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- Sampson, Joshua N., et al.
(författare)
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Analysis of Heritability and Shared Heritability Based on Genome-Wide Association Studies for 13 Cancer Types
- 2015
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Ingår i: Journal of the National Cancer Institute. - : Oxford University Press (OUP). - 0027-8874 .- 1460-2105. ; 107:12
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Tidskriftsartikel (refereegranskat)abstract
- Background: Studies of related individuals have consistently demonstrated notable familial aggregation of cancer. We aim to estimate the heritability and genetic correlation attributable to the additive effects of common single-nucleotide polymorphisms (SNPs) for cancer at 13 anatomical sites. Methods: Between 2007 and 2014, the US National Cancer Institute has generated data from genome-wide association studies (GWAS) for 49 492 cancer case patients and 34 131 control patients. We apply novel mixed model methodology (GCTA) to this GWAS data to estimate the heritability of individual cancers, as well as the proportion of heritability attributable to cigarette smoking in smoking-related cancers, and the genetic correlation between pairs of cancers. Results: GWAS heritability was statistically significant at nearly all sites, with the estimates of array-based heritability, h(l)(2), on the liability threshold (LT) scale ranging from 0.05 to 0.38. Estimating the combined heritability of multiple smoking characteristics, we calculate that at least 24% (95% confidence interval [CI] = 14% to 37%) and 7% (95% CI = 4% to 11%) of the heritability for lung and bladder cancer, respectively, can be attributed to genetic determinants of smoking. Most pairs of cancers studied did not show evidence of strong genetic correlation. We found only four pairs of cancers with marginally statistically significant correlations, specifically kidney and testes (rho = 0.73, SE = 0.28), diffuse large B-cell lymphoma (DLBCL) and pediatric osteosarcoma (rho = 0.53, SE = 0.21), DLBCL and chronic lymphocytic leukemia (CLL) (rho = 0.51, SE = 0.18), and bladder and lung (rho = 0.35, SE = 0.14). Correlation analysis also indicates that the genetic architecture of lung cancer differs between a smoking population of European ancestry and a nonsmoking Asian population, allowing for the possibility that the genetic etiology for the same disease can vary by population and environmental exposures. Conclusion: Our results provide important insights into the genetic architecture of cancers and suggest new avenues for investigation.
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- Ablikim, M., et al.
(författare)
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Analysis of D+ -> (K)over-bar(0)e(+)nu(e) and D+ -> pi(0)e(+)nu(e) semileptonic decays
- 2017
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Ingår i: Physical Review D. - : AMER PHYSICAL SOC. - 2470-0010 .- 2470-0029. ; 96:1
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Tidskriftsartikel (refereegranskat)abstract
- Using 2.93 fb(-1) of data taken at 3.773 GeV with the BESIII detector operated at the BEPCII collider, we study the semileptonic decays D+ -> (K) over bar (0)e(+)nu(e) and D+ -> pi(0)e(+)nu(e). We measure the absolute decay branching fractions B(D+ -> (K) over bar (0)e(+)nu(e)) = (8.60 +/- 0.06 +/- 0.15) x 10(-2) and B(D+ -> pi(0)e(+)nu(e)) = (3.63 +/- 0.08 +/- 0.05) x 10(-3), where the first uncertainties are statistical and the second systematic. We also measure the differential decay rates and study the form factors of these two decays. With the values of |V-cs| and |V-cd| from Particle Data Group fits assuming Cabibbo-Kobayashi-Maskawa (CKM) unitarity, we obtain the values of the form factors at q(2) = 0, f(+)(K)(0) = 0.725 +/- 0.004 +/- 0.012, and f(+)(pi)(0) = 0.622 +/- 0.012 +/- 0.003. Taking input from recent lattice QCD calculations of these form factors, we determine values of the CKM matrix elements |V-cs| = 0.944 +/- 0.005 +/- 0.015 +/- 0.024 and |V-cd| = 0.210 +/- 0.004 +/- 0.001 +/- 0.009, where the third uncertainties are theoretical.
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| 8. |
- Aad, G, et al.
(författare)
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- 2015
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swepub:Mat__t
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| 9. |
- Ablikim, M., et al.
(författare)
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Amplitude analysis of D0 → K -π+π+π-
- 2017
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Ingår i: Physical Review D. - 2470-0010 .- 2470-0029. ; 95:7
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Tidskriftsartikel (refereegranskat)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.
(författare)
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Amplitude analysis of the chi(c1) -> eta pi(+)pi(-) decays
- 2017
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Ingår i: Physical Review D. - : AMER PHYSICAL SOC. - 2470-0010 .- 2470-0029. ; 95:3
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Tidskriftsartikel (refereegranskat)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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