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Requirement for NF-κB signalling in a mouse model of lung adenocarcinoma

Author

Listed:
  • Etienne Meylan

    (Koch Institute for Integrative Cancer Research, and Howard Hughes Medical Institute, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, Massachusetts 02139, USA)

  • Alison L. Dooley

    (Koch Institute for Integrative Cancer Research, and Howard Hughes Medical Institute, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, Massachusetts 02139, USA)

  • David M. Feldser

    (Koch Institute for Integrative Cancer Research, and Howard Hughes Medical Institute, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, Massachusetts 02139, USA)

  • Lynn Shen

    (Koch Institute for Integrative Cancer Research, and Howard Hughes Medical Institute, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, Massachusetts 02139, USA)

  • Erin Turk

    (Koch Institute for Integrative Cancer Research, and Howard Hughes Medical Institute, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, Massachusetts 02139, USA)

  • Chensi Ouyang

    (Koch Institute for Integrative Cancer Research, and Howard Hughes Medical Institute, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, Massachusetts 02139, USA)

  • Tyler Jacks

    (Koch Institute for Integrative Cancer Research, and Howard Hughes Medical Institute, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, Massachusetts 02139, USA)

Abstract

Targeting KRAS cancers Mutations in genes of the RAS family are preset on about 20% of human cancers, making RAS proteins prime potential targets for cancer therapy. Direct targeting of RAS proteins has not so far been productive, but two papers published in this issue offer the prospect of alternative targets in a signalling pathway downstream of RAS. Using a synthetic lethality RNAi screen, Barbie et al. identify TBK1 as a kinase in the NF-κB signalling pathway that is essential for the survival of KRAS-transformed cells. TBK1 induces anti-apoptotic signals and may be a therapeutic cancer target. And in an elegant mouse model for lung cancer driven by Kras mutation and loss of p53, Meylan et al. show that NF-κB signalling is activated by the concerted actions of these two alterations and required for tumour initiation and tumour maintenance.

Suggested Citation

  • Etienne Meylan & Alison L. Dooley & David M. Feldser & Lynn Shen & Erin Turk & Chensi Ouyang & Tyler Jacks, 2009. "Requirement for NF-κB signalling in a mouse model of lung adenocarcinoma," Nature, Nature, vol. 462(7269), pages 104-107, November.
    • Handle: RePEc:nat:nature:v:462:y:2009:i:7269:d:10.1038_nature08462
    DOI: 10.1038/nature08462
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    Cited by:

    1. Paul K. Paik & Jia Luo & Ni Ai & Rachel Kim & Linda Ahn & Anup Biswas & Courtney Coker & Wanchao Ma & Phillip Wong & Darren J. Buonocore & W. Victoria Lai & Jamie E. Chaft & Swarnali Acharyya & Joan M, 2022. "Phase I trial of the TNF-α inhibitor certolizumab plus chemotherapy in stage IV lung adenocarcinomas," Nature Communications, Nature, vol. 13(1), pages 1-8, December.

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