Giant rafted pumice blocks from the most recent eruption of Taupo volcano, New Zealand: Insights from palaeomagnetic and textural data

Giant blocks of pumice lie strewn along a former shoreline of intracaldera Lake Taupo, New Zealand, and are the sole subaerial evidence of the most recent volcanism at the Taupo supervolcano. Geochemically they are identical to material erupted during the complex and multiphase 1.8 ka Taupo eruption, which they post-date by one to two decades. The blocks, some of which are >10 m long, show complex jointing patterns indicative of both surface chilling and continued interior expansion, as well as heterogeneous vesicularity, with dense rims (mean density 917 kg/m3) grading via an intervening transition zone (mean density 844 kg/m3) into a more highly vesicular interior (mean density 815 kg/m3). Analysis of thermal demagnetisation data indicates significant reorientation of the blocks as they cooled through a series of blocking temperatures. Some parts of block rims cooled to below 580 °C well before emplacement on the shore, whereas other parts in the interior and transition zones, which cooled more slowly, acquired different orientations before stranding. Some block interiors cooled after blocks were finally deposited, and record the direction of the 1.8 ka field. The blocks are believed to be derived from one or both of a pair of rhyolitic lava domes that developed on the bed of Lake Taupo several decades after the climactic Taupo eruption over the inferred vent area.These, and similar giant rafted pumice blocks in other marine and lacustrine settings raise a number of questions about how volatile-rich felsic magma can be erupted underwater with only limited thermal fragmentation. Furthermore, the prolonged flotation of out-sized fragments of vesiculated magma formed during subaqueous dome-growth contrasts with the rapid sinking of smaller pieces of hot plinian pumice under laboratory conditions. The genesis of pumice forming the blocks is not entirely clear. Most simply the blocks may represent part of a vesiculated carapace of a growing lava dome, broken loose as the dome grew and deformed then rising buoyantly to the surface. Parts of the carapace could also be released by local magma-water explosions. Some textures of the pumice, however, suggest fresher magma released from beneath the carapace. This may suggest that silicic dikes and pillows/pods intruded into a growing mound of silicic hyaloclastite, itself formed by quench fragmentation and thermal granulation of the dike margins. This fragmental cover would have inhibited cooling of a still-hot and actively vesiculating interior, which was then released to float to the surface by gravitational destabilisation and collapse of the growing pile. Following their formation, the large fragments of pumice floated to the lake's surface, where they were blown ashore to become embedded in accumulating transgressive shoreface sediments and continue cooling

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. 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; identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation; analyses timings and patterns of tumour evolution; describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity; and evaluates a range of more-specialized features of cancer genomes