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Su, Li

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Su, Li

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2005 - 200932010 - 201816

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Author's Publications: search.filters.isAuthorOfPublication.4949c74a-4bc6-415c-8b2a-3c516415bd35

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Now showing 1 - 10 of 19
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    Whole blood microRNA markers are associated with acute respiratory distress syndrome
    (Springer International Publishing, 2017) Zhu, Zhaozhong; Liang, Liming; Zhang, Ruyang; Wei, Yongyue; Su, Li; Tejera, Paula; Guo, Yichen; Wang, Zhaoxi; Lu, Quan; Baccarelli, Andrea; Zhu, Xi; Bajwa, Ednan; Taylor Thompson, B.; Shi, Guo-Ping; Christiani, David
    Background: MicroRNAs (miRNAs) can play important roles in inflammation and infection, which are common manifestations of acute respiratory distress syndrome (ARDS). We assessed if whole blood miRNAs were potential diagnostic biomarkers for human ARDS. Methods: This nested case-control study (N = 530) examined a cohort of ARDS patients and critically ill at-risk controls. Whole blood miRNA profiles and logistic regression analyses identified miRNAs correlated with ARDS. Stratification analysis also assessed selected miRNA markers for their role in sepsis and pneumonia associated with ARDS. Receiver operating characteristic (ROC) analysis evaluated miRNA diagnostic performance, along with Lung Injury Prediction Score (LIPS). Results: Statistical analyses were performed on 294 miRNAs, selected from 754 miRNAs after quality control screening. Logistic regression identified 22 miRNAs from a 156-patient discovery cohort as potential risk or protective markers of ARDS. Three miRNAs—miR-181a, miR-92a, and miR-424—from the discovery cohort remained significantly associated with ARDS in a 373-patient independent validation cohort (FDR q < 0.05) and meta-analysis (p < 0.001). ROC analyses demonstrated a LIPS baseline area-under-the-curve (AUC) value of ARDS of 0.708 (95% CI 0.651–0.766). Addition of miR-181a, miR-92a, and miR-424 to LIPS increased baseline AUC to 0.723 (95% CI 0.667–0.778), with a relative integrated discrimination improvement of 2.40 (p = 0.005) and a category-free net reclassification index of 27.21% (p = 0.01). Conclusions: miR-181a and miR-92a are risk biomarkers for ARDS, whereas miR-424 is a protective biomarker. Addition of these miRNAs to LIPS can improve the risk estimate for ARDS. Electronic supplementary material The online version of this article (10.1186/s40635-017-0155-0) contains supplementary material, which is available to authorized users.
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    Multi-Omics Analysis Reveals a HIF Network and Hub Gene EPAS1 Associated with Lung Adenocarcinoma
    (Elsevier, 2018) Wang, Zhaoxi; Wei, Yongyue; Zhang, Ruyang; Su, Li; Gogarten, Stephanie M.; Liu, Geoffrey; Brennan, Paul; Field, John K.; McKay, James D.; Lissowska, Jolanta; Swiatkowska, Beata; Janout, Vladimir; Bolca, Ciprian; Kontic, Milica; Scelo, Ghislaine; Zaridze, David; Laurie, Cathy C.; Doheny, Kimberly F.; Pugh, Elizabeth K.; Marosy, Beth A.; Hetrick, Kurt N.; Xiao, Xiangjun; Pikielny, Claudio; Hung, Rayjean J.; Amos, Christopher I.; Lin, Xihong; Christiani, David
    Recent technological advancements have permitted high-throughput measurement of the human genome, epigenome, metabolome, transcriptome, and proteome at the population level. We hypothesized that subsets of genes identified from omic studies might have closely related biological functions and thus might interact directly at the network level. Therefore, we conducted an integrative analysis of multi-omic datasets of non-small cell lung cancer (NSCLC) to search for association patterns beyond the genome and transcriptome. A large, complex, and robust gene network containing well-known lung cancer-related genes, including EGFR and TERT, was identified from combined gene lists for lung adenocarcinoma. Members of the hypoxia-inducible factor (HIF) gene family were at the center of this network. Subsequent sequencing of network hub genes within a subset of samples from the Transdisciplinary Research in Cancer of the Lung-International Lung Cancer Consortium (TRICL-ILCCO) consortium revealed a SNP (rs12614710) in EPAS1 associated with NSCLC that reached genome-wide significance (OR = 1.50; 95% CI: 1.31–1.72; p = 7.75 × 10−9). Using imputed data, we found that this SNP remained significant in the entire TRICL-ILCCO consortium (p = .03). Additional functional studies are warranted to better understand interrelationships among genetic polymorphisms, DNA methylation status, and EPAS1 expression.
