The new enclosures: critical perspectives on corporate land deals

The contributions to this collection use the tools of agrarian political economy to explore the rapid growth and complex dynamics of large-scale land deals in recent years, with a special focus on the implications of big land deals for property and labour regimes, labour processes and structures of accumulation. The first part of this introductory essay examines the implications of this agrarian political economy perspective. First we explore the continuities and contrasts between historical and contemporary land grabs, before examining the core underlying debate around large- versus small-scale farming futures. Next, we unpack the diverse contexts and causes of land grabbing today, highlighting six overlapping mechanisms. The following section turns to assessing the crisis narratives that frame the justifications for land deals, and the flaws in the argument around there being excess, empty or idle land available. Next the paper turns to an examination of the impacts of land deals, and the processes of inclusion and exclusion at play, before looking at patterns of resistance and constructions of alternatives. The final section introduces the papers in the collection.ESR

Pan-cancer analysis of whole genomes

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 promoter(4); 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 evolution(7); 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).Peer reviewe