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Volume 23 Issue 4, April 2017

In this issue (p 429), Katalin Susztak and colleagues tested whether two previously identified human risk alleles of APOL1 cause kidney disease when expressed as transgenes in mice. They find that expression of either risk allele, unlike that of a reference nonrisk allele, specifically in podocytes is sufficient to cause such disease in mice. Neither risk allele caused pathology when expressed in renal tubules. The cover shows a pseudocolored scanning electron micrograph of a glomerulus. Image credit: Dennis Kunkel Microscopy/Science Source.

Editorial

  • President Donald Trump's call to speed up drug approval by the US Food and Drug Administration (FDA) overlooks the fact that the agency has become faster over the past two decades. When considering changes to the drug-approval process, we should instead increase our investment in the many years of research that precede approval.

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Correction

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Correspondence

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News & Views

  • In a recent study, researchers generated a mouse model expressing variant APOL1 that recapitulates human kidney disease. Variant APOL1 leads to caspase-1-dependent pyroptosis, which opens the door for the development of new druggable targets to treat APOL1-mediated kidney disease.

    • Cheryl A Winkler
    • George W Nelson
    News & Views
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Review Article

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Brief Communication

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Article

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Letter

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Analysis

  • HRDetect represents a model integrating whole-genome sequencing mutation signatures associated with BRCA1 and BRCA2 deficiency. The implementation of this predictor across different tumor types identifies a larger proportion of patients displaying ‘BRCAness’ than previously recognized; they might derive benefit from platinum and PARP-inhibitor therapies.

    • Helen Davies
    • Dominik Glodzik
    • Serena Nik-Zainal
    Analysis
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