SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "WFRF:(Gong Jian) "

Sökning: WFRF:(Gong Jian)

  • Resultat 1-10 av 16
  • [1]2Nästa
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
1.
  • Fehringer, Gordon, et al. (författare)
  • Cross-Cancer Genome-Wide Analysis of Lung, Ovary, Breast, Prostate, and Colorectal Cancer Reveals Novel Pleiotropic Associations
  • 2016
  • Ingår i: Cancer research. - 1538-7445. ; 76:17, s. 5103-5114
  • Tidskriftsartikel (refereegranskat)abstract
    • Identifying genetic variants with pleiotropic associations can uncover common pathways influencing multiple cancers. We took a two-staged approach to conduct genome-wide association studies for lung, ovary, breast, prostate and colorectal cancer from the GAME-ON/GECCO Network (61,851 cases, 61,820 controls) to identify pleiotropic loci. Findings were replicated in independent association studies (55,789 cases, 330,490 controls). We identified a novel pleiotropic association at 1q22 involving breast and lung squamous cell carcinoma, with eQTL analysis showing an association with ADAM15/THBS3 gene expression in lung. We also identified a known breast cancer locus CASP8/ALS2CR12 associated with prostate cancer, a known cancer locus at CDKN2B-AS1 with different variants associated with lung adenocarcinoma and prostate cancer and confirmed the associations of a breast BRCA2 locus with lung and serous ovarian cancer. This is the largest study to date examining pleiotropy across multiple cancer-associated loci, identifying common mechanisms of cancer development and progression.
  •  
2.
  • Locke, Adam E, et al. (författare)
  • Genetic studies of body mass index yield new insights for obesity biology
  • 2015
  • Ingår i: Nature. - 0028-0836 .- 1476-4687. ; 518:7538, s. 197-206
  • Tidskriftsartikel (refereegranskat)abstract
    • Obesity is heritable and predisposes to many diseases. To understand the genetic basis of obesity better, here we conduct a genome-wide association study and Metabochip meta-analysis of body mass index (BMI), a measure commonly used to define obesity and assess adiposity, in up to 339,224 individuals. This analysis identifies 97 BMI-associated loci (P < 5 × 10−8), 56 of which are novel. Five loci demonstrate clear evidence of several independent association signals, and many loci have significant effects on other metabolic phenotypes. The 97 loci account for ~2.7% of BMI variation, and genome-wide estimates suggest that common variation accounts for >20% of BMI variation. Pathway analyses provide strong support for a role of the central nervous system in obesity susceptibility and implicate new genes and pathways, including those related to synaptic function, glutamate signalling, insulin secretion/action, energy metabolism, lipid biology and adipogenesis.
3.
  •  
4.
  • Thrift, Aaron P., et al. (författare)
  • Mendelian randomization study of height and risk of colorectal cancer
  • 2015
  • Ingår i: International Journal of Epidemiology. - 0300-5771 .- 1464-3685. ; 44:2, s. 662-672
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: For men and women, taller height is associated with increased risk of all cancers combined. For colorectal cancer (CRC), it is unclear whether the differential association of height by sex is real or is due to confounding or bias inherent in observational studies. We performed a Mendelian randomization study to examine the association between height and CRC risk. Methods: To minimize confounding and bias, we derived a weighted genetic risk score predicting height (using 696 genetic variants associated with height) in 10 226 CRC cases and 10 286 controls. Logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (95% CI) for associations between height, genetically predicted height and CRC. Results: Using conventional methods, increased height (per 10-cm increment) was associated with increased CRC risk (OR = 1.08, 95% CI = 1.02-1.15). In sex-specific analyses, height was associated with CRC risk for women (OR = 1.15, 95% CI = 1.05-1.26), but not men (OR = 0.98, 95% CI = 0.92-1.05). Consistent with these results, carrying greater numbers of (weighted) height-increasing alleles (per 1-unit increase) was associated with higher CRC risk for women and men combined (OR = 1.07, 95% CI = 1.01-1.14) and for women (OR = 1.09, 95% CI = 1.01-1.19). There was weaker evidence of an association for men (OR = 1.05, 95% CI = 0.96-1.15). Conclusion: We provide evidence for a causal association between height and CRC for women. The CRC-height association for men remains unclear and warrants further investigation in other large studies.
5.