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    A multi‐omic study reveals BTG2 as a reliable prognostic marker for early‐stage non‐small cell lung cancer
    (John Wiley and Sons Inc., 2018) Shen, Sipeng; Zhang, Ruyang; Guo, Yichen; Loehrer, Elizabeth; Wei, Yongyue; Zhu, Ying; Yuan, Qianyu; Moran, Sebastian; Fleischer, Thomas; Bjaanæs, Maria M.; Karlsson, Anna; Planck, Maria; Staaf, Johan; Helland, Åslaug; Esteller, Manel; Su, Li; Chen, Feng; Christiani, David
    B‐cell translocation gene 2 (BTG2) is a tumour suppressor protein known to be downregulated in several types of cancer. In this study, we investigated a potential role for BTG2 in early‐stage non‐small cell lung cancer (NSCLC) survival. We analysed BTG2 methylation data from 1230 early‐stage NSCLC patients from five international cohorts, as well as gene expression data from 3038 lung cancer cases from multiple cohorts. Three CpG probes (cg01798157, cg06373167, cg23371584) that detected BTG2 hypermethylation in tumour tissues were associated with lower overall survival. The prognostic model based on methylation could distinguish patient survival in the four cohorts [hazard ratio (HR) range, 1.51–2.21] and the independent validation set (HR = 1.85). In the expression analysis, BTG2 expression was positively correlated with survival in each cohort (HR range, 0.28–0.68), which we confirmed with meta‐analysis (HR = 0.61, 95% CI 0.54–0.68). The three CpG probes were all negatively correlated with BTG2 expression. Importantly, an integrative model of BTG2 methylation, expression and clinical information showed better predictive ability in the training set and validation set. In conclusion, the methylation and integrated prognostic signatures based on BTG2 are stable and reliable biomarkers for early‐stage NSCLC. They may have new applications for appropriate clinical adjuvant trials and personalized treatments in the future.
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    Global Metabolomic Profiling Reveals an Association of Metal Fume Exposure and Plasma Unsaturated Fatty Acids
    (Public Library of Science, 2013) Wei, Yongyue; Wang, Zhaoxi; Chang, Chiung-yu; Fan, Tianteng; Su, Li; Chen, Feng; Christiani, David
    Background: Welding-associated air pollutants negatively affect the health of exposed workers; however, their molecular mechanisms in causing disease remain largely unclear. Few studies have systematically investigated the systemic toxic effects of welding fumes on humans. Objectives: To explore the effects of welding fumes on the plasma metabolome, and to identify biomarkers for risk assessment of welding fume exposure. Methods: The two-stage, self-controlled exploratory study included 11 boilermakers from a 2011 discovery panel and 8 boilermakers from a 2012 validation panel. Plasma samples were collected pre- and post-welding fume exposure and analyzed by chromatography/mass spectrometry. Results: Eicosapentaenoic or docosapentaenoic acid metabolic changes post-welding were significantly associated with particulate (PM2.5) exposure (p<0.05). The combined analysis by linear mixed-effects model showed that exposure was associated with a statistically significant decline in metabolite change of eicosapentaenoic acid [(95% CI) = −0.013(−0.022∼−0.004); p = 0.005], docosapentaenoic acid n3 [(95% CI) = −0.010(−0.018∼−0.002); p = 0.017], and docosapentaenoic acid n6 [(95% CI) = −0.007(−0.013∼−0.001); p = 0.021]. Pathway analysis identified an association of the unsaturated fatty acid pathway with exposure (pStudy−2011 = 0.025; pStudy−2012 = 0.021; pCombined = 0.009). The functional network built by these fatty acids and their interactive genes contained significant enrichment of genes associated with various diseases, including neoplasms, cardiovascular diseases, and lipid metabolism disorders. Conclusions: High-dose exposure of metal welding fumes decreases unsaturated fatty acids with an exposure-response relationship. This alteration in fatty acids is a potential biological mediator and biomarker for exposure-related health disorders.
