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Sökning: WFRF:(Hu Zhibin)

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1.
  • Wang, Zhaoming, et al. (författare)
  • Imputation and subset-based association analysis across different cancer types identifies multiple independent risk loci in the TERT-CLPTM1L region on chromosome 5p15.33
  • 2014
  • Ingår i: Human Molecular Genetics. - 0964-6906 .- 1460-2083. ; 23:24, s. 6616-6633
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Genome-wide association studies (GWAS) have mapped risk alleles for at least 10 distinct cancers to a small region of 63 000 bp on chromosome 5p15.33. This region harbors the TERT and CLPTM1L genes; the former encodes the catalytic subunit of telomerase reverse transcriptase and the latter may play a role in apoptosis. To investigate further the genetic architecture of common susceptibility alleles in this region, we conducted an agnostic subset-based meta-analysis (association analysis based on subsets) across six distinct cancers in 34 248 cases and 45 036 controls. Based on sequential conditional analysis, we identified as many as six independent risk loci marked by common single-nucleotide polymorphisms: five in the TERT gene (Region 1: rs7726159, P = 2.10 × 10(-39); Region 3: rs2853677, P = 3.30 × 10(-36) and PConditional = 2.36 × 10(-8); Region 4: rs2736098, P = 3.87 × 10(-12) and PConditional = 5.19 × 10(-6), Region 5: rs13172201, P = 0.041 and PConditional = 2.04 × 10(-6); and Region 6: rs10069690, P = 7.49 × 10(-15) and PConditional = 5.35 × 10(-7)) and one in the neighboring CLPTM1L gene (Region 2: rs451360; P = 1.90 × 10(-18) and PConditional = 7.06 × 10(-16)). Between three and five cancers mapped to each independent locus with both risk-enhancing and protective effects. Allele-specific effects on DNA methylation were seen for a subset of risk loci, indicating that methylation and subsequent effects on gene expression may contribute to the biology of risk variants on 5p15.33. Our results provide strong support for extensive pleiotropy across this region of 5p15.33, to an extent not previously observed in other cancer susceptibility loci.</p>
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2.
  • Sampson, Joshua N., et al. (författare)
  • Analysis of Heritability and Shared Heritability Based on Genome-Wide Association Studies for 13 Cancer Types
  • 2015
  • Ingår i: Journal of the National Cancer Institute. - 0027-8874 .- 1460-2105. ; 107:12
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>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.</p>
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3.
  • Sampson, Joshua N., et al. (författare)
  • Analysis of Heritability and Shared Heritability Based on Genome-Wide Association Studies for 13 Cancer Types
  • 2015
  • Ingår i: Journal of the National Cancer Institute. - 0027-8874 .- 1460-2105. ; 107:12
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>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.</p><p>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.</p><p>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.</p><p>Conclusion: Our results provide important insights into the genetic architecture of cancers and suggest new avenues for investigation.</p>
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4.
  • Dai, Juncheng, et al. (författare)
  • Genome-wide association study of INDELs identified four novel susceptibility loci associated with lung cancer risk
  • 2020
  • Ingår i: International Journal of Cancer. - John Wiley & Sons. - 0020-7136 .- 1097-0215. ; 146:10, s. 2855-2864
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Genome-wide association studies (GWAS) have identified 45 susceptibility loci associated with lung ncer. Only less than SNPs, small insertions and deletions (INDELs) are the second most abundant netic polymorphisms in the human genome. INDELs are highly associated with multiple human seases, including lung cancer. However, limited studies with large-scale samples have been available to stematically evaluate the effects of INDELs on lung cancer risk. Here, we performed a large-scale meta- alysis to evaluate INDELs and their risk for lung cancer in 23,202 cases and 19,048 controls. Functional notations were performed to further explore the potential function of lung cancer risk INDELs. nditional analysis was used to clarify the relationship between INDELs and SNPs. Four new risk loci re identified in genome-wide INDEL analysis (1p13.2: rs5777156, Insertion, OR = 0.92, p = 9.10 x 10(- ; 4q28.2: rs58404727, Deletion, OR = 1.19, p = 5.25 x 10(-7); 12p13.31: rs71450133, Deletion, OR = 09, p = 8.83 x 10(-7); and 14q22.3: rs34057993, Deletion, OR = 0.90, p = 7.64 x 10(-8)). The eQTL alysis and functional annotation suggested that INDELs might affect lung cancer susceptibility by gulating the expression of target genes. After conducting conditional analysis on potential causal SNPs, e INDELs in the new loci were still nominally significant. Our findings indicate that INDELs could be tentially functional genetic variants for lung cancer risk. Further functional experiments are needed to tter understand INDEL mechanisms in carcinogenesis.</p>
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5.
  • Dai, Juncheng, et al. (författare)
  • Genome-wide association study of INDELs identified four novel susceptibility loci associated with lung cancer risk
  • ????
  • Ingår i: International Journal of Cancer. - John Wiley and Sons Inc.. - 0020-7136.
