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2. International cancer seminars: a focus on esophageal squamous cell carcinoma

Author

Murphy, G., McCormack, V., Abedi-Ardekani, B., Arnold, M., Camargo, M. C., Dar, N. A., Dawsey, S. M., Etemadi, A., Fitzgerald, R. C., Fleischer, D. E., Freedman, N. D., Goldstein, A. M., Gopal, S., Hashemian, M., Hu, N., Hyland, P. L., Kaimila, B., Kamangar, F., Malekzadeh, R., Mathew, C. G., Menya, D., Mulima, G., Mwachiro, M. M., Mwasamwaja, A., Pritchett, N., Qiao, Y.-L., Ribeiro-Pinto, L. F., Ricciardone, M., Schüz, J., Sitas, F., Taylor, P. R., Van Loon, K., Wang, S.-M., Wei, W.-Q., Wild, C. P., Wu, C., Abnet, C. C., Chanock, S. J., and Brennan, P.

Published
2017
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8. Validity and reliability of a new food frequency questionnaire compared to 24 h recalls and biochemical measurements: pilot phase of Golestan cohort study of esophageal cancer

Author

Malekshah, A F, Kimiagar, M, Saadatian-Elahi, M, Pourshams, A, Nouraie, M, Goglani, G, Hoshiarrad, A, Sadatsafavi, M, Golestan, B, Yoonesi, A, Rakhshani, N, Fahimi, S, Nasrollahzadeh, D, Salahi, R, Ghafarpour, A, Semnani, S, Steghens, J P, Abnet, C C, Kamangar, F, Dawsey, S M, Brennan, P, Boffetta, P, and Malekzadeh, R

Published
2006
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9. Histological precursors of oesophageal squamous cell carcinoma: results from a 13 year prospective follow up study in a high risk population

Author

Wang, G-Q, Abnet, C C, Shen, Q, Lewin, K J, Sun, X-D, Roth, M J, Qiao, Y-L, Mark, S D, Dong, Z-W, Taylor, P R, and Dawsey, S M

Subjects
Squamous cell carcinoma -- Diagnosis, Squamous cell carcinoma -- Surveys, Squamous cell carcinoma -- Risk factors, Endoscopic ultrasonography -- Diagnosis, Endoscopic ultrasonography -- Surveys, Biopsy -- Diagnosis, Health
Published
2005

16. Comparing Anthropometric Indicators of Visceral and General Adiposity as Determinants of Overall and Cardiovascular Mortality

Author

Nalini, M., Sharafkhah, M., Poustchi, H., Sepanlou, S. G., Pourshams, A., Radmard, A. R., Khoshnia, M., Gharavi, A., Dawsey, S. M., Abnet, C. C., Boffetta, P., Brennan, P., Sotoudeh, M., Nikmanesh, A., Shahin Merat, Etemadi, A., Shakeri, R., Malekzadeh, R., Kamangar, F., Nalini, Mahdi, Sharafkhah, Maryam, Poustchi, Hossein, Sepanlou, Sadaf G, Pourshams, Akram, Radmard, Amir Reza, Khoshnia, Masoud, Gharavi, Abdolsamad, Dawsey, Sanford M, Abnet, Christian C, Boffetta, Paolo, Brennan, Paul, Sotoudeh, Masoud, Nikmanesh, Arash, Merat, Shahin, Etemadi, Arash, Shakeri, Ramin, Malekzadeh, Reza, and Kamangar, Farin

Subjects
Adult, Male, Waist-Height Ratio, Waist-Hip Ratio, Intra-Abdominal Fat, Iran, Middle Aged, Cardiovascular, Article, Hip circumference, Cohort Studies, Cardiovascular Diseases, Risk Factors, Humans, Waist circumference, Female, Obesity, Mortality, Body mass index, Adiposity, Aged, Proportional Hazards Models
Abstract