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    Adiponectin Gene Polymorphisms and Acute Respiratory Distress Syndrome Susceptibility and Mortality
    (Public Library of Science, 2014) Ahasic, Amy M.; Zhao, Yang; Su, Li; Sheu, Chau-Chyun; Thompson, B. Taylor; Christiani, David
    Rationale: Adiponectin is an anti-inflammatory adipokine that is the most abundant gene product of adipose tissue. Lower levels have been observed in obesity, insulin resistance, and in critical illness. However, elevated levels early in acute respiratory failure have been associated with mortality. Polymorphisms in adiponectin-related genes (ADIPOQ, ADIPOR1, ADIPOR2) have been examined for relationships with obesity, insulin resistance and diabetes, cardiovascular disease, and to circulating adipokine levels, but many gaps in knowledge remain. The current study aims to assess the association between potentially functional polymorphisms in adiponectin-related genes with acute respiratory distress syndrome (ARDS) risk and mortality. Methods: Consecutive patients with risk factors for ARDS admitted to the ICU were enrolled and followed prospectively for development of ARDS. ARDS cases were followed through day 60 for all-cause mortality. 2067 patients were successfully genotyped using the Illumina CVD BeadChip high-density platform. Of these, 567 patients developed ARDS. Forty-four single nucleotide polymorphisms (SNPs) on ADIPOQ, ADIPOR1 and ADIPOR2 were successfully genotyped. Of these, 9 SNPs were hypothesized to be functional based on their location (promoter, exon, or 3′ untranslated region). These 9 SNPs were analyzed for association with ARDS case status and mortality among ARDS cases. Results: After multivariable analysis and adjustment for multiple comparisons, no SNPs were significantly associated with ARDS case status. Among ARDS cases, homozygotes for the minor allele of rs2082940 (ADIPOQ) had increased mortality (hazard ratio 2.61, 95% confidence interval 1.36–5.00, p = 0.0039) after adjustment for significant covariates. The significance of this association persisted after adjustment for multiple comparisons (FDR_q = 0.029). Conclusions: A common and potentially functional polymorphism in ADIPOQ may impact survival in ARDS. Further studies are required to replicate these results and to correlate genotype with circulating adiponectin levels.
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    Rare variants of large effect in BRCA2 and CHEK2 affect risk of lung cancer
    (Springer Nature, 2014) Wang, Yufei; McKay, James D; Rafnar, Thorunn; Wang, Zhaoming; Timofeeva, Maria N; Broderick, Peter; Zong, Xuchen; Laplana, Marina; Wei, Yongyue; Han, Younghun; Lloyd, Amy; Delahaye-Sourdeix, Manon; Chubb, Daniel; Gaborieau, Valerie; Wheeler, William; Chatterjee, Nilanjan; Thorleifsson, Gudmar; Sulem, Patrick; Liu, Geoffrey; Kaaks, Rudolf; Henrion, Marc; Kinnersley, Ben; Vallée, Maxime; LeCalvez-Kelm, Florence; Stevens, Victoria L; Gapstur, Susan M; Chen, Wei V; Zaridze, David; Szeszenia-Dabrowska, Neonilia; Lissowska, Jolanta; Rudnai, Peter; Fabianova, Eleonora; Mates, Dana; Bencko, Vladimir; Foretova, Lenka; Janout, Vladimir; Krokan, Hans E; Gabrielsen, Maiken Elvestad; Skorpen, Frank; Vatten, Lars Johan; Njølstad, Inger; Chen, Chu; Goodman, Gary; Benhamou, Simone; Vooder, Tonu; Välk, Kristjan; Nelis, Mari; Metspalu, Andres; Lener, Marcin; Lubiński, Jan; Johansson, Mattias; Vineis, Paolo; Agudo, Antonio; Clavel-Chapelon, Francoise; Bueno-de-Mesquita, H Bas; Trichopoulos, Dimitrios; Khaw, Kay-Tee; Johansson, Mikael; Weiderpass, Elisabete; Tjønneland, Anne; Riboli, Elio; Lathrop, Mark; Scelo, Ghislaine; Albanes, Demetrius; Caporaso, Neil E; Ye, Yuanqing; Gu, Jian; Wu, Xifeng; Spitz, Margaret R; Dienemann, Hendrik; Rosenberger, Albert; Su, Li; Matakidou, Athena; Eisen, Timothy; Stefansson, Kari; Risch, Angela; Chanock, Stephen J; Christiani, David; Hung, Rayjean J; Brennan, Paul; Landi, Maria Teresa; Houlston, Richard S; Amos, Christopher I
    We conducted imputation to the 1000 Genomes Project of four genome-wide association studies of lung cancer in populations of European ancestry (11,348 cases and 15,861 controls) and genotyped an additional 10,246 cases and 38,295 controls for follow-up. We identified large-effect genome-wide associations for squamous lung cancer with the rare variants BRCA2 p.Lys3326X (rs11571833, odds ratio (OR) = 2.47, P = 4.74 × 10−20) and CHEK2 p.Ile157Thr (rs17879961, OR = 0.38, P = 1.27 × 10−13). We also showed an association between common variation at 3q28 (TP63, rs13314271, OR = 1.13, P = 7.22 × 10−10) and lung adenocarcinoma that had been previously reported only in Asians. These findings provide further evidence for inherited genetic susceptibility to lung cancer and its biological basis. Additionally, our analysis demonstrates that imputation can identify rare disease-causing variants with substantive effects on cancer risk from preexisting genome-wide association study data.
