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Träfflista för sökning "WFRF:(Ta Michael) srt2:(2015-2019)"

Sökning: WFRF:(Ta Michael) > (2015-2019)

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  • Ju, Young Seok, et al. (författare)
  • Frequent somatic transfer of mitochondrial DNA into the nuclear genome of human cancer cells.
  • 2015
  • Ingår i: Genome Research. - : Cold Spring Harbor Laboratory. - 1549-5469 .- 1088-9051. ; 25:6, s. 814-824
  • Tidskriftsartikel (refereegranskat)abstract
    • Mitochondrial genomes are separated from the nuclear genome for most of the cell cycle by the nuclear double membrane, intervening cytoplasm, and the mitochondrial double membrane. Despite these physical barriers, we show that somatically acquired mitochondrial-nuclear genome fusion sequences are present in cancer cells. Most occur in conjunction with intranuclear genomic rearrangements, and the features of the fusion fragments indicate that nonhomologous end joining and/or replication-dependent DNA double-strand break repair are the dominant mechanisms involved. Remarkably, mitochondrial-nuclear genome fusions occur at a similar rate per base pair of DNA as interchromosomal nuclear rearrangements, indicating the presence of a high frequency of contact between mitochondrial and nuclear DNA in some somatic cells. Transmission of mitochondrial DNA to the nuclear genome occurs in neoplastically transformed cells, but we do not exclude the possibility that some mitochondrial-nuclear DNA fusions observed in cancer occurred years earlier in normal somatic cells.
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  • Dadaev, T, et al. (författare)
  • Fine-mapping of prostate cancer susceptibility loci in a large meta-analysis identifies candidate causal variants
  • 2018
  • Ingår i: Nature communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 9:1, s. 2256-
  • Tidskriftsartikel (refereegranskat)abstract
    • Prostate cancer is a polygenic disease with a large heritable component. A number of common, low-penetrance prostate cancer risk loci have been identified through GWAS. Here we apply the Bayesian multivariate variable selection algorithm JAM to fine-map 84 prostate cancer susceptibility loci, using summary data from a large European ancestry meta-analysis. We observe evidence for multiple independent signals at 12 regions and 99 risk signals overall. Only 15 original GWAS tag SNPs remain among the catalogue of candidate variants identified; the remainder are replaced by more likely candidates. Biological annotation of our credible set of variants indicates significant enrichment within promoter and enhancer elements, and transcription factor-binding sites, including AR, ERG and FOXA1. In 40 regions at least one variant is colocalised with an eQTL in prostate cancer tissue. The refined set of candidate variants substantially increase the proportion of familial relative risk explained by these known susceptibility regions, which highlights the importance of fine-mapping studies and has implications for clinical risk profiling.
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  • Gusev, A, et al. (författare)
  • Atlas of prostate cancer heritability in European and African-American men pinpoints tissue-specific regulation
  • 2016
  • Ingår i: Nature communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 7, s. 10979-
  • Tidskriftsartikel (refereegranskat)abstract
    • Although genome-wide association studies have identified over 100 risk loci that explain ∼33% of familial risk for prostate cancer (PrCa), their functional effects on risk remain largely unknown. Here we use genotype data from 59,089 men of European and African American ancestries combined with cell-type-specific epigenetic data to build a genomic atlas of single-nucleotide polymorphism (SNP) heritability in PrCa. We find significant differences in heritability between variants in prostate-relevant epigenetic marks defined in normal versus tumour tissue as well as between tissue and cell lines. The majority of SNP heritability lies in regions marked by H3k27 acetylation in prostate adenoc7arcinoma cell line (LNCaP) or by DNaseI hypersensitive sites in cancer cell lines. We find a high degree of similarity between European and African American ancestries suggesting a similar genetic architecture from common variation underlying PrCa risk. Our findings showcase the power of integrating functional annotation with genetic data to understand the genetic basis of PrCa.
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  • Matejcic, M, et al. (författare)
  • Author Correction: Germline variation at 8q24 and prostate cancer risk in men of European ancestry
  • 2019
  • Ingår i: Nature communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 10:1, s. 382-
  • Tidskriftsartikel (refereegranskat)abstract
    • The original version of this Article contained an error in the spelling of the author Manuela Gago-Dominguez, which was incorrectly given as Manuela G. Dominguez. This has now been corrected in both the PDF and HTML versions of the Article.
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  • Szulkin, R, et al. (författare)
  • Genome-wide association study of prostate cancer-specific survival
  • 2015
  • Ingår i: Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology. - 1538-7755. ; 24:11, s. 1796-1800
  • Tidskriftsartikel (refereegranskat)
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  • Takahashi, Harumi, et al. (författare)
  • Correlations between the enantio- and regio-selective metabolisms of warfarin
  • 2017
  • Ingår i: Pharmacogenomics (London). - : Future Medicine Ltd. - 1462-2416 .- 1744-8042. ; 18:2, s. 133-142
  • Tidskriftsartikel (refereegranskat)abstract
    • Aim: To clarify whether the activities of multiple CYPs associated with warfarin metabolism would be correlated with each other. Methods: Oral clearances (CLpo) of warfarin enantiomers were estimated in 378 Chinese, Caucasians and African-Americans. The partial metabolic clearances (CLm) for 7-hydroxywarfarin enantiomers were also measured. In addition, CLpo and CLm were determined in a patient on warfarin and rifampicin. Results: Correlations between CLpo for warfarin enantiomers existed across the three populations. In addition, there was a significant correlation between the CLm for 7-hydroxylation of warfarin enantiomers. Under induced conditions by rifampicin, there were significant correlations between the enantio-and regio-selective metabolisms of warfarin. Conclusion: Metabolic activities of CYP2C9, CYP1A2 and CYP3A4 may be regulated by common transcriptional mechanism(s).