BACKGROUND: It is unclear which anthropometric obesity indicator best predicts adverse health outcomes. This study aimed to investigate the association of body-mass index (BMI), waist circumference (WC), waist-to-height ratio (WHtR), waist-to-hip ratio (WHR), and hip-adjusted WC with all-cause and cardiovascular mortality. METHODS: 50045 people aged 40–75 (58% women, median BMI: 26.3kg/m(2)) participated in the population-based Golestan Cohort Study. We used Cox regression to estimate hazard ratios (HRs) and 95% confidence intervals (95% CI) for the association of obesity indicators with mortality. We also examined the association of these indicators with intermediate outcomes, including hypertension, blood glucose, dyslipidemia, carotid atherosclerosis, nonalcoholic fatty liver, and visceral abdominal fat. RESULTS: After a median follow-up of 10.9 years (success rate: 99.1%), 6651 deaths (2778 cardiovascular) occurred. Comparing 5(th) to the 1(st) quintile, HRs (95% CIs) for all-cause and cardiovascular mortality were 1.12 (1.02–1.22) and 1.59 (1.39–1.83) for BMI, 1.16 (1.07–1.27) and 1.66 (1.44–1.90) for WC, 1.28 (1.17–1.40) and 1.88 (1.63–2.18) for WHtR, 1.44 (1.32–1.58) and 2.04 (1.76–2.36) for WHR, and 1.84 (1.62–2.09) and 2.72 (2.23–3.32) for hip-adjusted WC, respectively. Hip-adjusted WC had the strongest associations with the intermediate outcomes. CONCLUSIONS: Indicators of visceral adiposity (e.g., hip-adjusted WC) were much stronger predictors of overall and cardiovascular mortality than were indicators of general adiposity (e.g., BMI). The full-strength effect of visceral adiposity becomes apparent only when both WC, as a risk factor, and hip circumference, as a protective factor, are individually and simultaneously taken into consideration.

Published
2019

18. Hazards of cigarettes, smokeless tobacco and waterpipe in a Middle Eastern Population: a Cohort Study of 50 000 individuals from Iran

Author

Etemadi, A., Khademi, H., Kamangar, F., Freedman, N. D., Abnet, C. C., Brennan, P., Malekzadeh, R., Golestan Cohort Study Team, Poustchi, H., Pourshams, A., Khoshnia, M., Gharavi, S., Norouzi, A., Merat, S., Jafari, E., Islami, F., Semnani, S., Pharoah, P. D. P., Boffetta, P., Dawsey, S. M., and Etemadi, A. and Khademi, H. and Kamangar, F. and Freedman, N.D. and Abnet, C.C. and Brennan, P. and Malekzadeh, R. and Golestan Cohort Study Team and Poustchi, H. and Pourshams, A. and Khoshnia, M. and Gharavi, S. and Norouzi, A. and Merat, S. and Jafari, E. and Islami, F. and Semnani, S. and Pharoah, P.D.P. and Boffetta, P. and Dawsey, S.M.

Subjects
Male, Tobacco, Smokeless, Health (social science), cohort analysi, Population, cigarette smoking, Iran, Tobacco, Waterpipe, Article, smoking, Cohort Studies, 03 medical and health sciences, 0302 clinical medicine, Environmental health, middle aged, statistics and numerical data, medicine, Humans, human, 030212 general & internal medicine, education, Socioeconomic status, Aged, education.field_of_study, Mortality, Premature, business.industry, Proportional hazards model, adult, Public Health, Environmental and Occupational Health, Cancer, smokeless tobacco, waterpipe tobacco, Adult, medicine.disease, mortality, Chewing tobacco, female, premature mortality, Tobacco, Smokele, Smokeless tobacco, 030220 oncology & carcinogenesis, Cohort, epidemiology, Cohort Studie, business, Cohort study
Abstract

Background There is limited information about the hazards of cigarettes, smokeless tobacco and waterpipe in the Middle East. The aim of this study was to determine the association between different types of tobacco use and earlier death in the Golestan Cohort Study. Methods The Study includes 50 045 adults (aged 40– 75 years) from north eastern Iran. The baseline questionnaire (2004–2008) assessed information about use of cigarettes, chewing tobacco (nass) and waterpipe. To assess the use of each type of tobacco compared with never tobacco users, we used Cox regression models adjusted for age, socioeconomic status, area of residence, education and other tobacco used, and stratified by sex, ethnicity and opium use. Results 17% of participants reported a history of cigarette smoking, 7.5% chewing tobacco (nass) and 1.1% smoking waterpipe, and these figures declined in the later birth cohorts. During a median follow-up of 8 years, 4524 deaths occurred (mean age 64.8 +9.9 years). Current (HR=1.44; 95% CI 1.28 to 1.61) and former (HR=1.35; 95% CI 1.16 to 1.56) cigarette smokers had higher overall mortality relative to never tobacco users. The highest cigarette-associated risk was for cancer death among current heavy smokers (HR=2.32; 95% CI 1.66 to 3.24). Current nass chewing was associated with overall mortality (HR=1.16; 95% CI 1.01 to 1.34), and there was a 61% higher risk of cancer death in people chewing nass more than five times a day. We observed an association between the cumulative lifetime waterpipe use (waterpipe-years≥28) and both overall (HR=1.66; 95% CI 1.11 to 2.47), and cancer mortality (HR=2.82; 95% CI 1.30 to 6.11). Conclusions Regular use of cigarettes, smokeless tobacco and waterpipe were associated with the risk of earlier death (particularly from cancer) in our cohort. © 2017, BMJ Publishing Group. All rights reserved.