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    Heart rate variability and DNA methylation levels are altered after short-term metal fume exposure among occupational welders: a repeated-measures panel study
    (BioMed Central, 2014) Fan, Tianteng; Fang, Shona C; Cavallari, Jennifer M; Barnett, Ian; Wang, Zhaoxi; Su, Li; Byun, Hyang-Min; Lin, Xihong; Baccarelli, Andrea; Christiani, David
    Background: In occupational settings, boilermakers are exposed to high levels of metallic fine particulate matter (PM2.5) generated during the welding process. The effect of welding PM2.5 on heart rate variability (HRV) has been described, but the relationship between PM2.5, DNA methylation, and HRV is not known. Methods: In this repeated-measures panel study, we recorded resting HRV and measured DNA methylation levels in transposable elements Alu and long interspersed nuclear element-1 (LINE-1) in peripheral blood leukocytes under ambient conditions (pre-shift) and right after a welding task (post-shift) among 66 welders. We also monitored personal PM2.5 level in the ambient environment and during the welding procedure. Results: The concentration of welding PM2.5 was significantly higher than background levels in the union hall (0.43 mg/m3 vs. 0.11 mg/m3, p < 0.0001). The natural log of transformed power in the high frequency range (ln HF) had a significantly negative association with PM2.5 exposure (β = -0.76, p = 0.035). pNN10 and pNN20 also had a negative association with PM2.5 exposure (β = -0.16%, p = 0.006 and β = -0.13%, p = 0.030, respectively). PM2.5 was positively associated with LINE-1 methylation [β = 0.79%, 5-methylcytosince (%mC), p = 0.013]; adjusted for covariates. LINE-1 methylation did not show an independent association with HRV. Conclusions: Acute decline of HRV was observed following exposure to welding PM2.5 and evidence for an epigenetic response of transposable elements to short-term exposure to high-level metal-rich particulates was reported. Electronic supplementary material The online version of this article (doi:10.1186/1471-2458-14-1279) contains supplementary material, which is available to authorized users.
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    Lung Adenocarcinoma with EGFR Amplification Has Distinct Clinicopathologic and Molecular Features in Never-Smokers
    (American Association for Cancer Research (AACR), 2009) Sholl, Lynette; Yeap, Beow; Iafrate, Anthony; Holmes-Tisch, A. J.; Chou, Y.-P.; Wu, Ming-Tsang; Goan, Y.-G.; Su, Li; Benedettini, E.; Yu, J.; Loda, Massimo; Janne, Pasi; Christiani, David; Chirieac, Lucian
    In a subset of lung adenocarcinomas the epidermal growth factor receptor (EGFR) is activated by kinase domain mutations and/or gene amplification, but the interaction between the two types of abnormalities is complex and unclear. We selected to study 99 consecutive never-smoking women of East Asian origin with lung adenocarcinomas that were characterized by histologic subtype. We analyzed EGFR mutations by PCR-capillary sequencing, EGFR copy number abnormalities by fluorescence and chromogenic in situ hybridization and quantitative PCR, and EGFR expression by immunohistochemistry with both specific antibodies against exon 19 deletion-mutated EGFR and total EGFR. We compared molecular and clinicopathologic features with disease-free survival. Lung adenocarcinomas with EGFR amplification had significantly more EGFR exon 19 deletion mutations than adenocarcinomas with disomy, low and high polysomy (100% v 54%, P=0.009). EGFR amplification occurred invariably on the mutated and not the wildtype allele (median mutated:wildtype ratios 14.0 v .33, P=0.003), was associated with solid histology (P=0.008), and advanced clinical stage (P=0.009). EGFR amplification was focally distributed in lung cancer specimens, mostly in regions with solid histology. Patients with EGFR amplification had a significantly worse outcome in univariate analysis (median disease-free survival 16 v 31 months, P=0.01) and when adjusted for stage (P=0.027). Lung adenocarcinomas with EGFR amplification have a unique association with exon 19 deletion mutations and demonstrate distinct clinicopathologic features associated with a significantly worsened prognosis. In these cases, EGFR amplification is heterogeneously distributed, mostly in areas with a solid histology.
