IDEAS home Printed from https://ideas.repec.org/a/nat/nature/v480y2011i7377d10.1038_nature10662.html
   My bibliography  Save this article

RAF inhibitor resistance is mediated by dimerization of aberrantly spliced BRAF(V600E)

Author

Listed:
  • Poulikos I. Poulikakos

    (Memorial Sloan-Kettering Cancer Center)

  • Yogindra Persaud

    (Human Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center)

  • Manickam Janakiraman

    (Human Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center)

  • Xiangju Kong

    (Jonsson Comprehensive Cancer Center, University of California at Los Angeles)

  • Charles Ng

    (Jonsson Comprehensive Cancer Center, University of California at Los Angeles)

  • Gatien Moriceau

    (Jonsson Comprehensive Cancer Center, University of California at Los Angeles)

  • Hubing Shi

    (Jonsson Comprehensive Cancer Center, University of California at Los Angeles)

  • Mohammad Atefi

    (Jonsson Comprehensive Cancer Center, University of California at Los Angeles)

  • Bjoern Titz

    (Jonsson Comprehensive Cancer Center, University of California at Los Angeles)

  • May Tal Gabay

    (Memorial Sloan-Kettering Cancer Center)

  • Maayan Salton

    (National Cancer Institute, NIH)

  • Kimberly B. Dahlman

    (Vanderbilt-Ingram Cancer Center)

  • Madhavi Tadi

    (Memorial Sloan-Kettering Cancer Center)

  • Jennifer A. Wargo

    (Massachusetts General Hospital Cancer Center)

  • Keith T. Flaherty

    (Massachusetts General Hospital Cancer Center)

  • Mark C. Kelley

    (Vanderbilt-Ingram Cancer Center)

  • Tom Misteli

    (National Cancer Institute, NIH)

  • Paul B. Chapman

    (Memorial Sloan-Kettering Cancer Center)

  • Jeffrey A. Sosman

    (Vanderbilt-Ingram Cancer Center)

  • Thomas G. Graeber

    (Jonsson Comprehensive Cancer Center, University of California at Los Angeles)

  • Antoni Ribas

    (Jonsson Comprehensive Cancer Center, University of California at Los Angeles
    Jonsson Comprehensive Cancer Center, University of California at Los Angeles)

  • Roger S. Lo

    (Jonsson Comprehensive Cancer Center, University of California at Los Angeles
    Jonsson Comprehensive Cancer Center, University of California at Los Angeles)

  • Neal Rosen

    (Memorial Sloan-Kettering Cancer Center
    Memorial Sloan-Kettering Cancer Center)

  • David B. Solit

    (Human Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center
    Memorial Sloan-Kettering Cancer Center)

Abstract

Although clinical trials have shown that RAF inhibitors prolong the survival of patients with BRAF-mutant melanoma, resistance inevitably develops; resistance is shown here to be frequently mediated by the expression of splicing variants of mutant BRAF.

Suggested Citation

  • Poulikos I. Poulikakos & Yogindra Persaud & Manickam Janakiraman & Xiangju Kong & Charles Ng & Gatien Moriceau & Hubing Shi & Mohammad Atefi & Bjoern Titz & May Tal Gabay & Maayan Salton & Kimberly B., 2011. "RAF inhibitor resistance is mediated by dimerization of aberrantly spliced BRAF(V600E)," Nature, Nature, vol. 480(7377), pages 387-390, December.
    • Handle: RePEc:nat:nature:v:480:y:2011:i:7377:d:10.1038_nature10662
    DOI: 10.1038/nature10662
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/nature10662
    File Function: Abstract
    Download Restriction: Access to the full text of the articles in this series is restricted.
    File URL: https://libkey.io/10.1038/nature10662?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    As the access to this document is restricted, you may want to search for a different version of it.

    Citations

    Citations are extracted by the CitEc Project, subscribe to its RSS feed for this item.
    as


    Cited by:

    1. Jiaxin Liang & Deyang Yu & Chi Luo & Christopher Bennett & Mark Jedrychowski & Steve P. Gygi & Hans R. Widlund & Pere Puigserver, 2023. "Epigenetic suppression of PGC1α (PPARGC1A) causes collateral sensitivity to HMGCR-inhibitors within BRAF-treatment resistant melanomas," Nature Communications, Nature, vol. 14(1), pages 1-12, December.
    2. Gholamreza Safaee Ardekani & Seyed Mehdi Jafarnejad & Larry Tan & Ardavan Saeedi & Gang Li, 2012. "The Prognostic Value of BRAF Mutation in Colorectal Cancer and Melanoma: A Systematic Review and Meta-Analysis," PLOS ONE, Public Library of Science, vol. 7(10), pages 1-10, October.

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:nature:v:480:y:2011:i:7377:d:10.1038_nature10662. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.