Preclinical efficacy of MEK inhibition in Nras-mutant AML

  • Michael R. Burgess
    Divisions of Hematology/Oncology, Department of Medicine and
  • Eugene Hwang
    Department of Pediatrics, University of California San Francisco, San Francisco, CA;
  • Ari J. Firestone
    Department of Pediatrics, University of California San Francisco, San Francisco, CA;
  • Tannie Huang
    Department of Pediatrics, University of California San Francisco, San Francisco, CA;
  • Jin Xu
    Department of Pediatrics, University of California San Francisco, San Francisco, CA;
  • Johannes Zuber
    Research Institute of Molecular Pathology, Vienna, Austria;
  • Natacha Bohin
    Department of Medicine, Division of Hematology/Oncology, University of Michigan, Ann Arbor, MI;
  • Tiffany Wen
    Department of Medicine, Division of Hematology/Oncology, University of Michigan, Ann Arbor, MI;
  • Scott C. Kogan
    Laboratory Medicine, University of California, San Francisco, San Francisco, CA;
  • Kevin M. Haigis
    Molecular Pathology Unit and Center for Cancer Research, Massachusetts General Hospital, Charlestown, MA;
  • Deepak Sampath
    Department of Translational Oncology, Genentech Inc., South San Francisco, CA;
  • Scott Lowe
    Howard Hughes Medical Institute;
  • Kevin Shannon
    Department of Pediatrics, University of California San Francisco, San Francisco, CA;
  • Qing Li
    Department of Medicine, Division of Hematology/Oncology, University of Michigan, Ann Arbor, MI;

書誌事項

公開日
2014-12-18
DOI
  • 10.1182/blood-2014-05-574582
公開者
American Society of Hematology

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説明

<jats:title>Key Points</jats:title> <jats:p>N-Ras expression is essential for the proliferative advantage of acute myeloid leukemias with oncogenic NRAS/Nras mutations. Mitogen-activated protein kinase kinase inhibition prolongs survival in Nras-mutant AML by reducing proliferation, but fails to undergo apoptosis.</jats:p>

収録刊行物

  • Blood

    Blood 124 (26), 3947-3955, 2014-12-18

    American Society of Hematology

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