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- Aad, G, et al.
(författare)
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- 2015
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swepub:Mat__t
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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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7. |
- Ablikim, M., et al.
(författare)
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Amplitude analysis of the KSKS system produced in radiative J /psi decays
- 2018
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Ingår i: Physical Review D. - : AMER PHYSICAL SOC. - 2470-0010 .- 2470-0029. ; 98:7
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Tidskriftsartikel (refereegranskat)abstract
- An amplitude analysis of the KSKS system produced in radiative J/psi decays is performed using the (1310.6 +/- 7.0) x 10(6) nip decays collected by the BESIII detector. Two approaches are presented. A mass-dependent analysis is performed by parametrizing the KSKS invariant mass spectrum as a sum of Breit-aligner line shapes. Additionally, a mass-independent analysis is performed to extract a piecewise function that describes the dynamics of the KSKS system while making minimal assumptions about the properties and number of poles in the amplitude. The dominant amplitudes in the mass-dependent analysis include the f(0)(1710), f(0)(2200), and f(2)'(1525). The mass-independent results, which are made available as input for further studies, are consistent with those of the mass-dependent analysis and are useful for a systematic study of hadronic interactions. The branching fraction of radiative J/psi decays to KSKS is measured to be (8.1 +/- 0.4) x 10(-4), where the uncertainty is systematic and the statistical uncertainty is negligible.
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- Ablikim, M., et al.
(författare)
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Branching fraction measurement of J/ψ→KSKL and search for J/ψ→KSKS
- 2017
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Ingår i: Physical Review D. - 2470-0010 .- 2470-0029. ; 96:11
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Tidskriftsartikel (refereegranskat)abstract
- Using a sample of 1.31 x 10(9) J/Psi events collected with the BESIII detector at the BEPCII collider, we study the decays of J/Psi -> KSKL and KSKS. The branching fraction of J/Psi -> KSKL is determined to be B(J/Psi -> KSKL) = (1.93 +/- 0.01 (stat) +/- 0.05 (syst)) x 10(-4), which significantly improves on previous measurements. No clear signal is observed for the J/Psi -> KSKS process, and the upper limit at the 95% confidence level for its branching fraction is determined to be B(J/Psi -> KSKS) < 1.4 x 10(-8), which improves on the previous searches by 2 orders in magnitude and reaches the order of the Einstein-Podolsky-Rosen expectation.
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9. |
- Ablikim, M., et al.
(författare)
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Branching fraction measurements of psi (3686) -> gamma chi(cJ)
- 2017
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Ingår i: Physical Review D. - 2470-0010 .- 2470-0029. ; 96:3
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Tidskriftsartikel (refereegranskat)abstract
- Using a sample of 106 million psi(3686) decays, the branching fractions of psi(3686) -> gamma chi(c0), psi(3686) -> gamma chi(c1), and psi(3686) -> gamma chi(c2) are measured with improved precision to be (9.389 +/- 0.014 +/- 0.332) %, (9.905 +/- 0.011 +/- 0.353) %, and (9.621 +/- 0.013 +/- 0.272) %, respectively, where the first uncertainties are statistical and the second ones are systematic. The product branching fractions of (psi 3686) -> gamma chi(c1), chi(c1) -> gamma J/psi (3686) -> gamma chi(c2), chi(c2) -> gamma J/psi and the branching fractions of chi(c1) -> gamma J/psi and chi(c2) -> gamma J/psi are also presented.
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- Ablikim, M., et al.
(författare)
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Evidence for e+e−→γηc(1S) at center-of-mass energies between 4.01 and 4.60 GeV
- 2017
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Ingår i: Physical Review D. - 2470-0010 .- 2470-0029. ; 96:5
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Tidskriftsartikel (refereegranskat)abstract
- We present first evidence for the process e(+)e(-) -> gamma eta(c)(1S) at six center-of-mass energies between 4.01 and 4.60 GeV using data collected by the BESIII experiment operating at BEPCII. We measure the Born cross section at each energy using a combination of twelve eta(c)(1S) decay channels. We also combine all six energies under various assumptions for the energy-dependence of the cross section. If the process is assumed to proceed via the Y(4260), we measure a peak Born cross section sigma(peak)(e(+)e(-) -> gamma eta(c)(1S)) = 2.11 +/- 0.49 (stat.) +/- 0.36 (syst.) pb with a statistical significance of 4.2 sigma.
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