Published
2016
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19. Research strategies for nutritional and physical activity epidemiology and cancer prevention

Author

Mahabir, S., Willett, W., Friedenreich, C., Lai, G., Boushey, Carol, Matthews, C., Sinha, R., Colditz, G., Rothwell, J., Reedy, J., Patel, A., Leitzmann, M., Fraser, G., Ross, S., Hursting, S., Abnet, C., Kushi, L., Taylor, P., Prentice, R., Mahabir, S., Willett, W., Friedenreich, C., Lai, G., Boushey, Carol, Matthews, C., Sinha, R., Colditz, G., Rothwell, J., Reedy, J., Patel, A., Leitzmann, M., Fraser, G., Ross, S., Hursting, S., Abnet, C., Kushi, L., Taylor, P., and Prentice, R.

Abstract

Very large international and ethnic differences in cancer rates exist, are minimally explained by genetic factors, and show the huge potential for cancer prevention. A substantial portion of the differences in cancer rates can be explained by modifiable factors, and many important relationships have been documented between diet, physical activity, and obesity, and incidence of important cancers. Other related factors, such as the microbiome and the metabolome, are emerging as important intermediary components in cancer prevention. It is possible with the incorporation of newer technologies and studies including long follow-up and evaluation of effects across the life cycle, additional convincing results will be produced. However, several challenges exist for cancer researchers; for example, measurement of diet and physical activity, and lack of standardization of samples for microbiome collection, and validation of metabolomic studies. The United States National Cancer Institute convened the Research Strategies for Nutritional and Physical Activity Epidemiology and Cancer Prevention Workshop on June 28-29, 2016, in Rockville, Maryland, during which the experts addressed the state of the science and areas of emphasis. This current paper reflects the state of the science and priorities for future research.

Published
2018

20. Association between telomere length and risk of cancer and non-neoplastic diseases: A Mendelian randomization study

Author

Collaboration, Telomeres Mendelian Randomization, Haycock, P, Burgess, S, Nounu, A, Zheng, J, Okoli, G, Bowden, J, Wade, K, Timpson, N, Evans, D, Willeit, P, Aviv, A, Gaunt, T, Hemani, G, Mangino, M, Ellis, H, Kurian, K, Pooley, K, Eeles, R, Lee, J, Fang, S, Chen, W, Law, M, Bowdler, L, Iles, M, Yang, Q, Worrall, B, Markus, H, Hung, R, Amos, C, Spurdle, A, Thompson, D, O'Mara, T, Wolpin, B, Amundadottir, L, Stolzenberg-Solomon, R, Trichopoulou, A, Onland-Moret, N, Lund, E, Duell, E, Canzian, F, Severi, G, Overvad, K, Gunter, M, Tumino, R, Svenson, U, van Rij, A, Baas, A, Bown, M, Samani, N, van t'Hof, F, Tromp, G, Jones, G, Kuivaniemi, H, Elmore, J, Johansson, M, Mckay, J, Scelo, G, Carreras-Torres, R, Gaborieau, V, Brennan, P, Bracci, P, Neale, R, Olson, S, Gallinger, S, Li, D, Petersen, G, Risch, H, Klein, A, Han, J, Abnet, C, Freedman, N, Taylor, P, Maris, J, Aben, K, Kiemeney, L, Vermeulen, S, Wiencke, J, Walsh, K, Wrensch, M, Rice, T, Turnbull, C, Litchfield, K, Paternoster, L, Standl, M, Abecasis, G, SanGiovanni, J, Li, Y, Mijatovic, V, Sapkota, Y, Low, S, Zondervan, K, Montgomery, G, Nyholt, D, van Heel, D, Hunt, K, Arking, D, Ashar, F, Sotoodehnia, N, Woo, D, Rosand, J, Comeau, M, Brown, W, Silverman, E, Hokanson, J, Cho, M, Hui, J, Ferreira, M, Thompson, P, Morrison, A, Felix, J, Smith, N, Christiano, A, Petukhova, L, Betz, R, Fan, X, Zhang, X, Zhu, C, Langefeld, C, Thompson, S, Wang, F, Lin, X, Schwartz, D, Fingerlin, T, Rotter, J, Cotch, M, Jensen, R, Munz, M, Dommisch, H, Schaefer, A, Han, F, Ollila, H, Hillary, R, Albagha, O, Ralston, S, Zeng, C, Zheng, W, Shu, X, Reis, A, Uebe, S, Hüffmeier, U, Kawamura, Y, Otowa, T, Sasaki, T, Hibberd, M, Davila, S, Xie, G, Siminovitch, K, Bei, J, Zeng, Y, Försti, A, Chen, B, Landi, S, Franke, A, Fischer, A, Ellinghaus, D, Flores, C, Noth, I, Ma, S, Foo, J, Liu, J, Kim, J, Cox, D, Delattre, O, Mirabeau, O, Skibola, C, Tang, C, Garcia-Barcelo, M, Chang, K, Su, W, Chang, Y, Martin, N, Gordon, S, Wade, T, Lee, C, Kubo, M, Cha, P, Nakamura, Y, Levy, D, Kimura, M, Hwang, S, Hunt, S, Spector, T, Soranzo, N, Manichaikul, A, Barr, R, Kahali, B, Speliotes, E, Yerges-Armstrong, L, Cheng, C, Jonas, J, Wong, T, Fogh, I, Lin, K, Powell, J, Rice, K, Relton, C, Martin, R, Davey Smith, G, Erasmus MC other, Epidemiology, and Pediatrics