  • Tidskriftsartikel (refereegranskat)abstract
    • Genome-wide association studies (GWAS) have identified 45 susceptibility loci associated with lung cancer. Only less than SNPs, small insertions and deletions (INDELs) are the second most abundant genetic polymorphisms in the human genome. INDELs are highly associated with multiple human diseases, including lung cancer. However, limited studies with large-scale samples have been available to systematically evaluate the effects of INDELs on lung cancer risk. Here, we performed a large-scale meta-analysis to evaluate INDELs and their risk for lung cancer in 23,202 cases and 19,048 controls. Functional annotations were performed to further explore the potential function of lung cancer risk INDELs. Conditional analysis was used to clarify the relationship between INDELs and SNPs. Four new risk loci were identified in genome-wide INDEL analysis (1p13.2: rs5777156, Insertion, OR = 0.92, p = 9.10 × 10−8; 4q28.2: rs58404727, Deletion, OR = 1.19, p = 5.25 × 10−7; 12p13.31: rs71450133, Deletion, OR = 1.09, p = 8.83 × 10−7; and 14q22.3: rs34057993, Deletion, OR = 0.90, p = 7.64 × 10−8). The eQTL analysis and functional annotation suggested that INDELs might affect lung cancer susceptibility by regulating the expression of target genes. After conducting conditional analysis on potential causal SNPs, the INDELs in the new loci were still nominally significant. Our findings indicate that INDELs could be potentially functional genetic variants for lung cancer risk. Further functional experiments are needed to better understand INDEL mechanisms in carcinogenesis.
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6.
  • Dai, Juncheng, et al. (författare)
  • Systematic analyses of regulatory variants in DNase I hypersensitive sites identified two novel lung cancer susceptibility loci
  • 2019
  • Ingår i: Carcinogenesis. - Oxford University Press. - 0143-3334 .- 1460-2180. ; 40:3, s. 432-440
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>DNase I hypersensitive sites (DHS) are abundant in regulatory elements, such as promoter, enhancer and transcription factor binding sites. Many studies have revealed that disease-associated variants were concentrated in DHS-related regions. However, limited studies are available on the roles of DHS-related variants in lung cancer. In this study, we performed a large-scale case-control study with 20 871 lung cancer cases and 15 971 controls to evaluate the associations between regulatory genetic variants in DHS and lung cancer susceptibility. The expression quantitative trait loci (eQTL) analysis and pathway-enrichment analysis were performed to identify the possible target genes and pathways. In addition, we performed motif-based analysis to explore the lung-cancer-related motifs using sequence kernel association test. Two novel variants, rs186332 in 20q13.3 (C&gt;T, odds ratio [OR] = 1.17, 95% confidence interval [95% CI]: 1.10-1.24, P = 8.45 x 10(-7)) and rs4839323 in 1p13.2 (T&gt;C, OR = 0.92, 95% CI: 0.89-0.95, P = 1.02 x 10(-6)) showed significant association with lung cancer risk. The eQTL analysis suggested that these two SNPs might regulate the expression of MRGBP and SLC16A1, respectively. What's more, the expression of both MRGBP and SLC16A1 was aberrantly elevated in lung tumor tissues. The motif-based analysis identified 10 motifs related to the risk of lung cancer (P &lt; 1.71 x 10(-4)). Our findings suggested that variants in DHS might modify lung cancer susceptibility through regulating the expression of surrounding genes. This study provided us a deeper insight into the roles of DHS-related genetic variants for lung cancer.</p>
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7.
  • Dai, Juncheng, et al. (författare)
  • Systematic analyses of regulatory variants in DNase I hypersensitive sites identified two novel lung cancer susceptibility loci
  • 2019
  • Ingår i: Carcinogenesis. - Oxford University Press. - 0143-3334. ; 40:3, s. 432-440
  • Tidskriftsartikel (refereegranskat)abstract
    • DNase I hypersensitive sites (DHS) are abundant in regulatory elements, such as promoter, enhancer and transcription factor binding sites. Many studies have revealed that disease-associated variants were concentrated in DHS-related regions. However, limited studies are available on the roles of DHS-related variants in lung cancer. In this study, we performed a large-scale case-control study with 20 871 lung cancer cases and 15 971 controls to evaluate the associations between regulatory genetic variants in DHS and lung cancer susceptibility. The expression quantitative trait loci (eQTL) analysis and pathway-enrichment analysis were performed to identify the possible target genes and pathways. In addition, we performed motif-based analysis to explore the lung-cancer-related motifs using sequence kernel association test. Two novel variants, rs186332 in 20q13.3 (C>T, odds ratio [OR] = 1.17, 95% confidence interval [95% CI]: 1.10-1.24, P = 8.45 × 10-7) and rs4839323 in 1p13.2 (T>C, OR = 0.92, 95% CI: 0.89-0.95, P = 1.02 × 10-6) showed significant association with lung cancer risk. The eQTL analysis suggested that these two SNPs might regulate the expression of MRGBP and SLC16A1, respectively. What's more, the expression of both MRGBP and SLC16A1 was aberrantly elevated in lung tumor tissues. The motif-based analysis identified 10 motifs related to the risk of lung cancer (P < 1.71 × 10-4). Our findings suggested that variants in DHS might modify lung cancer susceptibility through regulating the expression of surrounding genes. This study provided us a deeper insight into the roles of DHS-related genetic variants for lung cancer.
