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- Campbell, PJ, et al.
(författare)
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Pan-cancer analysis of whole genomes
- 2020
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Ingår i: Nature. - : Springer Science and Business Media LLC. - 1476-4687 .- 0028-0836. ; 578:7793, s. 82-
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Tidskriftsartikel (refereegranskat)abstract
- Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale1–3. 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 promoter4; identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation5,6; analyses timings and patterns of tumour evolution7; describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity8,9; and evaluates a range of more-specialized features of cancer genomes8,10–18.
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- Barlo, Alexander, M.Sc. Eng. 1994-
(författare)
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Failure Prediction of Complex Load Cases in Sheet Metal Forming : Emphasis on Non-Linear Strain Paths, Stretch-Bending and Edge Effects
- 2023
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Licentiatavhandling (övrigt vetenskapligt/konstnärligt)abstract
- With the increased focus on reducing carbon emissions in today’s society, several industries have to overcome new challenges, where especially the automotive industry is under a lot of scrutiny to deliver improved and more environmentally friendly products. To meet the demands from customers and optimize vehicles aerodynamically, new cars often contain complex body geometries, together with advanced materials that are introduced to reduce the total vehicle weight. With the introduction of the complex body components and advanced materials,one area in the automotive industry that has to overcome these challenges is manufacturing engineering, and in particular the departments working with the sheet metal forming process. In this process complex body component geometries can lead to non-linear strain paths and stretch bending load cases, and newly introduced advanced materials can be prone to exhibit behaviour of edge cracks not observed in conventional sheet metals. This thesis takes it onset in the challenges seen in industry today with predicting failure of the three complex load cases: Non-Linear Strain Paths, Stretch-Bending,and Edge Cracks. Through Finite Element simulation attempts are made to accurately predict failure caused by aforementioned load cases in industrial components or experimental setups in an effort to develop post-processing methods that are applicable to all cases.
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- Bäck, M, et al.
(författare)
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Open Up your Science in EHJ Open
- 2021
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Ingår i: European heart journal open. - : Oxford University Press (OUP). - 2752-4191. ; 1:1, s. oeab021-
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Tidskriftsartikel (refereegranskat)
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| 20. |
- Campbell, L, et al.
(författare)
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Intimate Partner Violence During COVID-19 Restrictions: A Study of 30 Countries From the I-SHARE Consortium
- 2023
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Ingår i: Journal of interpersonal violence. - : SAGE Publications. - 1552-6518 .- 0886-2605. ; 38:11-12, s. 7115-7142
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Tidskriftsartikel (refereegranskat)abstract
- Intimate partner violence (IPV) causes substantial physical and psychological trauma. Restrictions introduced in response to the COVID-19 pandemic, including lockdowns and movement restrictions, may exacerbate IPV risk and reduce access to IPV support services. This cross-sectional study examines IPV during COVID-19 restrictions in 30 countries from the International Sexual HeAlth and REproductive Health (I-SHARE) study conducted from July 20th, 2020, to February, 15th, 2021. IPV was a primary outcome measure adapted from a World Health Organization multicountry survey. Mixed-effects modeling was used to determine IPV correlates among participants stratified by cohabitation status. The sample included 23,067 participants from 30 countries. A total of 1,070/15,336 (7.0%) participants stated that they experienced IPV during COVID-19 restrictions. A total of 1,486/15,336 (9.2%) participants stated that they had experienced either physical or sexual partner violence before the restrictions, which then decreased to 1,070 (7.0%) after the restrictions. In general, identifying as a sexual minority and experiencing greater economic vulnerability were associated with higher odds of experiencing IPV during COVID-19 restrictions, which were accentuated among participants who were living with their partners. Greater stringency of COVID-19 restrictions and living in urban or semi-urban areas were associated with lower odds of experiencing IPV in some settings. The I-SHARE data suggest a substantial burden of IPV during COVID-19 restrictions. However, the restrictions were correlated with reduced IPV in some settings. There is a need for investing in specific support systems for survivors of IPV during the implementation of restrictions designed to contain infectious disease outbreaks.
