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Suppression of lung adenocarcinoma progression by Nkx2-1

Author

Listed:
  • Monte M. Winslow

    (David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
    Ludwig Center for Molecular Oncology, Massachusetts Institute of Technology)

  • Talya L. Dayton

    (David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology)

  • Roel G. W. Verhaak

    (Dana-Farber Cancer Institute, Harvard University
    Broad Institute)

  • Caroline Kim-Kiselak

    (David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
    Ludwig Center for Molecular Oncology, Massachusetts Institute of Technology)

  • Eric L. Snyder

    (David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology)

  • David M. Feldser

    (David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology)

  • Diana D. Hubbard

    (Dana-Farber Cancer Institute, Harvard University
    Broad Institute)

  • Michel J. DuPage

    (David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology)

  • Charles A. Whittaker

    (David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology)

  • Sebastian Hoersch

    (David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology)

  • Stephanie Yoon

    (David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology)

  • Denise Crowley

    (David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology)

  • Roderick T. Bronson

    (Tufts University Veterinary School)

  • Derek Y. Chiang

    (Dana-Farber Cancer Institute, Harvard University
    Broad Institute
    University of North Carolina)

  • Matthew Meyerson

    (Dana-Farber Cancer Institute, Harvard University
    Broad Institute)

  • Tyler Jacks

    (David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
    Ludwig Center for Molecular Oncology, Massachusetts Institute of Technology
    Massachusetts Institute of Technology
    Howard Hughes Medical Institute, Massachusetts Institute of Technology)

Abstract

Nkx2-1 as an oncogene and tumour-suppressor In a mouse model of lung cancer driven by activated K-Ras and p53 loss, Jacks and colleagues describe a method for tracing individual metastases back to the primary tumours, allowing non-metastatic lesions to be distinguished from metastatic lesions in the same animal. A comparison of gene-expression signatures between metastatic and non-metastatic tumours with human lung cancers led to the identification of Nkx2-1/TTF-1 as a gene that is down-regulated during tumour progression in mice, and associated with poorer outcome in patients. Nkx2-1 loss promotes metastasis at least in part by regulating Hmga2, resulting in de-differentiation. Thus Nkx2-1, previously identified as a lung-cancer oncogene, can also function as a suppressor of lung-cancer progression.

Suggested Citation

  • Monte M. Winslow & Talya L. Dayton & Roel G. W. Verhaak & Caroline Kim-Kiselak & Eric L. Snyder & David M. Feldser & Diana D. Hubbard & Michel J. DuPage & Charles A. Whittaker & Sebastian Hoersch & St, 2011. "Suppression of lung adenocarcinoma progression by Nkx2-1," Nature, Nature, vol. 473(7345), pages 101-104, May.
    • Handle: RePEc:nat:nature:v:473:y:2011:i:7345:d:10.1038_nature09881
    DOI: 10.1038/nature09881
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    Cited by:

    1. Zhiyuan Cheng & Ning Cheng & Dian Shi & Xiaoyu Ren & Ting Gan & Yana Bai & Kehu Yang, 2019. "The Relationship between Nkx2.1 and DNA Oxidative Damage Repair in Nickel Smelting Workers: Jinchang Cohort Study," IJERPH, MDPI, vol. 16(1), pages 1-15, January.

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