Type II migration strikes back – an old paradigm for planet migration in discs

In this paper, we analyse giant gap-opening planet migration in proto-planetary discs, focusing on the type II migration regime. According to standard type II theory, planets migrate at the same rate as the gas in the disc, as they are coupled to the disc viscous evolution; however, recent studies questioned this paradigm, suggesting that planets migrate faster than the disc material. We study the problem through 2D long-time simulations of systems consistent with type II regime, using the hydrodynamical grid code FARGO3D. Even though our simulations confirm the presence of an initial phase characterized by fast migration, they also reveal that the migration velocity slows down and eventually reaches the theoretical prediction if we allow the system to evolve for enough time. We find the same tendency to evolve towards the theoretical predictions at later times when we analyse the mass flow through the gap and the torques acting on the planet. This transient is related to the initial conditions of our (and previous) simulations, and is due to the fact that the shape of the gap has to adjust to a new profile, once the planet is set into motion. Secondly, we test whether the type II theory expectation that giant planet migration is driven by viscosity is consistent with our simulation by comparing simulations with the same viscosity and different disc masses (or vice versa). We find a good agreement with the theory, since when the discs are characterized by the same viscosity, the migration properties are the same

Inward and outward migration of massive planets: moving towards a stalling radius

Stars and planetary system

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