Intrusive memories are disruptive to daily functioning and detrimental to well-being; unfortunately, the presence of these memories is a defining characteristic of post-traumatic stress disorder (PTSD). Although increasingly understood as a memory disorder, current trauma management and recovery strategies for PTSD do not often take principal memory theories into account. Many common practices, such as delayed processing after trauma exposure and spaced therapy sessions, might inadvertently strengthen the retention of intrusive memories in the long-term. In this paper, model simulations show that altering the timing of different presentations of emotional stimuli might affect subsequent intrusions. Experimentally, we demonstrated through a two-day within-subject image presentation task that when emotional images are presented in spaced intervals (as opposed to consecutive, "massed" presentation), the perceived frequency of intrusions for the mass-presented emotional images during the 24 hours after first exposure were significantly lower than spaced images. Our study presents a novel strategy that can potentially mitigate the frequency of intrusive post-traumatic memories, highlighting the advantages of translational applications of computational cognitive models to mental health.

In the published version of this paper, the list of members of the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium and their affiliations contained minor errors in the affiliations. The original Article has been corrected to include the corrected list.

Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale^1-3. Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4-5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete. Chromothripsis, in which many clustered structural variants arise in a single catastrophic event, is frequently an early event in tumour evolution; in acral melanoma, for example, these events precede most somatic point mutations and affect several cancer-associated genes simultaneously. Cancers with abnormal telomere maintenance often originate from tissues with low replicative activity and show several mechanisms of preventing telomere attrition to critical levels. Common and rare germline variants affect patterns of somatic mutation, including point mutations, structural variants and somatic retrotransposition. A collection of papers from the PCAWG Consortium describes non-coding mutations that drive cancer beyond those in the TERT promoter⁴; identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation^5,6; analyses timings and patterns of tumour evolution⁷; describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity^8,9; and evaluates a range of more-specialized features of cancer genomes^8,10-18.