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| 21. |
- Carlevaro-Fita, J, et al.
(författare)
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Cancer LncRNA Census reveals evidence for deep functional conservation of long noncoding RNAs in tumorigenesis
- 2020
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Ingår i: Communications biology. - : Springer Science and Business Media LLC. - 2399-3642. ; 3:1, s. 56-
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Tidskriftsartikel (refereegranskat)abstract
- Long non-coding RNAs (lncRNAs) are a growing focus of cancer genomics studies, creating the need for a resource of lncRNAs with validated cancer roles. Furthermore, it remains debated whether mutated lncRNAs can drive tumorigenesis, and whether such functions could be conserved during evolution. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, we introduce the Cancer LncRNA Census (CLC), a compilation of 122 GENCODE lncRNAs with causal roles in cancer phenotypes. In contrast to existing databases, CLC requires strong functional or genetic evidence. CLC genes are enriched amongst driver genes predicted from somatic mutations, and display characteristic genomic features. Strikingly, CLC genes are enriched for driver mutations from unbiased, genome-wide transposon-mutagenesis screens in mice. We identified 10 tumour-causing mutations in orthologues of 8 lncRNAs, including LINC-PINT and NEAT1, but not MALAT1. Thus CLC represents a dataset of high-confidence cancer lncRNAs. Mutagenesis maps are a novel means for identifying deeply-conserved roles of lncRNAs in tumorigenesis.
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- Kitagawa, M, et al.
(författare)
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Dual blockade of the lipid kinase PIP4Ks and mitotic pathways leads to cancer-selective lethality
- 2017
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Ingår i: Nature communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 8:1, s. 2200-
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Tidskriftsartikel (refereegranskat)abstract
- Achieving robust cancer-specific lethality is the ultimate clinical goal. Here, we identify a compound with dual-inhibitory properties, named a131, that selectively kills cancer cells, while protecting normal cells. Through an unbiased CETSA screen, we identify the PIP4K lipid kinases as the target of a131. Ablation of the PIP4Ks generates a phenocopy of the pharmacological effects of PIP4K inhibition by a131. Notably, PIP4Ks inhibition by a131 causes reversible growth arrest in normal cells by transcriptionally upregulating PIK3IP1, a suppressor of the PI3K/Akt/mTOR pathway. Strikingly, Ras activation overrides a131-induced PIK3IP1 upregulation and activates the PI3K/Akt/mTOR pathway. Consequently, Ras-transformed cells override a131-induced growth arrest and enter mitosis where a131’s ability to de-cluster supernumerary centrosomes in cancer cells eliminates Ras-activated cells through mitotic catastrophe. Our discovery of drugs with a dual-inhibitory mechanism provides a unique pharmacological strategy against cancer and evidence of cross-activation between the Ras/Raf/MEK/ERK and PI3K/AKT/mTOR pathways via a Ras˧PIK3IP1˧PI3K signaling network.
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- Larsson, Magnus, et al.
(författare)
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Aerodynamic Identification using Neural Networks
- 1997
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Rapport (övrigt vetenskapligt/konstnärligt)abstract
- The use of neural networks and efficient identification algorithms in aerodynamic modeling could substantially reduce the time and work effort in going from wind tunnel and flight test data to model. The model is globally differentiable and can be inspected in any way desired. A number of structured and black box sigmoid type neural net models have been identified for mainly the C z aerodynamic coefficient in the region 0 ffi ff 60 ffi , where the aerodynamic coefficients behave highly nonlinear. The estimation data has been directly extracted from an existing aerodatabase for a generic fighter aircraft, that also has been used for validation. All available data has been used for estimation and the data is considered noiseless, so only the approximation properties of the different models are tested. Somewhat surprisingly, it is found that pure black box models with the same number of parameters as structured models utilizing physical insight, often perform better.
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| 45. |
- Larsson, SC, et al.
(författare)
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Dairy foods and risk of stroke
- 2009
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Ingår i: Epidemiology (Cambridge, Mass.). - 1531-5487. ; 20:3, s. 355-360
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Tidskriftsartikel (refereegranskat)
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