<i>PDGFRA</i> Activating Mutations in Gastrointestinal Stromal Tumors

DOI Web Site 被引用文献100件
  • Michael C. Heinrich
    Department of Medicine,
  • Christopher L. Corless
    Department of Pathology, Oregon Health & Science University Cancer Institute and Portland VA Medical Center, Portland, OR 97201, USA.
  • Anette Duensing
    Department of Pathology, Brigham and Women's Hospital, 75 Francis Street, Boston, MA 02115, USA, and Harvard Medical School, Boston, MA 02115, USA.
  • Laura McGreevey
    Department of Medicine,
  • Chang-Jie Chen
    Department of Pathology, Brigham and Women's Hospital, 75 Francis Street, Boston, MA 02115, USA, and Harvard Medical School, Boston, MA 02115, USA.
  • Nora Joseph
    Department of Pathology, Brigham and Women's Hospital, 75 Francis Street, Boston, MA 02115, USA, and Harvard Medical School, Boston, MA 02115, USA.
  • Samuel Singer
    Department of Surgery, Memorial Sloan-Kettering Cancer Institute, New York, NY 10021, USA.
  • Diana J. Griffith
    Department of Medicine,
  • Andrea Haley
    Department of Medicine,
  • Ajia Town
    Department of Medicine,
  • George D. Demetri
    Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA.
  • Christopher D. M. Fletcher
    Department of Pathology, Brigham and Women's Hospital, 75 Francis Street, Boston, MA 02115, USA, and Harvard Medical School, Boston, MA 02115, USA.
  • Jonathan A. Fletcher
    Department of Pathology, Brigham and Women's Hospital, 75 Francis Street, Boston, MA 02115, USA, and Harvard Medical School, Boston, MA 02115, USA.

抄録

<jats:p> Most gastrointestinal stromal tumors (GISTs) have activating mutations in the KIT receptor tyrosine kinase, and most patients with GISTs respond well to Gleevec, which inhibits KIT kinase activity. Here we show that ∼35% (14 of 40) of GISTs lacking <jats:italic>KIT</jats:italic> mutations have intragenic activation mutations in the related receptor tyrosine kinase, platelet-derived growth factor receptor α ( <jats:italic>PDGFRA</jats:italic> ). Tumors expressing KIT or PDGFRA oncoproteins were indistinguishable with respect to activation of downstream signaling intermediates and cytogenetic changes associated with tumor progression. Thus, <jats:italic>KIT</jats:italic> and <jats:italic>PDGFRA</jats:italic> mutations appear to be alternative and mutually exclusive oncogenic mechanisms in GISTs. </jats:p>

収録刊行物

  • Science

    Science 299 (5607), 708-710, 2003-01-31

    American Association for the Advancement of Science (AAAS)

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