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    Associated Links Among Smoking, Chronic Obstructive Pulmonary Disease, and Small Cell Lung Cancer: A Pooled Analysis in the International Lung Cancer Consortium
    (Elsevier, 2015) Huang, Ruyi; Wei, Yongyue; Hung, Rayjean J.; Liu, Geoffrey; Su, Li; Zhang, Ruyang; Zong, Xuchen; Zhang, Zuo-Feng; Morgenstern, Hal; Brüske, Irene; Heinrich, Joachim; Hong, Yun-Chul; Kim, Jin Hee; Cote, Michele; Wenzlaff, Angela; Schwartz, Ann G.; Stucker, Isabelle; Mclaughlin, John; Marcus, Michael W.; Davies, Michael P.A.; Liloglou, Triantafillos; Field, John K.; Matsuo, Keitaro; Barnett, Matt; Thornquist, Mark; Goodman, Gary; Wang, Yi; Chen, Size; Yang, Ping; Duell, Eric J.; Andrew, Angeline S.; Lazarus, Philip; Muscat, Joshua; Woll, Penella; Horsman, Janet; Dawn Teare, M.; Flugelman, Anath; Rennert, Gad; Zhang, Yan; Brenner, Hermann; Stegmaier, Christa; van der Heijden, Erik H.F.M.; Aben, Katja; Kiemeney, Lambertus; Barros-Dios, Juan; Pérez-Ríos, Monica; Ruano-Ravina, Alberto; Caporaso, Neil E.; Bertazzi, Pier Alberto; Landi, Maria Teresa; Dai, Juncheng; Shen, Hongbing; Fernandez-Tardon, Guillermo; Rodriguez-Suarez, Marta; Tardon, Adonina; Christiani, David
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    Socioeconomic status is associated with reduced lung function in China: an analysis from a large cross-sectional study in Shanghai
    (BioMed Central, 2016) Gaffney, Adam; Hang, Jing-qing; Lee, Mi-Sun; Su, Li; Zhang, Feng-ying; Christiani, David
    Background: An inverse association between socioeconomic status and pulmonary function has emerged in many studies. However, the mediating factors in this relationship are poorly understood, and might be expected to differ between countries. We sought to investigate the relationship between socioeconomic status and lung function in China, a rapidly industrializing nation with unique environmental challenges, and to identify potentially-modifiable environmental mediators. Methods: We used data from the Shanghai Putuo Study, a cross-sectional study performed in Shanghai, China. Participants completed a questionnaire and spirometry. The primary exposure was socioeconomic status, determined by education level. The primary outcomes were FEV1 and FVC percent predicted. Multiple linear regressions were used to test this association, and the percent explained by behavioral, environmental, occupational, and dietary variables was determined by adding these variables to a base model. Results: The study population consisted of a total of 22,878 study subjects that were 53.3 % female and had a mean age of 48. In the final multivariate analysis, the effect estimates for FEV1 and FVC percent predicted for low socioeconomic status (compared to high) were statistically significant at a p-value of <0.01. Smoking, biomass exposure, mode of transportation to work, a diet low in fruits or vegetables, and occupational category partially attenuated the relationship between SES and lung function. In a fully-adjusted age-stratified analysis, the socioeconomic disparity in lung function widened with increasing age. Conclusions: We found cross-sectional evidence of socioeconomic disparities in pulmonary function in Shanghai. These differences increased with age and were partially explained by potentially modifiable exposures.