Effects of comorbid ADHD with learning disabilities on anxiety, depression, and aggression in adults

Objective: ADHD and learning disabilities (LD) frequently coexist and there are indications that comorbidity may increase the risk of psychopathology. Method: The current study examined the gender distribution and frequency of comorbidity and its impact on the prevalence of symptoms of anxiety,&nbsp; depression, and aggression in a clinic sample of 80 adults with ADHD, aged 18 to 58 years. More individuals were diagnosed with ADHD+LD than ADHD only, with no difference in this distribution according to gender. Results: A factorial multivariate analysis of variance indicated that females with ADHD+LD displayed more cognitive depression than females with ADHD only and than males with ADHD+LD and ADHD only. However,individuals with ADHD only and individuals with ADHD+LD did not differ on overall anxiety, depression or aggression. Likewise, males and females did not differ on measures of psychopathology. Conclusion: This study lays the foundation for continued research into the characteristics and comorbidities of adults with ADHD.<br /

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