henri Mondor, 94000 Créteil, France.
      Authors
    • Calderaro J 3
    (1 author)
  • 4. INSERM, UMR-1053, Université de Bordeaux, 33076 Bordeaux, France.
      Authors
    • Taouji S 4
    • Balabaud C 4
    • Chevet E 4
    (3 authors)
  • 5. Department of Pathology, Assistance Publique-Hôpitaux de Paris, Cochin Hospital, 75014 Paris, France.
      Authors
    • Terris B 5
    (1 author)
    • Show all (13)

ORCIDs linked to this article

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Cancer Cell, 01 Apr 2014, 25(4):428-441
https://doi.org/10.1016/j.ccr.2014.03.005 PMID: 24735922 

A comment on this article appears in "Next-generation genomic profiling of hepatocellular adenomas: a new era of individualized patient care." Cancer Cell. 2014 Apr 14;25(4):409-11.

Abstract 

Hepatocellular adenomas (HCA) are benign liver tumors predominantly developed in women using oral contraceptives. Here, exome sequencing identified recurrent somatic FRK mutations that induce constitutive kinase activity, STAT3 activation, and cell proliferation sensitive to Src inhibitors. We also found uncommon recurrent mutations activating JAK1, gp130, or β-catenin. Chromosome copy number and methylation profiling revealed patterns that correlated with specific gene mutations and tumor phenotypes. Finally, integrative analysis of HCAs transformed to hepatocellular carcinoma revealed β-catenin mutation as an early alteration and TERT promoter mutations as associated with the last step of the adenoma-carcinoma transition. In conclusion, we identified the genomic diversity in benign hepatocyte proliferation, several therapeutic targets, and the key genomic determinants of the adenoma-carcinoma transformation sequence.

Full text links 

Read article at publisher's site: https://doi.org/10.1016/j.ccr.2014.03.005

Read article for free, from open access legal sources, via Unpaywall: http://www.cell.com/article/S1535610814000907/pdfUnpaywall

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