Wei Zheng

Vanderbilt University, Nashville, Michigan, United States

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Publications (518)3338.61 Total impact

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    ABSTRACT: In a three-stage genome-wide association study among East Asian women including 22,780 cases and 24,8 controls, we identified 3 genetic loci newly associated with breast cancer risk, including rs4950 at q32. (in intron 2 of the ZC3H11A gene; P = 8.82 × 0 −9), rs0474352 at 5q4.3 (near the ARRDC3 gene; P = .67 × 0 −9) and rs2290203 at 5q26. (in intron 4 of the PRC1 gene; P = 4.25 × 0 −8). We replicated these associations in 6,003 cases and 4,335 controls of European ancestry (P = 0.030, 0.004 and 0.00, respectively). Data from the ENCODE Project suggest that variants rs4950 and rs0474352 might be located in an enhancer region and transcription factor binding sites, respectively. This study provides additional insights into the genetics and biology of breast cancer. Breast cancer is one of the most common malignancies among women worldwide. Genetic factors have a substantial role in breast cancer etiology 1,2 . Thus far, genome-wide association studies (GWAS) have identified approximately 75 genetic loci associated with breast cancer risk 2–5 . With the exception of the studies we have conducted among East Asian women 6–9 and one study conducted among women of African ancestry 10 , all other published GWAS have been conducted among women of European ancestry. Genetic risk variants identified thus far from GWAS explain only about 10% of familial risk for breast cancer in East Asian women 3 . Given the dif-ferences in genetic architecture and environmental exposures for women of European and East Asian ancestry, additional GWAS need to be conducted among East Asian women to study the genetic basis of breast cancer risk. The current study was conducted as part of the Asia Breast Cancer Consortium (ABCC) to search for additional susceptibility loci for breast cancer. Included in this study are data obtained from 22,780 breast cancer cases and 24,181 controls who were recruited in 14 studies conducted in multiple Asian countries (Supplementary Table 1). The discovery stage (stage 1) included 2 GWAS in which 5,285 Chinese women (SBCGS-1) and 4,777 Korean women (SeBCS1) were scanned primarily using Affymetrix Genome-Wide Human SNP Array 6.0, which consists of 906,602 SNPs. After applying quality control filters described previously 6,9,11 , 5,152 Chinese women (2,867 cases and 2,285 controls; 677,157 SNPs) and 4,298 Korean women (2,246 cases and 2,052 controls; 555,117 SNPs) remained in the cur-rent analysis. Imputation was conducted for each study following the MACH algorithm 12 using HapMap 2 release 22 CHB (Han Chinese in Beijing, China) and JPT (Japanese in Tokyo, Japan) data (2,416,663 SNPs) as the reference. Only SNPs with a high imputation quality score (RSQR ≥ 0.50) were analyzed for associations with breast can-cer risk. In the analyses of data from Chinese and Korean women, a total of 1,930,412 and 1,907,146 SNPs, respectively, were included. A meta-analysis of these GWAS data was conducted using a fixed-effects, inverse variance meta-analysis with the METAL program 13 . There was little evidence of inflation in the association test statis-tics for the studies included in stage 1 (genomic inflation factors (λ): λ = 1.0426 for SBCGS-1, λ = 1.0431 for SeBCS1 and λ = 1.0499 for both studies combined; Supplementary Fig. 1). When scaled to a study of 1,000 cases and 1,000 controls, λ 1,000 values were 1.02, 1.02 and 1.01, respectively. To select SNPs for stage 2 replication, we used the following criteria: (i) association P < 0.05 in the stage 1 meta-analysis results; (ii) the
    Nature Genetics 07/2014; · 35.21 Impact Factor
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    ABSTRACT: Chronic inflammation is associated with increased risk of multiple cancers, including breast cancer. Adipose tissues produce proinflammatory cytokines, and obesity is a risk factor for postmenopausal breast cancer. We evaluated the association of regular use of nonsteroidal anti-inflammatory drugs (NSAIDs) with breast cancer risk, overall and by body mass index (BMI) and tumor subtypes defined by estrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2 status. We conducted a population-based, case-control study involving 5,078 women aged 25-75 years who were recruited primarily from the Nashville metropolitan area of Tennessee. Multivariate unconditional logistic regression models were used to estimate odds ratios and 95 % confidence intervals for breast cancer risk after adjusting for multiple potential confounding factors. Regular use of any NSAID was associated with significantly reduced breast cancer risk (OR 0.78; 95 % CI 0.69-0.89). This association was observed for regular use of baby aspirin only (OR 0.82, 95 % CI 0.69-0.99), other NSAIDs only (OR 0.81, 95 % CI 0.69-0.95), and both baby aspirin and other NSAIDs (OR 0.52, 95 % CI 0.40-0.69). These significant inverse associations were found among overweight women (BMI ≥25 kg/m(2)) overall and by subtypes of breast cancer, but not among women with BMI <25 kg/m(2) (P for interaction = 0.023). Regular use of NSAIDs was inversely associated with breast cancer risk, particularly among overweight women. Overweight women may benefit more from the protective effects of NSAID use than normal-weight women.