  • Wood, Andrew R, et al. (författare)
  • Defining the role of common variation in the genomic and biological architecture of adult human height
  • 2014
  • Ingår i: Nature Genetics. - 1061-4036 .- 1546-1718. ; 46:11, s. 1173-1186
  • Tidskriftsartikel (refereegranskat)abstract
    • Using genome-wide data from 253,288 individuals, we identified 697 variants at genome-wide significance that together explained one-fifth of the heritability for adult height. By testing different numbers of variants in independent studies, we show that the most strongly associated ∼2,000, ∼3,700 and ∼9,500 SNPs explained ∼21%, ∼24% and ∼29% of phenotypic variance. Furthermore, all common variants together captured 60% of heritability. The 697 variants clustered in 423 loci were enriched for genes, pathways and tissue types known to be involved in growth and together implicated genes and pathways not highlighted in earlier efforts, such as signaling by fibroblast growth factors, WNT/β-catenin and chondroitin sulfate-related genes. We identified several genes and pathways not previously connected with human skeletal growth, including mTOR, osteoglycin and binding of hyaluronic acid. Our results indicate a genetic architecture for human height that is characterized by a very large but finite number (thousands) of causal variants.
6.
  • Erzurumluoglu, A Mesut, et al. (författare)
  • Meta-analysis of up to 622,409 individuals identifies 40 novel smoking behaviour associated genetic loci
  • 2019
  • Ingår i: Molecular Psychiatry. - Nature Publishing Group. - 1359-4184 .- 1476-5578.
  • Tidskriftsartikel (refereegranskat)abstract
    • Smoking is a major heritable and modifiable risk factor for many diseases, including cancer, common respiratory disorders and cardiovascular diseases. Fourteen genetic loci have previously been associated with smoking behaviour-related traits. We tested up to 235,116 single nucleotide variants (SNVs) on the exome-array for association with smoking initiation, cigarettes per day, pack-years, and smoking cessation in a fixed effects meta-analysis of up to 61 studies (up to 346,813 participants). In a subset of 112,811 participants, a further one million SNVs were also genotyped and tested for association with the four smoking behaviour traits. SNV-trait associations with P < 5 × 10-8 in either analysis were taken forward for replication in up to 275,596 independent participants from UK Biobank. Lastly, a meta-analysis of the discovery and replication studies was performed. Sixteen SNVs were associated with at least one of the smoking behaviour traits (P < 5 × 10-8) in the discovery samples. Ten novel SNVs, including rs12616219 near TMEM182, were followed-up and five of them (rs462779 in REV3L, rs12780116 in CNNM2, rs1190736 in GPR101, rs11539157 in PJA1, and rs12616219 near TMEM182) replicated at a Bonferroni significance threshold (P < 4.5 × 10-3) with consistent direction of effect. A further 35 SNVs were associated with smoking behaviour traits in the discovery plus replication meta-analysis (up to 622,409 participants) including a rare SNV, rs150493199, in CCDC141 and two low-frequency SNVs in CEP350 and HDGFRP2. Functional follow-up implied that decreased expression of REV3L may lower the probability of smoking initiation. The novel loci will facilitate understanding the genetic aetiology of smoking behaviour and may lead to the identification of potential drug targets for smoking prevention and/or cessation.
  •  
7.
  • Figueroa, Jonine D., et al. (författare)
  • Identification of a novel susceptibility locus at 13q34 and refinement of the 20p12.2 region as a multi-signal locus associated with bladder cancer risk in individuals of European ancestry
  • 2016
  • Ingår i: Human Molecular Genetics. - Oxford University Press. - 0964-6906. ; 25:6, s. 1203-1214
  • Tidskriftsartikel (refereegranskat)abstract
    • Candidate gene and genome-wide association studies (GWAS) have identified 15 independent genomic regions associated with bladder cancer risk. In search for additional susceptibility variants, we followed up on four promising single-nucleotide polymorphisms (SNPs) that had not achieved genome-wide significance in 6911 cases and 11 814 controls (rs6104690, rs4510656, rs5003154 and rs4907479, P < 1 × 10−6), using additional data from existing GWAS datasets and targeted genotyping for studies that did not have GWAS data. In a combined analysis, which included data on up to 15 058 cases and 286 270 controls, two SNPs achieved genome-wide statistical significance: rs6104690 in a gene desert at 20p12.2 (P = 2.19 × 10−11) and rs4907479 within the MCF2L gene at 13q34 (P = 3.3 × 10−10). Imputation and fine-mapping analyses were performed in these two regions for a subset of 5551 bladder cancer cases and 10 242 controls. Analyses at the 13q34 region suggest a single signal marked by rs4907479. In contrast, we detected two signals in the 20p12.2 region—the first signal is marked by rs6104690, and the second signal is marked by two moderately correlated SNPs (r2 = 0.53), rs6108803 and the previously reported rs62185668. The second 20p12.2 signal is more strongly associated with the risk of muscle-invasive (T2-T4 stage) compared with non-muscle-invasive (Ta, T1 stage) bladder cancer (case–case P ≤ 0.02 for both rs62185668 and rs6108803). Functional analyses are needed to explore the biological mechanisms underlying these novel genetic associations with risk for bladder cancer.