Subjects
0301 basic medicine, Adult, Male, Cancer Research, Single-nucleotide polymorphism, Genome-wide association study, Disease, Bioinformatics, Polymorphism, Single Nucleotide, Risk Assessment, Article, 03 medical and health sciences, Telomere Homeostasis, SDG 3 - Good Health and Well-being, Neoplasms, Mendelian randomization, Journal Article, medicine, Humans, Genetic Predisposition to Disease, Càncer, Germ-Line Mutation, Aged, Cancer, Aged, 80 and over, business.industry, Nucleotides, Odds ratio, Mendelian Randomization Analysis, Middle Aged, Telomere, medicine.disease, Nucleòtids, 030104 developmental biology, Stem cell division, Oncology, Cardiovascular Diseases, Urological cancers Radboud Institute for Health Sciences [Radboudumc 15], Female, ICEP, business, Genome-Wide Association Study, Bristol Population Health Science Institute
Abstract

Importance The causal direction and magnitude of the association between telomere length and incidence of cancer and non-neoplastic diseases is uncertain owing to the susceptibility of observational studies to confounding and reverse causation. Objective To conduct a Mendelian randomization study, using germline genetic variants as instrumental variables, to appraise the causal relevance of telomere length for risk of cancer and non-neoplastic diseases. Data Sources Genomewide association studies (GWAS) published up to January 15, 2015. Study Selection GWAS of noncommunicable diseases that assayed germline genetic variation and did not select cohort or control participants on the basis of preexisting diseases. Of 163 GWAS of noncommunicable diseases identified, summary data from 103 were available. Data Extraction and Synthesis Summary association statistics for single nucleotide polymorphisms (SNPs) that are strongly associated with telomere length in the general population. Main Outcomes and Measures Odds ratios (ORs) and 95%confidence intervals (CIs) for disease per standard deviation (SD) higher telomere length due to germline genetic variation. Results Summary data were available for 35 cancers and 48 non-neoplastic diseases, corresponding to 420 081 cases (median cases, 2526 per disease) and 1 093 105 controls (median, 6789 per disease). Increased telomere length due to germline genetic variation was generally associated with increased risk for site-specific cancers. The strongest associations (ORs [95%CIs] per 1-SD change in genetically increased telomere length) were observed for glioma, 5.27 (3.15-8.81); serous low-malignant-potential ovarian cancer, 4.35 (2.39-7.94); lung adenocarcinoma, 3.19 (2.40-4.22); neuroblastoma, 2.98 (1.92-4.62); bladder cancer, 2.19 (1.32-3.66); melanoma, 1.87 (1.55-2.26); testicular cancer, 1.76 (1.02-3.04); kidney cancer, 1.55 (1.08-2.23); and endometrial cancer, 1.31 (1.07-1.61). Associations were stronger for rarer cancers and at tissue sites with lower rates of stem cell division. There was generally little evidence of association between genetically increased telomere length and risk of psychiatric, autoimmune, inflammatory, diabetic, and other non-neoplastic diseases, except for coronary heart disease (OR, 0.78 [95%CI, 0.67-0.90]), abdominal aortic aneurysm (OR, 0.63 [95%CI, 0.49-0.81]), celiac disease (OR, 0.42 [95%CI, 0.28-0.61]) and interstitial lung disease (OR, 0.09 [95%CI, 0.05-0.15]). Conclusions and Relevance It is likely that longer telomeres increase risk for several cancers but reduce risk for some non-neoplastic diseases, including cardiovascular diseases.

