Prevention and intervention programs targeting sexual abuse in individuals with mild intellectual disability: A systematic review

Contains fulltext : 232083.pdf (Publisher’s version ) (Open Access)Introduction: Compared to their non-disabled peers, individuals with mild intellectual disability (MID) are at higher risk of becoming a victim of sexual abuse and more vulnerable to its disruptive effects. This review provides an overview of content and effectiveness of prevention and intervention programs targeting sexual abuse in individuals with MID. Methods: PRISMA guidelines were followed and quality and effectiveness of the programs were evaluated taking into account the rating of the Quality Assessment Tool for Quantitative Studies (QATQS). Results: Twelve studies were included. In prevention programs role-play prevailed, whereas the content of intervention programs varied. All studies received a "weak" QATQS rating. By consequence, effectiveness of the program was downgraded to "unclear" in ten, and "ineffective" in two studies. Conclusion: Further development of programs and higher quality of research is needed to investigate whether they are effective in preventing sexual abuse or reducing its consequences in individuals with MID.24 p

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