Cancer therapeutic resistance articles within Nature

Featured

  • News & Views |

    The efficacy of the anticancer drug vemurafenib, which is used to treat metastatic melanoma, is plagued by acquired resistance. A picture of how such resistance develops is emerging. See Letter p.387

    • Hugo Lavoie
    •  & Marc Therrien

  • News & Views |

    The promise of an exciting new drug that inhibits the mutant B-RAF protein in skin cancer is marred by the fact that most patients relapse within a year. Fresh data hint at how such resistance emerges. See Letters p.968 & p.973

    • David Solit
    •  & Charles L. Sawyers

  • News & Views |

    Resistance of tumour cells to chemotherapy can severely affect the efficacy of this anticancer treatment. The non-tumour cells of the organ in which the tumour resides may aid the emergence of such resistance.

    • Urban Emmenegger
    •  & Robert S. Kerbel

  • News |

    Learning how melanoma fights back may yield new therapies.

    • Heidi Ledford

  • Letter |

    Recent data from early clinical trials in melanoma patients carrying mutations in the B-RAF gene have shown promising results with the B-RAF kinase inhibitor PLX4032; however, many patients eventually develop resistance to this treatment. Two papers now uncover possible mechanisms of resistance to PLX4032. One paper shows that upregulation of MAP3K8 (which encodes COT) can confer resistance of melanoma cells to B-RAF inhibitors, whereas another paper found that melanomas can acquire resistance due to mutations of N-RAS or increased expression of PDGFRβ. Each of these resistance mechanisms seems to apply to at least some patients on recent PLX4032 trial, whereas, surprisingly, so far no secondary B-RAF mutations have been observed.

    • Cory M. Johannessen
    • , Jesse S. Boehm
    •  & Levi A. Garraway

  • Letter |

    Recent data from early clinical trials in melanoma patients carrying mutations in the B-RAF gene have shown promising results with the B-RAF kinase inhibitor PLX4032; however, many patients eventually develop resistance to this treatment. Two papers now uncover possible mechanisms of resistance to PLX4032. One paper shows that upregulation of MAP3K8 (which encodes COT) can confer resistance of melanoma cells to B-RAF inhibitors, whereas another paper found that melanomas can acquire resistance due to mutations of N-RAS or increased expression of PDGFRβ. Each of these resistance mechanisms seems to apply to at least some patients on recent PLX4032 trial, whereas, surprisingly, so far no secondary B-RAF mutations have been observed.

    • Ramin Nazarian
    • , Hubing Shi
    •  & Roger S. Lo

  • News & Views |

    Some cancer cells that become tolerant to a drug remain resistant even after its withdrawal, yet these cells eventually become sensitive to the drug again. The underlying molecular mechanism is unusual.

    • Paul Workman
    •  & Jon Travers

Browse broader subjects

Browse Cancer therapeutic resistance across other nature.com journals