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  • Willeit, Peter, et al. (författare)
  • Inflammatory markers and extent and progression of early atherosclerosis : Meta-analysis of individual-participant-data from 20 prospective studies of the PROG-IMT collaboration
  • 2016
  • Ingår i: European Journal of Preventive Cardiology. - : Oxford University Press (OUP). - 2047-4873 .- 2047-4881. ; 23:2, s. 194-205
  • Tidskriftsartikel (refereegranskat)abstract
    • BackgroundLarge-scale epidemiological evidence on the role of inflammation in early atherosclerosis, assessed by carotid ultrasound, is lacking. We aimed to quantify cross-sectional and longitudinal associations of inflammatory markers with common-carotid-artery intima-media thickness (CCA-IMT) in the general population. MethodsInformation on high-sensitivity C-reactive protein, fibrinogen, leucocyte count and CCA-IMT was available in 20 prospective cohort studies of the PROG-IMT collaboration involving 49,097 participants free of pre-existing cardiovascular disease. Estimates of associations were calculated within each study and then combined using random-effects meta-analyses. ResultsMean baseline CCA-IMT amounted to 0.74mm (SD=0.18) and mean CCA-IMT progression over a mean of 3.9 years to 0.011mm/year (SD=0.039). Cross-sectional analyses showed positive linear associations between inflammatory markers and baseline CCA-IMT. After adjustment for traditional cardiovascular risk factors, mean differences in baseline CCA-IMT per one-SD higher inflammatory marker were: 0.0082mm for high-sensitivity C-reactive protein (p<0.001); 0.0072mm for fibrinogen (p<0.001); and 0.0025mm for leucocyte count (p=0.033). Inflammatory load', defined as the number of elevated inflammatory markers (i.e. in upper two quintiles), showed a positive linear association with baseline CCA-IMT (p<0.001). Longitudinal associations of baseline inflammatory markers and changes therein with CCA-IMT progression were null or at most weak. Participants with the highest inflammatory load' had a greater CCA-IMT progression (p=0.015). ConclusionInflammation was independently associated with CCA-IMT cross-sectionally. The lack of clear associations with CCA-IMT progression may be explained by imprecision in its assessment within a limited time period. Our findings for inflammatory load' suggest important combined effects of the three inflammatory markers on early atherosclerosis.
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  • Aad, G., et al. (författare)
  • 2015
  • Ingår i: Physical Review C (Nuclear Physics). - 0556-2813 .- 1089-490X. ; 92:3
  • Tidskriftsartikel (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2015
  • Ingår i: The European Physical Journal C. - : Springer Science and Business Media LLC. - 1434-6052. ; 75:7
  • Tidskriftsartikel (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2015
  • Ingår i: The European Physical Journal C. - : Springer Science and Business Media LLC. - 1434-6052. ; 75:7
  • Tidskriftsartikel (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2015
  • Tidskriftsartikel (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2015
  • Ingår i: The European Physical Journal C. - : Springer Science and Business Media LLC. - 1434-6052. ; 75:9
  • Tidskriftsartikel (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2015
  • Ingår i: Physical Review D (Particles, Fields, Gravitation and Cosmology). - 1550-2368 .- 1550-7998. ; 91:11, s. 112011-
  • Tidskriftsartikel (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2015
  • Ingår i: Physical Review Letters. - 1079-7114 .- 0031-9007. ; 115:9
  • Tidskriftsartikel (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2015
  • Ingår i: Journal of High Energy Physics. - : Springer-Verlag New York. - 1029-8479 .- 1126-6708. ; :9
  • Tidskriftsartikel (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2015
  • Tidskriftsartikel (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2015
  • Ingår i: Physical Review D (Particles, Fields, Gravitation and Cosmology). - 1550-2368 .- 1550-7998. ; 92:1
  • Tidskriftsartikel (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2015
  • Ingår i: Journal of High Energy Physics. - : Springer. - 1029-8479 .- 1126-6708. ; :12
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  • Aad, G., et al. (författare)
  • 2015
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  • Aad, G., et al. (författare)
  • 2015
  • Ingår i: Journal of High Energy Physics. - : Societa Italiana di Fisica. - 1029-8479 .- 1126-6708. ; :8
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  • Aad, G., et al. (författare)
  • 2015
  • Ingår i: Journal of High Energy Physics. - : Societa Italiana di Fisica. - 1029-8479 .- 1126-6708. ; :9
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  • Aad, G., et al. (författare)
  • 2015
  • Ingår i: Physical Review Letters. - : American Physical Society. - 1079-7114 .- 0031-9007. ; 114:23
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  • Aad, G., et al. (författare)
  • 2015
  • Ingår i: Physical Review Letters. - : American Physical Society. - 1079-7114 .- 0031-9007. ; 114:22
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  • Aad, G., et al. (författare)
  • 2015
  • Ingår i: Journal of High Energy Physics. - 1029-8479 .- 1126-6708. ; :8
  • Tidskriftsartikel (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2015
  • Ingår i: Physical Review D (Particles, Fields, Gravitation and Cosmology). - 1550-2368 .- 1550-7998. ; 92:9
  • Tidskriftsartikel (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2015
  • Ingår i: Physical Review Letters. - 1079-7114 .- 0031-9007. ; 115:13
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  • Aad, G., et al. (författare)
  • 2015
  • Ingår i: Physical Review Letters. - 1079-7114 .- 0031-9007. ; 115:3
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  • Aad, G., et al. (författare)
  • 2015
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  • Aad, G., et al. (författare)
  • 2015
  • Ingår i: Physical Review Letters. - 1079-7114 .- 0031-9007. ; 115:3
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