Published
2017
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21. Dairy food intake and all-cause, cardiovascular disease, and cancer mortality: The Golestan Cohort Study

Author

Farvid, M. S., Malekshah, A. F., Pourshams, A., Poustchi, H., Sepanlou, S. G., Sharafkhah, M., Khoshnia, M., Farvid, M., Abnet, C. C., Kamangar, F., Dawsey, S. M., Brennan, P., Pharoah, P. D., Boffetta, P., Willett, W. C., Malekzadeh, R., and Farvid, M.S. and Malekshah, A.F. and Pourshams, A. and Poustchi, H. and Sepanlou, S.G. and Sharafkhah, M. and Khoshnia, M. and Farvid, M. and Abnet, C.C. and Kamangar, F. and Dawsey, S.M. and Brennan, P. and Pharoah, P.D. and Boffetta, P. and Willett, W.C. and Malekzadeh, R.

Subjects
Male, food intake, Iran, digestive system cancer, cardiovascular disease, Cheese, cancer mortality, middle aged, vegetable, grain, Cancer, milk, Middle Aged, Cardiovascular disease, Yogurt, Golestan Cohort Study, Diet Survey, Dairy product, aged, female, Milk, dairy product, food consumption, epidemiology, Female, food product, prospective study, Human, cohort analysi, Article, yoghurt, cancer, cheese, male, adverse effect, follow up, human, Dairy Product, Mortality, health risk, Iran, Cardiovascular Disease, red meat, questionnaire, public health, adult, fruit, mortality, major clinical study, Prospective Studie, Proportional Hazards Model, mortality risk, Neoplasm, diet, neoplasm, proportional hazards model, Golestan
Abstract

We investigated the association between dairy product consumption and all-cause, cardiovascular disease (CVD), and cancer mortality in the Golestan Cohort Study, a prospective cohort study launched in January 2004 in Golestan Province, northeastern Iran. A total of 42,403 men and women participated in the study and completed a diet questionnaire at enrollment. Cox proportional hazards models were used to estimate hazard ratios and 95% confidence intervals. We documented 3,291 deaths (1,467 from CVD and 859 from cancer) during 11 years of follow-up (2004-2015). The highest quintile of total dairy product consumption (versus the lowest) was associated with 19% lower all-cause mortality risk (hazard ratio (HR) = 0.81, 95% confidence interval (CI): 0.72, 0.91; Ptrend = 0.006) and 28% lower CVD mortality risk (HR = 0.72, 95% CI: 0.60, 0.86; Ptrend = 0.005). High consumption of low-fat dairy food was associated with lower risk of all-cause (HR = 0.83, 95% CI: 0.73, 0.94; Ptrend = 0.002) and CVD (HR = 0.74, 95% CI: 0.61, 0.89; Ptrend = 0.001) mortality. We noted 11% lower all-cause mortality and 16% lower CVD mortality risk with high yogurt intake. Cheese intake was associated with 16% lower all-cause mortality and 26% lower CVD mortality risk. Higher intake of high-fat dairy food and milk was not associated with all-cause or CVD mortality. Neither intake of individual dairy products nor intake of total dairy products was significantly associated with overall cancer mortality. High consumption of dairy products, especially yogurt and cheese, may reduce the risk of overall and CVD mortality. © 2017 The Author.

Published
2017

23. Household fuel use and cardiovascular disease mortality

Author

Mitter, S. S., Vedanthan, R., Islami, F., Pourshams, A., Khademi, H., Kamangar, F., Abnet, C. C., Dawsey, S. M., Pharoah, P. D., Brennan, P., Fuster, V., Boffetta, P., Malekzadeh, R., Mitter, S.S., Vedanthan, R., Islami, F., Pourshams, A., Khademi, H., Kamangar, F., Abnet, C.C., Dawsey, S.M., Pharoah, P.D., Brennan, P., Fuster, V., Boffetta, P., and Malekzadeh, R.