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8.
  • 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. - 0008-5472 .- 1538-7445. ; 76:17, s. 5103-5114
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>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.</p>
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9.
  • Fu, Le, et al. (författare)
  • Ultrastrong Translucent Glass Ceramic with Nanocrystalline, Biomimetic Structure.
  • 2018
  • Ingår i: Nano letters. - 1530-6992. ; 18:11, s. 7146-7154
  • Tidskriftsartikel (refereegranskat)abstract
    • Transparent/translucent glass ceramics (GCs) have broad applications in biomedicine, armor, energy, and constructions. However, GCs with improved optical properties typically suffer from impaired mechanical properties, compared to traditional sintered full-ceramics. We present a method of obtaining high-strength, translucent GCs by preparing ZrO2-SiO2 nanocrystalline glass ceramics (NCGCs) with a microstructure of monocrystalline ZrO2 nanoparticles (NPs), embedded in an amorphous SiO2 matrix. The ZrO2-SiO2 NCGC with a composition of 65%ZrO/35%SiO2 (molar ratio, 65Zr) achieved an average flexural strength of 1 GPa. This is one of the highest flexural strength values ever reported for GCs. ZrO2 NPs bond strongly with SiO2 matrix due to the formation of a thin (2-3 nm) amorphous Zr/Si interfacial layer between the ZrO2 NPs and SiO2 matrix. The diffusion of Si atoms into the ZrO2 NPs forms a Zr-O-Si superlattice. Electron tomography results show that some of the ZrO2 NPs are connected in one direction, forming in situ ZrO2 nanofibers (with length of ∼500 nm), and that the ZrO2 nanofibers are stacked in an ordered way in all three dimensions. The nanoarchitecture of the ZrO2 nanofibers mimics the architecture of mineralized collagen fibril in cortical bone. Strong interface bonding enables efficient load transfer from the SiO2 matrix to the 3D nanoarchitecture built by ZrO2 nanofibers and NPs, and the 3D nanoarchitecture carries the majority of the external load. These two factors synergistically contribute to the high strength of the 65Zr NCGC. This study deepens our fundamental understanding of the microstructure-mechanical strength relationship, which could guide the design and manufacture of other high-strength, translucent GCs.
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10.
  • Fu, Le, et al. (författare)
  • Ultrastrong translucent glass ceramic with nanocrystalline, biomimetic structure
  • 2018
  • Ingår i: Nano letters (Print). - 1530-6984 .- 1530-6992. ; 18:11, s. 7146-7154
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Transparent/translucent glass ceramics (GCs) have broad applications in biomedicine, armor, energy, and constructions. However, GCs with improved optical properties typically suffer from impaired mechanical properties, compared to traditional sintered full-ceramics. We present a method of obtaining high-strength, translucent GCs by preparing ZrO<sub>2</sub>-SiO<sub>2</sub> nanocrystalline glass ceramics (NCGCs), with a microstructure of monocrystalline ZrO<sub>2</sub> nanoparticles (NPs), embedded in an amorphous SiO<sub>2</sub> matrix. The ZrO<sub>2</sub>-SiO<sub>2</sub> NCGC with a composition of 65%ZrO<sub>2</sub>-35%SiO<sub>2</sub> (molar ratio, 65Zr) achieved an average flexural strength of 1 GPa. This is one of the highest flexural strength values ever reported for GCs. ZrO<sub>2</sub> NPs have a core-shell structure, and the shell is a thin (2–3 nm) amorphous Zr/Si interfacial layer that provides strong bonding between the ZrO<sub>2</sub> NPs and SiO<sub>2</sub> matrix. The diffusion of Si atoms into the ZrO<sub>2</sub> NPs forms a Zr-O-Si superlattice. Electron tomography results show that some of the ZrO<sub>2</sub> NPs are connected in one direction, forming <em>in situ</em> ZrO<sub>2 </sub>nanofibers (with length of ~500 nm), and that the ZrO<sub>2</sub> nanofibers are stacked in an ordered way in all three dimensions. The nano-architecture of the ZrO<sub>2</sub> nanofibers mimics the architecture of mineralized collagen fibril in cortical bone. Strong interface bonding enables efficient load transfer from the SiO<sub>2</sub> matrix to the 3D nano-architecture built by ZrO<sub>2</sub> nanofibers and NPs, and the 3D nano-architecture carries the majority of the external load. These two factors synergistically contribute to the high strength of the 65Zr NCGC. This study deepens our fundamental understanding of the microstructure-mechanical strength relationship, which could guide the design and manufacture of other high-strength, translucent GCs.</p>
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