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| 2. |
- Campbell, PJ, et al.
(author)
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Pan-cancer analysis of whole genomes
- 2020
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In: Nature. - : Springer Science and Business Media LLC. - 1476-4687 .- 0028-0836. ; 578:7793, s. 82-
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Journal article (peer-reviewed)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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| 3. |
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| 4. |
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| 5. |
- Bravo, L, et al.
(author)
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- 2021
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swepub:Mat__t
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| 6. |
- Niemi, MEK, et al.
(author)
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- 2021
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swepub:Mat__t
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| 7. |
- Tabiri, S, et al.
(author)
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- 2021
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swepub:Mat__t
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| 8. |
- Kanai, M, et al.
(author)
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- 2023
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swepub:Mat__t
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| 9. |
- Ablikim, M., et al.
(author)
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Amplitude analysis of D0 → K -π+π+π-
- 2017
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In: Physical Review D. - 2470-0010 .- 2470-0029. ; 95:7
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Journal article (peer-reviewed)abstract
- We present an amplitude analysis of the decay D0 → K -π+π+π- based on a data sample of 2.93 fb−1 acquired by the BESIII detector at the ψ(3770) resonance. With a nearly background free sample of about 16000 events, we investigate the substructure of the decay and determine the relative fractions and the phases among the different intermediate processes. Our amplitude model includes the two-body decays D0 → ¯K*0ρ0, D0 → K−a+1(1260) and D0 → K−1(1270)π+, the three-body decays D0 →¯K*0π+π− and D0 → K−π+ρ0, as well as the four-body nonresonant decay D0 → K−π+π+π−. The dominant intermediate process is D0 → K−a+1(1260), accounting for a fit fraction of 54.6%.
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| 10. |
- Ablikim, M., et al.
(author)
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Amplitude analysis of the chi(c1) -> eta pi(+)pi(-) decays
- 2017
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In: Physical Review D. - : AMER PHYSICAL SOC. - 2470-0010 .- 2470-0029. ; 95:3
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Journal article (peer-reviewed)abstract
- Using 448.0 x 10(6) psi(3686) events collected with the BESIII detector, an amplitude analysis is performed for psi(3686) -> gamma chi(c1), chi(c1) ->eta pi(+)pi(-) decays. The most dominant two- body structure observed is a(0)(980)(+/-) pi(-/+); a(0)(980)(+/-) -> eta pi(+/-.) line shape is modeled using a dispersion relation, and a significant nonzero a(0) (980) coupling to the eta'pi channel is measured. We observe chi(c1) -> a(2)(1700)pi production for the first time, with a significance larger than 17 sigma. The production of mesons with exotic quantum numbers, J(PC) = 1(-+), is investigated, and upper limits for the branching fractions chi(c1) -> pi(1)(1400)(+/-)pi(-/+) , chi(c1) -> pi(1)(1600)(+/-)pi(-/+) and chi(c1) -> pi 1(2015)(+/-)pi(-/+) with subsequent pi(1)(X)(+/-) -> eta pi(+/-) decay, are determined.
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