Subjects
Air pollution - global disease
Abstract

Background - Household air pollution is the third largest risk factor for global disease burden, but direct links with cardiovascular disease mortality are limited. This study aimed to evaluate the relationship between household fuel use and cardiovascular disease mortality. Methods and Results - The Golestan Cohort Study in northeastern Iran enrolled 50 045 individuals 40 to 75 years of age between 2004 and 2008 and collected data on lifetime household fuel use and other baseline exposures. Participants were followed up through 2012 with a 99% successful follow-up rate. Cox proportional hazards models were fitted to calculate hazard ratios for associations between pehen (local dung), wood, kerosene/diesel, or natural gas burning for cooking and heating and all-cause and cause-specific mortality, with adjustment for lifetime exposure to each of these fuels and potential confounders. A total of 3073 participants (6%) died during follow-up; 78% of these deaths were attributable to noncommunicable diseases, including cardiovascular, oncological, and respiratory illnesses. Adjusted 10-year hazard ratios from kerosene/diesel burning were 1.06 (95% confidence interval, 1.02-1.10) and 1.11 (95% confidence interval, 1.06-1.17) for all-cause and cardiovascular mortality, respectively. Subtype-specific analyses revealed a significant increase in ischemic heart disease (10-year hazard ratio, 1.14; 95% confidence interval, 1.06-1.21) and a trend toward cerebrovascular accident (10-year hazard ratio, 1.08; 95% confidence interval, 0.99-1.17) mortality. Stratification by sex revealed a potential signal for increased risk for all-cause and cardiovascular disease mortality among women compared with men, with similar risk for ischemic heart disease mortality. Conclusions - Household exposure to high-pollution fuels was associated with increased risk for all-cause and cardiovascular disease mortality. Replicating these results worldwide would support efforts to reduce such exposures. © 2016 American Heart Association, Inc.

Published
2016

25. Polymorphisms in genes in the androgen pathway and risk of Barrett’s esophagus and esophageal adenocarcinoma

Author

Ek, W. E., Lagergren, K., Cook, M., Wu, A. H., Abnet, C. C., Levine, D., Chow, W-H., Bernstein, L., Risch, H. A., Shaheen, N. J., Bird, N. C., Corley, D. A., Hardie, L. J., Fitzgerald, R. C., Gammon, M. D., Romero, Y., Liu, G., Ye, W., Vaughan, T. L., MacGregor, S., Whiteman, D. C., Westberg, L., and Lagergren, J.

Subjects
Adult, Male, Risk, Jumonji Domain-Containing Histone Demethylases, Esophageal Neoplasms, Steroid 17-alpha-Hydroxylase, Oxidoreductases, N-Demethylating, Adenocarcinoma, Middle Aged, Polymorphism, Single Nucleotide, Article, Barrett Esophagus, Humans, Female, Genetic Predisposition to Disease, Aged
Abstract

The strong male predominance in Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC) remains inadequately explained, but sex hormones might be involved. We hypothesized that single nucleotide polymorphisms (SNPs) in the androgen pathway influence risk of developing BE and EAC. This genetic-epidemiological analysis included 14 studies from Australia, Europe and North America. Polymorphisms in 16 genes coding for the androgen pathway were analyzed using a gene-based approach: versatile gene-based test association study. This method evaluates associations between a trait and all SNPs within a specific gene rather than each SNP marker individually as in a conventional GWAS. The data were stratified for sex, body-mass index, waist-to-hip ratio, tobacco smoking and gastroesophageal reflux status. Included were data from 1,508 EAC patients, 2,383 BE patients and 2,170 control participants. SNPs within the gene CYP17A1 were associated with risk of BE in the sexes combined (p = 0.002) and in males (p = 0.003), but not in females separately (p = 0.3). This association was found in tobacco smokers (p = 0.003) and in BE patients without reflux (p = 0.004), but not in nonsmokers (p = 0.2) or those with reflux (p = 0.036). SNPs within JMJD1C were associated with risk of EAC in females (p = 0.001). However, none of these associations replicated in a subsequent sample. Fourteen other genes studied did not reach statistically significant levels of association with BE, EAC or the combination of BE and EAC, after correcting for the number of genes included in the analysis. In conclusion, genetic variants in the androgen-related genes CYP17A1 and JMJD1C might be associated with risk of BE and EAC, respectively, but replication data with larger sample sizes are needed.