    Breast Cancer Research and Treatment 07/2014; · 4.47 Impact Factor
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    ABSTRACT: A higher adherence to dietary recommendations, such as the Dietary Approaches to Stop Hypertension (DASH) and the Alternative Healthy Eating Index (AHEI), has been associated with lower morbidity and mortality from chronic diseases in Western populations. However, the health benefits of following the Dietary Guidelines for Chinese remain unknown.OBJECTIVE: We examined adherence to the Chinese Food Pagoda (CHFP) in association with total and cause-specific mortality and compared associations with those of the DASH and AHEI.DESIGN: Participants included 61,239 men and 73,216 women (aged 40-74 y) from 2 population-based prospective studies in Shanghai, China. Habitual dietary intakes were assessed at baseline in-person interviews by using validated food-frequency questionnaires. Deaths and underlying causes were identified through the Shanghai Vital Statistics Registry and follow-up home visits.RESULTS: We documented 2954 deaths in men and 4348 deaths in women during mean follow-ups of 6.5 and 12.0 y, respectively. A higher CHFP score was associated with lower total mortality with multivariable-adjusted HRs of 0.67 (95% CI: 0.60, 0.75) in men and 0.87 (95% CI: 0.80, 0.95) in women when extreme quartiles were compared (both P-trend < 0.005). Decreased risks associated with a higher CHFP score were observed for cardiovascular disease, cancer, and diabetes mortality, particularly in men. A significantly lower total mortality was shown for adherence to specific recommendations on vegetables, fruit, legumes, fish, and eggs but not grains, dairy, meat, fat, and salt. A higher DASH score and AHEI also predicted lower mortality from all causes, cardiovascular disease, and diabetes but not cancer.CONCLUSIONS: A greater compliance with Chinese or US dietary guidelines is associated with lower total mortality in Chinese adults. Favorable associations are more evident in men than women and more consistent for cardiometabolic mortality than cancer mortality.
    American Journal of Clinical Nutrition 06/2014; · 6.50 Impact Factor
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    ABSTRACT: Indoor air pollution (IAP) caused by cooking has been associated with lung cancer risk in retrospective case-control studies in developing and rural countries. We report the association of cooking conditions, fuel use, oil use and risk of lung cancer in a developed urban population in a prospective cohort of women in Shanghai. A total of 71,320 never smoking women were followed from 1996 through 2009 and 429 incident lung cancer cases were identified. Questionnaires collected information on household living and cooking practices for the women's three most recent residences and utilization of cooking fuel and oil, and ventilation conditions. Cox proportional hazards regression estimated the association for kitchen ventilation conditions, cooking fuels, and use of cooking oils for the risk of lung cancer by hazard ratios (HR) with 95% confidence intervals (95% CI). Ever poor kitchen ventilation was associated with a 49% increase in lung cancer risk (HR: 1.49; 95% CI: 1.15-1.95) compared to never poor ventilation. Ever use of coal was not significantly associated. However, ever coal use with poor ventilation (HR: 1.69; 95% CI: 1.22-2.35) and twenty or more years of using coal (HR: 2.03; 95% CI: 1.35-3.05) was significantly associated compared to no exposure to coal or poor ventilation. Cooking oil use was not significantly associated. These results demonstrate that IAP from poor ventilation of coal combustion increases the risk of lung cancer and is an important public health issue in cities across China where people may have lived in homes with inadequate kitchen ventilation. © 2014 Wiley Periodicals, Inc.
