Nature 414, 165-166 (2001) In Fig. 1b of this Brief Communication, the legend and text did not make it clear that two different groups of ten sheep were used in the study to give overall n 5 20. A reanalysis of the data using a post-hoc Tukey test (rather than a paired t-test, as originally stated) revealed some small errors that altered the significance values slightly; however, there is no overall change in the results. The maximum retest interval was 801 rather than 800 days, and 100-500 trials were conducted for 1-6 weeks (not 400-500 trials for 4-6 weeks, as published). A revised version of Fig. 1b showing the corrected statistical changes and an expanded legend incorporating further methodological detail are available as Supplementary Information to this Corrigendum.Supplementary Information is linked to the online version of this Corrigendum at www.nature.com/nature.

No abstract

No abstract

Resistance to temozolomide and radiotherapy is a major problem for patients with glioblastoma but may be overcome using the poly(ADP-ribose) polymerase inhibitor ABT-888. Using two primary glioblastoma xenografts, the efficacy of ABT-888 combined with radiotherapy and/or temozolomide was evaluated. Treatment with ABT-888 combined with temozolomide resulted in significant survival prolongation (GBM12: 55.1%, P = 0.005; GBM22: 54.4%, P = 0.043). ABT-888 had no effect with radiotherapy alone but significantly enhanced survival in GBM12 when combined with concurrent radiotherapy/ temozolomide. With multicycle therapy, ABT-888 further extended the survival benefit of temozolomide in the inherently sensitive GBM12 and GBM22 xenograft lines. However, after in vivo selection for temozolomide resistance, the derivative GBM12TMZ and GBM22TMZ lines were no longer sensitized by ABT-888 in combination with temozolomide, and a similar lack of efficacy was observed in two other temozolomide-resistant tumor lines. Thus, the sensitizing effects of ABT-888 were limited to tumor lines that have not been previously exposed to temozolomide, and these results suggest that patients with newly diagnosed glioblastoma may be more likely to respond to combined temozolomide/poly(ADP-ribose) polymerase inhibitor therapy than patients with recurrent disease.

Clinically approved PARP inhibitors (PARPi) have a mild adverse effect profile and are well tolerated as continuous daily oral therapy. We review the evidence that justifies the repurposing of PARPi to block the proliferation of severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) and combat the life‐threatening sequelae of coronavirus disease 2019 (COVID‐19) by several mechanisms. PARPi can effectively decrease IL‐6, IL‐1 and TNF‐α levels (key interleukins in SARS‐CoV‐2‐induced cytokine storm) and can alleviate subsequent lung fibrosis, as demonstrated in murine experiments and clinical trials. PARPi can tune macrophages towards a tolerogenic phenotype. PARPi may also counteract SARS‐CoV‐2‐induced and inflammation‐induced cell death and support cell survival. PARPi is effective in animal models of acute respiratory distress syndrome (ARDS), asthma and ventilator‐induced lung injury. PARPi may potentiate the effectiveness of tocilizumab, anakinra, sarilumab, adalimumab, canakinumab or siltuximab therapy. The evidence suggests that PARPi would benefit COVID‐19 patients and trials should be undertaken.