Published
2015

26. Impact of smoking and smoking cessation on cardiovascular events and mortality among older adults: Meta-analysis of Individual participant data from prospective cohort studies of the CHANCES consortium

Author

Mons, U., Müezzinler, A., Gellert, C., Schöttker, B., Abnet, C. C., Bobak, M., De Groot, L., Freedman, N. D., Jansen, E., Kee, F., Kromhout, D., Kuulasmaa, K., Tiina, L., O'Doherty, M. G., Bas, B. -D. -M., Orfanos, P., Peters, A., Van Der Schouw, Y. T., Wilsgaard, T., Wolk, A., Trichopoulou, A., Boffetta, P., Brenner, H., Baceviciene, M., Boer, J. M. A., Drygas, W., Eriksson, S., Feskens, E., Gafarov, V., Gardiner, J., Håkansson, N., Jansson, J. -H., Jousilahti, P., Kampman, E., Kontto, J., Kubinova, R., Leenders, M., Linneberg, A., Løchen, M. -L., Lorbeer, R., Malyutina, S., Mathiesen, E. B., Melhus, H., Michaëlsson, K., Njølstad, I., Orsini, N., Pajak, A., Pikhart, H., Pisinger, C., Salomaa, V., Sánchez, M. -J., Sans, S., Schaan, B., Schneider, A., Siganos, G., Söderberg, S., Streppel, M., Tamošiunas, A., Veronesi, G., Waterham, E., Wennberg, P., Mons, U., Müezzinler, A., Gellert, C., Schöttker, B., Abnet, C.C., Bobak, M., De Groot, L., Freedman, N.D., Jansen, E., Kee, F., Kromhout, D., Kuulasmaa, K., Tiina, L., O'Doherty, M.G., Bas, B.-D.-M., Orfanos, P., Peters, A., Van Der Schouw, Y.T., Wilsgaard, T., Wolk, A., Trichopoulou, A., Boffetta, P., Brenner, H., Baceviciene, M., Boer, J.M.A., Drygas, W., Eriksson, S., Feskens, E., Gafarov, V., Gardiner, J., Håkansson, N., Jansson, J.-H., Jousilahti, P., Kampman, E., Kontto, J., Kubinova, R., Leenders, M., Linneberg, A., Løchen, M.-L., Lorbeer, R., Malyutina, S., Mathiesen, E.B., Melhus, H., Michaëlsson, K., Njølstad, I., Orsini, N., Pajak, A., Pikhart, H., Pisinger, C., Salomaa, V., Sánchez, M.-J., Sans, S., Schaan, B., Schneider, A., Siganos, G., Söderberg, S., Streppel, M., Tamošiunas, A., Veronesi, G., Waterham, E., and Wennberg, P.

Subjects
Medicine (all), Smoking - cardiovascular mortality - stroke
Abstract

OBJECTIVE: To investigate the impact of smoking and smoking cessation on cardiovascular mortality, acute coronary events, and stroke events in people aged 60 and older, and to calculate and report risk advancement periods for cardiovascular mortality in addition to traditional epidemiological relative risk measures. DESIGN: Individual participant meta-analysis using data from 25 cohorts participating in the CHANCES consortium. Data were harmonised, analysed separately employing Cox proportional hazard regression models, and combined by meta-analysis. RESULTS: Overall, 503 905 participants aged 60 and older were included in this study, of whom 37 952 died from cardiovascular disease. Random effects meta-analysis of the association of smoking status with cardiovascular mortality yielded a summary hazard ratio of 2.07 (95% CI 1.82 to 2.36) for current smokers and 1.37 (1.25 to 1.49) for former smokers compared with never smokers. Corresponding summary estimates for risk advancement periods were 5.50 years (4.25 to 6.75) for current smokers and 2.16 years (1.38 to 2.39) for former smokers. The excess risk in smokers increased with cigarette consumption in a dose-response manner, and decreased continuously with time since smoking cessation in former smokers. Relative risk estimates for acute coronary events and for stroke events were somewhat lower than for cardiovascular mortality, but patterns were similar. CONCLUSIONS: Our study corroborates and expands evidence from previous studies in showing that smoking is a strong independent risk factor of cardiovascular events and mortality even at older age, advancing cardiovascular mortality by more than five years, and demonstrating that smoking cessation in these age groups is still beneficial in reducing the excess risk. © 2015 BMJ Publishing Group Ltd.