    International journal of cancer. Journal international du cancer. 06/2014;
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    ABSTRACT: Known genetic loci explain only a small proportion of the familial relative risk of colorectal cancer (CRC). We conducted a genome-wide association study of CRC in East Asians with 14,963 cases and 31,945 controls and identified 6 new loci associated with CRC risk (P = 3.42 [times] 10-8 to 9.22 [times] 10-21) at 10q22.3, 10q25.2, 11q12.2, 12p13.31, 17p13.3 and 19q13.2. Two of these loci map to genes (TCF7L2 and TGFB1) with established roles in colorectal tumorigenesis. Four other loci are located in or near genes involved in transcriptional regulation (ZMIZ1), genome maintenance (FEN1), fatty acid metabolism (FADS1 and FADS2), cancer cell motility and metastasis (CD9), and cell growth and differentiation (NXN). We also found suggestive evidence for three additional loci associated with CRC risk near genome-wide significance at 8q24.11, 10q21.1 and 10q24.2. Furthermore, we replicated 22 previously reported CRC-associated loci. Our study provides insights into the genetic basis of CRC and suggests the in
    Nature Genetics 06/2014; 46(6):533-542. · 35.21 Impact Factor
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    ABSTRACT: Epidemiologic studies of occupational lead exposure have suggested increased risks of cancers of the brain, kidney, lung, meninges, and stomach; however, the totality of the evidence is inconsistent. To clarify whether lead is a carcinogen, we investigated the relationship between occupational lead exposure and risks of these five cancer sites in two prospective cohort studies in Shanghai, China.
    Occupational and environmental medicine. 06/2014; 71 Suppl 1:A42.
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    ABSTRACT: The association between benzene exposure and non-Hodgkin lymphoma (NHL) has been the subject of debate, and an IARC working group recently concluded for the first time that there is now limited evidence to support this association in humans. We evaluated the relationship between occupational benzene exposure and NHL risk among 73 087 women in a population-based cohort study of women in Shanghai.
    Occupational and environmental medicine. 06/2014; 71 Suppl 1:A40-1.
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    ABSTRACT: Purpose Systemic oxidative stress has been implicated in the pathogenesis and progression of many chronic diseases, including breast cancer. No studies have investigated F2-isoprostanes (F2-IsoPs), valid biomarkers of systemic oxidative stress, in association with breast cancer prognosis. We conducted a nested case–control study in a prospective breast cancer survivor cohort to investigate systemic oxidative stress and survival. Methods Urinary levels of F2-IsoPs and its major urinary metabolite (2,3-dinor-5,6-dihydro-15-F2t-IsoP, F2-IsoP-M) were measured post-cancer treatment using gas chromatography/negative ion chemical ionization mass spectrometry for 57 deceased breast cancer patients (cases) and 103 surviving patients (controls) matched 1:2 on age at diagnosis, stage, and diagnosis year. Odds ratios (ORs) and 95 % confidence intervals (CIs) were derived from conditional logistic regression models. Results In unadjusted models, elevated F2-IsoP levels categorized based on the median value [≥1.73; <1.73 (reference)] were nonsignificantly inversely associated with mortality (OR 0.51, 95 % CI 0.24–1.10). After adjustment for potential confounders, elevated F2-IsoP levels were significantly associated with mortality (OR 0.36, 95 % CI 0.14–0.96). The inverse association was marginally significant when F2-IsoP was categorized based on tertiles (p trend = 0.08). In contrast, elevated F2-IsoP-M levels, categorized based on the median level [≥0.91; < 0.91(reference)], were associated with a statistically nonsignificant increased risk of mortality in both unadjusted and adjusted models (adjusted OR 1.39, 95 % CI 0.62–3.09). Conclusion Results suggest a role for oxidative stress biomarkers in breast cancer survival; however, as this is the first study to date, additional larger studies are needed.
    Cancer Causes and Control 06/2014; 25(6). · 3.20 Impact Factor
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    ABSTRACT: We investigated the relationship between telomere length and lung cancer in a pooled analysis from three prospective cohort studies: the Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial, conducted among men and women in the United States, and previously published data from the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) trial conducted among male smokers in Finland, and the Shanghai Women's Health Study (SWHS), which is comprised primarily of never-smokers. The pooled population included 847 cases and 847 controls matched by study, age, and sex. Leukocyte telomere length was measured by a monochrome multiplex quantitative PCR assay. We used conditional logistic regression models to calculate odds ratios (OR) and their 95% confidence intervals (CI) for the association between telomere length and lung cancer risk, adjusted for age and pack-years of smoking. Longer telomere length was associated with increased lung cancer risk in the pooled analysis (OR(95% CI) by quartile: 1.00; 1.24(0.90-1.71); 1.27(0.91-1.78); and 1.86(1.33-2.62); P-trend=0.000022). Findings were consistent across the three cohorts and strongest for subjects with very long telomere length, i.e., lung cancer risks for telomere length (OR(95% CI)) in the upper half of the fourth quartile were 2.41(1.28-4.52), 2.16(1.11-4.23) and 3.02(1.39-6.58) for the PLCO trial, the ATBC trial, and the SWHS, respectively. In addition, the association persisted among cases diagnosed more than six years after blood collection and was particularly evident for female adenocarcinoma cases. Telomere length in white blood cell DNA may be a biomarker of future increased risk of lung cancer in diverse populations.
