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Somatic mutations in the kinase domain of the MET/hepatocyte growth factor receptor gene in childhood hepatocellular carcinomas

  1. Author:
    Park, W. S.
    Dong, S. M.
    Kim, S. Y.
    Na, E. Y.
    Shin, M. S.
    Pi, J. H.
    Kim, B. J.
    Bae, J. H.
    Hong, Y. K.
    Lee, K. S.
    Lee, S. H.
    Yoo, N. J.
    Jang, J. J.
    Pack, S.
    Zhuang, Z. P.
    Schmidt, L.
    Zbar, B.
    Lee, J. Y.

  2. Author Address

    Lee JY Catholic Univ, Coll Med, Dept Pathol Seoul 137701 South Korea Catholic Univ, Coll Med, Dept Pathol Seoul 137701 South Korea Catholic Univ, Coll Med, Canc Res Inst Seoul 137701 South Korea Seoul Natl Univ, Coll Med, Dept Pathol Seoul 110799 South Korea NCI, Pathol Lab Bethesda, MD 20892 USA NCI, Frederick Canc Res & Dev Ctr, Immunobiol Lab Frederick, MD 21702 USA Sci Applicat Int Corp, Intramural Res Support Program Frederick, MD USA
    1. Year: 1999
  2. Journal: Cancer Research
    1. 59
    2. 2
    3. Pages: 307-310
  4. Type of Article: Article
  1. Abstract:

    The MET protooncogene encodes a transmembrane tyrosine kinase identified as the receptor of a polypeptide known as hepatocyte growth factor/scatter factor. We performed PCR-based single-strand conformational polymorphism and sequencing analysis of the tyrosine kinase domain of the MET gene (exon 15-19) in 75 primary liver cancers. Three missense mutations were detected exclusively in 10 childhood hepatocellular carcinomas (HCCs), while no mutations were detected in 16 adult HCCs, 21 cholangiocarcinomas, or 28 hepatoblastomas. The extremely short incubation period from hepatitis B virus infection to the genesis of childhood HCC as compared with the adult HCC suggests that there may be an additional mechanism that accelerates the carcinogenesis of childhood HCC. Our results indicate that mutations of the tyrosine kinase domain of the MET gene may be involved in the acceleration of the carcinogenesis in childhood HCC. [References: 20]

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