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- Bravo, L, et al.
(författare)
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- 2021
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swepub:Mat__t
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- Tabiri, S, et al.
(författare)
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- 2021
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swepub:Mat__t
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- Glasbey, JC, et al.
(författare)
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- 2021
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swepub:Mat__t
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| 4. |
- 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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| 5. |
- Ahyow, LC, et al.
(författare)
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Bed occupancy rates and hospital-acquired Clostridium difficile infection: a cohort study
- 2013
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Ingår i: Infection control and hospital epidemiology. - : Cambridge University Press (CUP). - 1559-6834 .- 0899-823X. ; 34:10, s. 1062-1069
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Tidskriftsartikel (refereegranskat)abstract
- An emergent strain (ribotype 027) of Clostridium difficile infection (CDI) has been implicated in epidemics worldwide. Organizational factors such as bed occupancy have been associated with an increased incidence of CDI; however, the data are sparse, and the association has not been widely demonstrated. We investigated the association of bed occupancy and CDI within a large hospital organization in the United Kingdom.Objective.To establish whether bed occupancy rates are a significant risk factor for CDI in the general ward setting.Methods.A retrospective cohort study was carried out on data from 2006 to 2008. Univariate and multivariate Cox regression modeling was used to examine the strength and significance of the associations. Variables included patient characteristics, antibiotic policy exposure, case mix, and bed occupancy rates.Results.A total of 1,589 cases of hospital-acquired CDI were diagnosed (1.7% of admissions), with an overall infection rate of 2.16 per 1,000 patient-days. Median bed occupancy was 93.3% (interquartile range, 83.3%–100%) Univariate and multivariate analyses showed positive and statistically significant associations. In the adjusted model, patients on wards with occupancy rates of 80%–89.9% had rates of CDI that were 56% higher (hazard ratio, 1.56 [95% confidence interval, 1.18–2.04]; P<.001) compared with baseline (0%–69.9% occupancy). CDI rates were 55% higher for patients on wards with maximal bed occupancy (100%).Conclusions.There is strong evidence of an association between high bed occupancy and CDI. Without effective interventions at high levels of bed occupancy, the economic benefits sought from reducing bed numbers may be negated by the increased risk of CDI.
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- Bower, H, et al.
(författare)
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Continued improvement in survival of acute myeloid leukemia patients: an application of the loss in expectation of life
- 2016
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Ingår i: Blood cancer journal. - : Springer Science and Business Media LLC. - 2044-5385. ; 6, s. e390-
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Tidskriftsartikel (refereegranskat)abstract
- We evaluated temporal trends in survival of Swedish acute myeloid leukemia (AML) patients diagnosed between 1973 and 2011 using relative survival ratios (RSRs) and a measure called the loss in expectation of life (LEL). RSRs increased most for patients <60 years at diagnosis during the first calendar periods, but between 1997–2005 and 2006–2011 the most pronounced increase was for those aged 61–70 years at diagnosis; RSR changed from 0.16 (95% confidence interval (CI): 0.13–0.19) to 0.28 (95% CI: 0.23–0.33), respectively. The LEL for males aged 35 years at diagnosis was 41.0 (95% CI: 40.1–41.8) years in 1975 and 19.5 (95% CI: 16.4–22.5) years in 2011. For males aged 65 years, the corresponding figures were 13.8 (95% CI: 13.7–14.0) and 12.0 (95% CI: 11.3–12.8). Conditional LEL estimates suggested that patients who survive 5 years postdiagnosis have shorter remaining lifespan than the general population. The proportion of expected life lost (PELL) suggested that male 65-year-old patients lost 75% of their life expectancy in 2005 and 66% if they were diagnosed in 2011. Survival continued to increase to 2011, with larger improvements in those aged 61–70 years at diagnosis. The LEL and PELL are intuitive measures that may be useful in communicating survival statistics to patients, clinicians and health-care providers.
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