    Cancer research. 05/2014;
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    ABSTRACT: Background: Previous studies on the association between one-carbon dietary factors and gastric cancer risk have been inconsistent. Methods: We investigated this association using data from a prospective study, the Shanghai Women's Health Study (1997-2010), including 323 distal gastric cancer cases identified from 73,009 Chinese women. Hazard ratios and 95% confidence intervals were estimated using Cox proportional hazard regression after adjusting for confounders. Results: Overall, no statistically significant association of gastric cancer was observed with dietary intake of folate, methionine, or B vitamins. However, when stratified by menopausal status, higher intake of riboflavin was associated with decreased gastric cancer risk in premenopausal women with HR of 0.35 (95% CI: 0.17, 0.73), 0.48 (0.24, 0.97), 0.28 ( 0.12, 0.65), and 0.23 (0.07, 0.91), respectively, for the quintile 2 to 5 intake groups compared to the lowest quintile intake (p for trend=0.02]. Among premenopausal women, highest intake of folate was associated with increased gastric cancer risk (HR: 2.62; 95% CI: 1.04, 6.59). There were no statistically significant associations observed among postmenopausal women. Conclusions: These results suggest dietary factors involved in one-carbon metabolism are associated with gastric cancer risk among premenopausal women. Impact: Riboflavin may be a protective factor and folate may be a risk factor for premenopausal gastric cancer.
    Cancer Epidemiology Biomarkers &amp Prevention 04/2014; · 4.56 Impact Factor
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    ABSTRACT: & Aims: Genetic and epigenetic alterations contribute to the pathogenesis of colorectal cancer (CRC). There is considerable molecular heterogeneity among colorectal tumors, which appears to arise as polyps progress to cancer. This heterogeneity results in different pathways to tumorigenesis. Although epigenetic and genetic alterations have been detected in conventional tubular adenomas, little is known about how these affect progression to CRC. We compared methylomes of normal colon mucosa, tubular adenomas, and colorectal cancers to determine how epigenetic alterations might contribute to cancer formation. We conducted genome-wide array-based studies and comprehensive data analyses of aberrantly methylated loci in 41 normal colon tissue, 42 colon adenomas, and 64 cancers using HumanMethylation450 arrays. We found genome-wide alterations in DNA methylation in the non-tumor colon mucosa adjacent to tubular adenomas and cancers. Three classes of cancers and 2 classes of adenomas were identified based on their DNA methylation patterns. The adenomas separated into classes of high-frequency methylation (adenoma-H), and low-frequency methylation (adenoma-L). Within the adenoma-H class a subset of adenomas had mutant KRAS. Additionally, the adenoma-H class had DNA methylation signatures similar to those of cancers with low or intermediate levels of methylation, whereas the adenoma-L class had methylation signatures similar to that of non-tumor colon tissue. The CpGs sites that were differentially methylated in these signatures are located in intragenic and intergenic regions. Genome-wide alterations in DNA methylation occur during early stages of progression of tubular adenomas to cancer. These findings reveal heterogeneity in the pathogenesis of colorectal cancer, even at the adenoma step of the process.
    Gastroenterology 04/2014; · 12.82 Impact Factor
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    ABSTRACT: Previous epidemiological studies of circulating folate concentration and colorectal cancer have reported inconsistent results. We evaluated associations of pre-diagnostic plasma folate concentration with colorectal cancer risk in a case-control study nested within the Shanghai Men's Health Study (2002-2010). Included herein are 288 cases who were diagnosed with incident colorectal cancer and 575 controls who were individually matched to cases on baseline characteristics. Folate concentrations in plasma were measured by microbiological assay. Multivariate conditional logistic regression was used to assess associations of plasma folate concentrations with colorectal cancer risk. Plasma folate was non-significantly but positively associated with colorectal cancer risk. Odds ratios (OR) and 95% confidence intervals (CI) were 1.38 (0.95-2.02) for the middle tertile of plasma folate concentrations and 1.33 (0.90-1.98) for the highest compared with the lowest tertile. The positive association reached statistical significance for the highest tertile of folate concentrations for men with late-stage colorectal cancer (OR=2.66; 95% CI=1.03-6.86) and for the middle tertile for cases diagnosed within the first 4 years after blood collection (OR=1.72; 95% CI=1.02-2.92) and for men in the high BMI group (OR=1.88; 95% CI=1.14-3.11). In our study population, where folic acid fortification of the food supply and vitamin supplement use are uncommon, plasma folate concentration was positively associated with colorectal cancer risk among men who may have had preneoplastic lesions. These findings need to be confirmed in studies with specific assessment of preneoplastic lesions and repeated measurements of folate level over time. © 2014 Wiley Periodicals, Inc.
    International Journal of Cancer 04/2014; · 6.20 Impact Factor
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    ABSTRACT: A high body mass index (BMI) is a major risk factor for several chronic diseases, but the biology underlying these associations is not well-understood. Dyslipidemia, inflammation, and elevated levels of growth factors and sex steroid hormones explain some of the increased disease risk, but other metabolic factors not yet identified may also play a role. In order to discover novel metabolic biomarkers of BMI, we used non-targeted metabolomics to assay 317 metabolites in blood samples from 947 participants and examined the cross-sectional associations between metabolite levels and BMI. Participants were from three studies in the United States and China. Height, weight, and potential confounders were ascertained by questionnaire (US studies) or direct measurement (Chinese study). Metabolite levels were measured using liquid-phase chromatography and gas chromatography coupled with mass spectrometry. We evaluated study-specific associations using linear regression, adjusted for age, gender, and smoking, and we estimated combined associations using random effects meta-analysis. The meta-analysis revealed 37 metabolites significantly associated with BMI, including 19 lipids, 12 amino acids, and 6 others, at the Bonferroni significance threshold (P < 0.00016). Eighteen of these associations had not been previously reported, including histidine, an amino acid neurotransmitter, and butyrylcarnitine, a lipid marker of whole-body fatty acid oxidation. Heterogeneity by study was minimal (all P heterogeneity > 0.05). In total, 110 metabolites were associated with BMI at the P < 0.05 level. These findings establish a baseline for the BMI metabolome, and suggest new targets for researchers attempting to clarify mechanistic links between BMI and disease risk.
    Metabolomics 04/2014; 10(2). · 4.43 Impact Factor
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    ABSTRACT: Tobacco smoking is a major risk factor for many diseases. We sought to quantify the burden of tobacco-smoking-related deaths in Asia, in parts of which men's smoking prevalence is among the world's highest. We performed pooled analyses of data from 1,049,929 participants in 21 cohorts in Asia to quantify the risks of total and cause-specific mortality associated with tobacco smoking using adjusted hazard ratios and their 95% confidence intervals. We then estimated smoking-related deaths among adults aged ≥45 y in 2004 in Bangladesh, India, mainland China, Japan, Republic of Korea, Singapore, and Taiwan-accounting for ∼71% of Asia's total population. An approximately 1.44-fold (95% CI = 1.37-1.51) and 1.48-fold (1.38-1.58) elevated risk of death from any cause was found in male and female ever-smokers, respectively. In 2004, active tobacco smoking accounted for approximately 15.8% (95% CI = 14.3%-17.2%) and 3.3% (2.6%-4.0%) of deaths, respectively, in men and women aged ≥45 y in the seven countries/regions combined, with a total number of estimated deaths of ∼1,575,500 (95% CI = 1,398,000-1,744,700). Among men, approximately 11.4%, 30.5%, and 19.8% of deaths due to cardiovascular diseases, cancer, and respiratory diseases, respectively, were attributable to tobacco smoking. Corresponding proportions for East Asian women were 3.7%, 4.6%, and 1.7%, respectively. The strongest association with tobacco smoking was found for lung cancer: a 3- to 4-fold elevated risk, accounting for 60.5% and 16.7% of lung cancer deaths, respectively, in Asian men and East Asian women aged ≥45 y. Tobacco smoking is associated with a substantially elevated risk of mortality, accounting for approximately 2 million deaths in adults aged ≥45 y throughout Asia in 2004. It is likely that smoking-related deaths in Asia will continue to rise over the next few decades if no effective smoking control programs are implemented. Please see later in the article for the Editors' Summary.
    PLoS Medicine 04/2014; 11(4):e1001631. · 15.25 Impact Factor
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    ABSTRACT: Evidence for the association of diet and gastric cancer is equivocal, and the majority of previous studies have not evaluated the interaction of diet and infection with Helicobacter pylori, the leading risk factor for gastric cancer. We examined these associations among 226 cases and 451 controls nested within a prospective cohort. Dietary intakes were calculated from validated food frequency questionnaires. Blood levels of 15 antibodies to Helicobacter pylori proteins were assessed using multiplex serology. Odds ratios (ORs) were calculated using logistic regression. Among individuals infected with high-risk Helicobacter pylori (sero-positivity to 5-6 virulent H. pylori proteins), increasing intake of red meat, heme iron, and sodium increased risk (comparing highest tertile to lowest: ORs [95% confidence interval {CI}]: 1.85 [1.01-3.40]; 1.95 [1.06-3.57]; and 1.76 [0.91-3.43], respectively) while increasing intake of fruit decreased gastric cancer risk (comparing highest tertile of intake to lowest: OR [95% CI]: 0.52 [0.28-0.94]). No associations of diet with risk were found among individuals infected with low-risk H. pylori (P for interaction for red meat and sodium: 0.02 and 0.01, respectively). In this population with over 90% prevalence of CagA-positive H. pylori infection, categorizing individuals using H. pylori multiplex serology may identify individuals for whom a diet intervention may be effective.
    Nutrition and Cancer 03/2014; · 2.70 Impact Factor
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    ABSTRACT: Exposure to certain phenols is ubiquitous due to their use in many consumer and personal care products. However, predictors of exposure have not been well characterized in most populations. To identify predictors of exposure and assess reproducibility of phenol concentrations across serial spot urine samples among Chinese adults. We measured 2,4-dichlorophenol, 2,5-dichlorophenol, butyl paraben, methyl paraben, propyl paraben, benzophenone-3, bisphenol A, and triclosan in urine collected during 1997-2006 among 50 participants of the Shanghai Women's Health Study cohort and during 2002-2006 among 50 participants of the Shanghai Men's Health Study cohort. We investigated predictors of concentrations using the Satterthwaite t-test and assessed reproducibility among serial samples using intraclass correlation coefficients (ICC) and Spearman correlation coefficients (SCC). Creatinine-corrected phenol concentrations were generally higher among women than men. Participants who took medicine in the past 24 hours had higher concentrations of propyl paraben. Cigarette smoking was associated with lower concentrations of propyl and methyl parabens among men. Bottled water consumption was associated with higher bisphenol A, 2,4-dichlorophenol, and 2,5-dichlorophenol concentrations among women. Among men, reproducibility across serial samples was moderate for 2,4-dichlorophenol and 2,5-dichlorophenol (ICC=0.54-0.60, SCC=0.43-0.56), but lower for other analytes (ICC=0.20-0.29). Reproducibility among women was low (ICC=0.13-0.39), but increased when restricted to morning-only urine samples. Among these 100 Shanghai residents, urinary phenol concentrations varied by sex, smoking, and consumption of bottled water. Our results suggest that a single urine sample may be adequate for ranking exposure to the precursors of 2,4-dichlorophenol and 2,5-dichlorophenol among men and, under certain circumstances, among women.
    Environmental Health Perspectives 03/2014; · 7.26 Impact Factor
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    ABSTRACT: Glycated hemoglobin (HbA1C) is used as a measure of glycemic control and also as a diagnostic criterion for diabetes mellitus. To discover novel loci harbouring common variants associated with HbA1C in East Asians, we conducted a meta-analysis of 13 genome wide association studies (N=21,026). We replicated our findings in 3 additional studies comprising 11,576 individuals of East Asian ancestry. 10 variants showed associations that reached genome wide significance in the discovery dataset of which 9 [4 novel variants at TMEM79 (P-value 1.3 × 10(-23)), HBS1L/MYB (8.5 × 10(-15)), MYO9B (9.0 × 10(-12)) and CYBA (1.1 × 10(-8)) as well as 5 variants at loci that had been previously identified (CDKAL1, G6PC2/ABCB11, GCK, ANK1, and FN3K)] showed consistent evidence of association in replication datasets. These variants explained 1.76% of the variance in HbA1C. Several of these variants (TMEM79, HBS1L/MYB, CYBA, MYO9B, ANK1, and FN3K) showed no association with either blood glucose or type 2 diabetes. Amongst individuals with non-diabetic levels of fasting glucose (<7.0 mmol/l) but elevated (>=6.5%) HbA1c, 36.1% had HbA1C<6.5% after adjustment for these 6 variants. . Our East Asian GWAS meta-analysis has identified novel variants associated with HbA1C as well as demonstrating that the effects of known variants are largely transferable across ethnic groups. Variants affecting erythrocyte parameters rather than glucose metabolism may be relevant to the use of HbA1C for diagnosing diabetes in these populations.
    Diabetes 03/2014; · 7.90 Impact Factor
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    ABSTRACT: Cholelithiasis and cholecystectomy have been proposed as risk factors for liver cancer, but findings have been inconsistent. We assessed this association using data from the Shanghai Women's and Men's Health Studies. History of cholelithiasis and cholecystectomy were reported at baseline and follow-up interviews, and liver cancer diagnoses were ascertained from the Shanghai Cancer Registry and Vital Statistics Unit. Adjusted hazard ratios (aHRs) and 95% CIs were calculated after adjustment for potential confounders. A history of cholelithiasis and cholecystectomy was reported by 9.5% and 3.6% of participants at baseline, respectively. After a total of 859 882 person-years of follow-up for women and 391 093 for men, incident liver cancer was detected in 160 women and 252 men. A positive association was observed between a history of cholelithiasis or cholecystectomy and liver cancer in men (aHR 1.46; 95% CI 1.02 to 2.07) and women (aHR 1.55; 95% CI 1.06 to 2.26). Similar results were observed for cholelithiasis only, but cholecystectomy did not reach statistical significance. There was no strong evidence for detection bias of liver cancer due to cholelithiasis or cholecystectomy. Our study suggests that cholelithiasis and possibly cholecystectomy may increase the risk of liver cancer.
    Journal of epidemiology and community health 02/2014; · 3.04 Impact Factor
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    ABSTRACT: The association of dietary fiber intake with colorectal cancer risk is established. However, the association may differ between cigarette smokers and nonsmokers. We evaluated this hypothesis in a large colonoscopy-based case-control study. Dietary fiber intakes were estimated by self-administered food frequency questionnaire. Unconditional logistic regression analysis was used to estimate ORs and 95% CIs with adjustment for potential confounders. Analysis also was stratified by cigarette smoking and sex. High dietary fiber intake was associated with reduced risk of colorectal polyps (P-trend = 0.003). This association was found to be stronger among cigarette smokers (P-trend = 0.006) than nonsmokers (P-trend = 0.21), although the test for multiplicative interaction was not statistically significant (P = 0.11). This pattern of association was more evident for high-risk adenomatous polyps (ADs), defined as advanced or multiple ADs (P-interaction smoking and dietary fiber intake = 0.09). Among cigarette smokers who smoked ≥23 y, a 38% reduced risk of high-risk ADs was found to be associated with high intake of dietary fiber compared with those in the lowest quartile fiber intake group (P-trend = 0.004). No inverse association with dietary fiber intake was observed for low-risk ADs, defined as single nonadvanced ADs. Cigarette smoking may modify the association of dietary fiber intake with the risk of colorectal polyps, especially high-risk ADs, a well-established precursor of colorectal cancer.
    Journal of Nutrition 02/2014; · 4.20 Impact Factor
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    ABSTRACT: Uncertainty remains on the relationship between a family history of liver cancer and liver cancer risk in prospective cohort studies in a general population. Thus, we examined this association in 133,014 participants in the Shanghai Women's and Men's Health Studies. Family history of liver cancer was categorized through dichotomous and proportional score approaches. Hazard ratios (HRs) and 95% confidence intervals (CIs) were derived using the Cox proportional hazards models with adjustment for potential confounders. A meta-analysis of observational studies through December 2013 on liver cancer risk in relation to family history of liver cancer was also performed. Study-specific risk estimates were combined using fixed or random effects models depending on whether significant heterogeneity was detected. For the Shanghai Women's and Men's Health Studies, 299 liver cancer cases were identified during follow-up through 2010. Family history of liver cancer was associated with liver cancer risk using both binary indicator (HR=2.60, 95%CI: 1.77-3.80) and proportional score (high-risk vs. minimal-risk category: HR=3.03, 95%CI: 1.73-5.31), with increasing HRs for increasing score categories. The Meta-analysis also showed an increased risk for those with a family history of liver cancer (RR=2.55, 95% CI: 2.05-3.16). Family history of liver cancer was related to increased risk of liver cancer in Chinese population. This risk is particularly high for those with an affected mother. The "dose-response" of risk with an increasing family history score of liver cancer might further facilitate future cancer prevention programs on identifying individuals with the highest potential liver cancer risk. © 2014 Wiley Periodicals, Inc.
