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XPO1-dependent nuclear export is a druggable vulnerability in KRAS-mutant lung cancer

Author

Listed:
  • Jimi Kim

    (UTSW Medical Center)

  • Elizabeth McMillan

    (UTSW Medical Center)

  • Hyun Seok Kim

    (Severance Biomedical Science Institute, Yonsei University College of Medicine)

  • Niranjan Venkateswaran

    (Internal Medicine, UTSW Medical Center)

  • Gurbani Makkar

    (UTSW Medical Center)

  • Jaime Rodriguez-Canales

    (MD Anderson Cancer Center)

  • Pamela Villalobos

    (MD Anderson Cancer Center)

  • Jasper Edgar Neggers

    (KU Leuven Department of Microbiology and Immunology)

  • Saurabh Mendiratta

    (UTSW Medical Center)

  • Shuguang Wei

    (Biochemistry, UTSW Medical Center)

  • Yosef Landesman

    (Karyopharm Therapeutics)

  • William Senapedis

    (Karyopharm Therapeutics)

  • Erkan Baloglu

    (Karyopharm Therapeutics)

  • Chi-Wan B. Chow

    (MD Anderson Cancer Center)

  • Robin E. Frink

    (Hamon Center, UTSW Medical Center)

  • Boning Gao

    (Hamon Center, UTSW Medical Center)

  • Michael Roth

    (Biochemistry, UTSW Medical Center)

  • John D. Minna

    (Hamon Center, UTSW Medical Center)

  • Dirk Daelemans

    (KU Leuven Department of Microbiology and Immunology)

  • Ignacio I. Wistuba

    (MD Anderson Cancer Center)

  • Bruce A. Posner

    (Biochemistry, UTSW Medical Center)

  • Pier Paolo Scaglioni

    (Internal Medicine, UTSW Medical Center)

  • Michael A. White

    (UTSW Medical Center)

Abstract

A multi-genomic approach identifies the addiction of KRAS-mutant lung cancer cells to XPO1-dependent nuclear export, offering a new therapeutic opportunity.

Suggested Citation

  • Jimi Kim & Elizabeth McMillan & Hyun Seok Kim & Niranjan Venkateswaran & Gurbani Makkar & Jaime Rodriguez-Canales & Pamela Villalobos & Jasper Edgar Neggers & Saurabh Mendiratta & Shuguang Wei & Yosef, 2016. "XPO1-dependent nuclear export is a druggable vulnerability in KRAS-mutant lung cancer," Nature, Nature, vol. 538(7623), pages 114-117, October.
    • Handle: RePEc:nat:nature:v:538:y:2016:i:7623:d:10.1038_nature19771
    DOI: 10.1038/nature19771
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    Cited by:

    1. Wei Liu & Hongchao Cao & Jing Wang & Areeg Elmusrati & Bing Han & Wei Chen & Ping Zhou & Xiyao Li & Stephen Keysar & Antonio Jimeno & Cun-Yu Wang, 2024. "Histone-methyltransferase KMT2D deficiency impairs the Fanconi anemia/BRCA pathway upon glycolytic inhibition in squamous cell carcinoma," Nature Communications, Nature, vol. 15(1), pages 1-18, December.
    2. Anja Deutzmann & Delaney K. Sullivan & Renumathy Dhanasekaran & Wei Li & Xinyu Chen & Ling Tong & Wadie D. Mahauad-Fernandez & John Bell & Adriane Mosley & Angela N. Koehler & Yulin Li & Dean W. Felsh, 2024. "Nuclear to cytoplasmic transport is a druggable dependency in MYC-driven hepatocellular carcinoma," Nature Communications, Nature, vol. 15(1), pages 1-13, December.

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