Improved Squeaky Wheel Optimisation for Driver Scheduling

This paper presents a technique called Improved Squeaky Wheel Optimisation for driver scheduling problems. It improves the original Squeaky Wheel Optimisations effectiveness and execution speed by incorporating two additional steps of Selection and Mutation which implement evolution within a single solution. In the ISWO, a cycle of Analysis-Selection-Mutation-Prioritization-Construction continues until stopping conditions are reached. The Analysis step first computes the fitness of a current solution to identify troublesome components. The Selection step then discards these troublesome components probabilistically by using the fitness measure, and the Mutation step follows to further discard a small number of components at random. After the above steps, an input solution becomes partial and thus the resulting partial solution needs to be repaired. The repair is carried out by using the Prioritization step to first produce priorities that determine an order by which the following Construction step then schedules the remaining components. Therefore, the optimisation in the ISWO is achieved by solution disruption, iterative improvement and an iterative constructive repair process performed. Encouraging experimental results are reported

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