  •  
8.
  • Gong, Cheng, et al. (författare)
  • Large eddy simulation of hydrogen combustion in supersonic flows using an Eulerian stochastic fields method
  • 2017
  • Ingår i: International Journal of Hydrogen Energy. - Elsevier. - 0360-3199. ; 42:2, s. 1264-1275
  • Tidskriftsartikel (refereegranskat)abstract
    • An Eulerian Monte-Carlo approach, the so-called Eulerian stochastic fields (ESF) method is implemented and evaluated for simulation of non-premixed hydrogen/air combustion in supersonic flows. The ESF method is integrated into a compressible flow large eddy simulation (LES) solver, and validated on a supersonic combustor with a strut as flame-holder. Comparison with experimental data and with results from a well-stirred reactor (WSR) model demonstrates the advantage of the LES-ESF method for simulation of local-extinction and re-ignition phenomena. The hydrogen/air flame structure and the stabilization of the combustion process in the supersonic combustor are analysed based on the present LES-ESF method. Oscillation of the recirculation zones is found to be the dominant mechanism for the local-extinction/re-ignition and the flame stabilization under the present condition.
  •  
9.
  •  
10.
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 1-10 av 16
  • [1]2Nästa
Åtkomst
fritt online (6)
Typ av publikation
tidskriftsartikel (14)
konferensbidrag (1)
doktorsavhandling (1)
Typ av innehåll
refereegranskat (15)
övrigt vetenskapligt (1)
Författare/redaktör
Kooperberg, Charles (9)
Chang-Claude, Jenny (6)
Haiman, Christopher ... (6)
Stancáková, Alena, (6)
Langenberg, Claudia (6)
Scott, Robert A (6)
visa fler...
Le Marchand, Loïc (6)
Mangino, Massimo (6)
Luan, Jian'an (6)
Esko, Tonu (6)
Hayward, Caroline (6)
Stringham, Heather M ... (6)
Müller-Nurasyid, Mar ... (6)
Yengo, Loïc, (5)
Schumacher, Fredrick ... (5)
Berndt, Sonja I (5)
Amin, Najaf, (5)
Teumer, Alexander, (5)
Blangero, John, (5)
Gudnason, Vilmundur, (5)
Hartman, Catharina A ... (5)
Hofman, Albert, (5)
Montgomery, Grant W. ... (5)
Nauck, Matthias, (5)
Kuusisto, Johanna, (5)
Rose, Lynda M (5)
Zhao, Wei, (5)
Hunter, David J. (5)
Jackson, Anne U. (5)
Heard-Costa, Nancy L ... (5)
Winkler, Thomas W. (5)
Feitosa, Mary F. (5)
Kutalik, Zoltan (5)
Sanna, Serena (5)
Campbell, Harry (5)
Bergman, Richard N. (5)
Collins, Francis S. (5)
Wright, Alan F. (5)
Harris, Tamara B. (5)
Abecasis, Goncalo R. (5)
Nolte, Ilja M (5)
Tanaka, Toshiko (5)
Kumari, Meena (5)
James, Alan L (5)
Beilby, John (5)
Wong, Andrew (5)
Kleber, Marcus E. (5)
van Vliet-Ostaptchou ... (5)
Smith, Jennifer A., (5)
Faul, Jessica D., (5)
visa färre...
Lärosäte
Uppsala universitet (10)
Umeå universitet (9)
Karolinska Institutet (9)
Göteborgs universitet (5)
Lunds universitet (5)
Högskolan Dalarna (2)
visa fler...
Högskolan i Gävle (1)
visa färre...
Språk
Engelska (16)
Forskningsämne (UKÄ/SCB)
Medicin och hälsovetenskap (12)
Naturvetenskap (2)
Teknik (2)

År

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy