Trace Clustering for User Behavior Mining

Business information systems support a large variety of business processes and tasks, yet organizations rarely understand how users interact with these systems. User Behavior Mining aims to address this by applying process mining techniques to UI logs, i.e., detailed records of interactions with a system\u27s user interface. Insights gained from this type of data hold great potential for usability engineering and task automation, but the complexity of UI logs can make them challenging to analyze. In this paper, we explore trace clustering as a means to structure UI logs and reduce this complexity. In particular, we apply different trace clustering approaches to a real-life UI log and show that the cluster-level process models reveal useful information about user behavior. At the same time, we find configurations in which trace clustering fails to generate satisfactory partitions. Our results also demonstrate that recently proposed representation learning techniques for process traces can be effectively employed in a realistic setting

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