    International Journal of Cancer 02/2014; · 6.20 Impact Factor

Publication Stats

10k Citations
3,338.61 Total Impact Points


  • 2001–2014
    • Vanderbilt University
      • • Division of Epidemiology
      • • Department of Medicine
      • • Vanderbilt Epidemiology Center
      • • Vanderbilt-Ingram Cancer Center (VICC)
      • • Center for Health Services Research
      Nashville, Michigan, United States
  • 1987–2014
    • Shanghai Cancer Institute
      Shanghai, Shanghai Shi, China
  • 2013
    • University of Minnesota Duluth
      Duluth, Minnesota, United States
    • Harvard Medical School
      • Department of Medicine
      Boston, MA, United States
    • Nanjing Medical University
      • Department of Epidemiology and Biostatistics
      Nanjing, Jiangsu Sheng, China
    • University of Cambridge
      Cambridge, England, United Kingdom
    • Institute of Cancer Research
      Londinium, England, United Kingdom
  • 2012–2013
    • Renji Hospital
      Shanghai, Shanghai Shi, China
    • University of Texas MD Anderson Cancer Center
      Houston, Texas, United States
  • 2010–2013
    • Imperial College London
      • • Department of Epidemiology and Biostatistics
      • • Department of Primary Care and Public Health
      London, ENG, United Kingdom
    • Mayo Clinic - Rochester
      • Department of Health Science Research
      Rochester, MN, United States
  • 2011–2012
    • University of Southern California
      • Department of Preventive Medicine
      Los Angeles, CA, United States
    • Montreal Heart Institute
      Montréal, Quebec, Canada
    • U.S. Food and Drug Administration
      Washington, Washington, D.C., United States
    • University of Hawaiʻi at Mānoa
      • Office of Public Health Studies
      Honolulu, HI, United States
    • Icahn School of Medicine at Mount Sinai
      Manhattan, New York, United States
    • Queensland Institute of Medical Research
      Brisbane, Queensland, Australia
    • University of North Carolina at Chapel Hill
      • Department of Epidemiology
      Chapel Hill, NC, United States
    • Cancer Institute and Hospital, Chinese Academy of Medical Sciences
      Peping, Beijing, China
  • 2010–2012
    • Seoul National University Hospital
      • Department of Surgery
      Sŏul, Seoul, South Korea
  • 2007–2012
    • Shanghai Municipal Center for Disease Control and Prevention
      Shanghai, Shanghai Shi, China
    • Shanghai Jiao Tong University
      Shanghai, Shanghai Shi, China
    • Government of the People's Republic of China
      Peping, Beijing, China
    • Harvard University
      • Department of Epidemiology
      Boston, MA, United States
  • 1992–2012
    • National Cancer Institute (USA)
      • • Division of Cancer Epidemiology and Genetics
      • • Occupational and Environmental Epidemiology
      Bethesda, MD, United States
  • 2005–2011
    • Fudan University
      • • School of Public Health
      • • Department of Health Statistics and Social Medicine
      • • Cancer Hospital
      Shanghai, Shanghai Shi, China
  • 2007–2010
    • Gateway-Vanderbilt Cancer Treatment Center
      Clarksville, Tennessee, United States
  • 2005–2010
    • National Institutes of Health
      • • Division of Cancer Epidemiology and Genetics
      • • Branch of Occupational and Environmental Epidemiology
      Bethesda, MD, United States
  • 2009
    • Northwestern University
      • Department of Preventive Medicine
      Evanston, IL, United States
  • 2004–2008
    • Meharry Medical College
      • Department of Surgery
      Nashville, Tennessee, United States
    • University of Texas at Brownsville and Texas Southmost College
      Brownsville, Texas, United States
    • Europaeische Akademie Bozen - Accademia Europea Bolzano
      Bozen, Trentino-Alto Adige, Italy
  • 2002–2008
    • Yale University
      New Haven, Connecticut, United States
    • Mayo Foundation for Medical Education and Research
      • Department of Health Sciences Research
      Scottsdale, AZ, United States
    • Unité Inserm U1077
      Caen, Lower Normandy, France
  • 1999–2006
    • University of South Carolina
      • Department of Epidemiology & Biostatistics
      Columbia, South Carolina, United States
  • 2003
    • Yale-New Haven Hospital
      New Haven, Connecticut, United States
    • Wake Forest School of Medicine
      • Center for Cancer Genomics
      Winston-Salem, NC, United States
  • 1998
    • Zhejiang Medical University
      Hang-hsien, Zhejiang Sheng, China