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Cancer

A targeted treatment with off-target risks

Nature volume 542, pages 424–425 (2017)Cite this article

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It emerges that blood-cancer-targeting drugs that block a tumour-survival pathway also activate a mutation-causing enzyme in mice and in human cells. This might have implications for the clinical use of these drugs. See Letter p.489

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Figure 1: Inhibition of a B-cell-receptor signalling pathway might increase the number of harmful mutations.

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  • 22 February 2017

    A new reference 10 has been added, in acknowledgement of the fact that this paper was the first to report that PI3Kδ suppresses expression of AID.

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Authors and Affiliations

  1. David A. Fruman is in the Department of Molecular Biology and Biochemistry, University of California, Irvine, Irvine, California 92697, USA.,

    David A. Fruman

  2. Susan O'Brien is at the Chao Family Comprehensive Cancer Center, University of California, Irvine, Orange, California 92868, USA.,

    Susan O'Brien

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  1. David A. Fruman
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  2. Susan O'Brien
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Correspondence to David A. Fruman.

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Fruman, D., O'Brien, S. A targeted treatment with off-target risks. Nature 542, 424–425 (2017). https://doi.org/10.1038/nature21504

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