Published
2015

27. Gene-environment interactions in cancer epidemiology: A national cancer institute think tank report

Author

Hutter, C. M., Mechanic, L. E., Chatterjee, N., Kraft, P., Gillanders, E. M., Abnet, C. C., Amos, C., Balshaw, D., Bickeböller, H., Bierut, L. J., Boffetta, P., Bondy, M., Chanock, S., Chen, H. -S., Cox, N., Vivo, I. D., Divi, R., Dupuis, J., Ellison, G., Fallin, M. D., Gauderman, W. J., Gillanders, E., Haiman, C., Hutter, C., Simonds, N. I., Iversen, E., Khoury, M. J., Marchand, L. L., McAllister, K., Mechanic, L., Peters, U., Prentice, R., Rebbeck, T., Reedy, J., Rothman, N., Schully, S., Seminara, D., Shaughnessy, D., Shete, S., Spiegelman, D., Stram, D. O., BALDWIN, THOMAS DONALD, Wang, M., WANG, WENPING, WEINBERG, CAREN HELENE, Winn, D. M., Witte, J. S., Hutter, C.M., Mechanic, L.E., Chatterjee, N., Kraft, P., Gillanders, E.M., Abnet, C.C., Amos, C., Balshaw, D., Bickeböller, H., Bierut, L.J., Boffetta, P., Bondy, M., Chanock, S., Chen, H.-S., Cox, N., Vivo, I.D., Divi, R., Dupuis, J., Ellison, G., Fallin, M.D., Gauderman, W.J., Gillanders, E., Haiman, C., Hutter, C., Simonds, N.I., Iversen, E., Khoury, M.J., Marchand, L.L., McAllister, K., Mechanic, L., Peters, U., Prentice, R., Rebbeck, T., Reedy, J., Rothman, N., Schully, S., Seminara, D., Shaughnessy, D., Shete, S., Spiegelman, D., Stram, D.O., Thomas, D., Wang, M., Wang, W., Weinberg, C., Winn, D.M., and Witte, J.S.

Subjects
Gene-environment interactions, complex phenotypes, genetic epidemiology
Abstract

Cancer risk is determined by a complex interplay of genetic and environmental factors. Genome-wide association studies (GWAS) have identified hundreds of common (minor allele frequency [MAF] > 0.05) and less common (0.01 < MAF < 0.05) genetic variants associated with cancer. The marginal effects of most of these variants have been small (odds ratios: 1.1-1.4). There remain unanswered questions on how best to incorporate the joint effects of genes and environment, including gene-environment (G × E) interactions, into epidemiologic studies of cancer. To help address these questions, and to better inform research priorities and allocation of resources, the National Cancer Institute sponsored a "Gene-Environment Think Tank" on January 10-11, 2012. The objective of the Think Tank was to facilitate discussions on (1) the state of the science, (2) the goals of G × E interaction studies in cancer epidemiology, and (3) opportunities for developing novel study designs and analysis tools. This report summarizes the Think Tank discussion, with a focus on contemporary approaches to the analysis of G × E interactions. Selecting the appropriate methods requires first identifying the relevant scientific question and rationale, with an important distinction made between analyses aiming to characterize the joint effects of putative or established genetic and environmental factors and analyses aiming to discover novel risk factors or novel interaction effects. Other discussion items include measurement error, statistical power, significance, and replication. Additional designs, exposure assessments, and analytical approaches need to be considered as we move from the current small number of success stories to a fuller understanding of the interplay of genetic and environmental factors. © 2013 WILEY PERIODICALS, INC.

Published
2013

28. Serum pepsinogen 1 and anti‐<italic>Helicobacter pylori</italic> IgG antibodies as predictors of gastric cancer risk in Finnish males.

Author

Song, M., Camargo, M. C., Weinstein, S. J., Murphy, G., Freedman, N. D., Koshiol, J., Stolzenberg‐Solomon, R. Z., Abnet, C. C., Männistö, S., Albanes, D., and Rabkin, C. S.

Subjects
BLOOD serum analysis, PEPSINOGEN, HELICOBACTER pylori, IMMUNOGLOBULIN G, STOMACH cancer risk factors, FINNS, DISEASES
Abstract

Summary: Background: Serum pepsinogen 1 (SPG1) and anti‐Helicobacter pylori serology have been used for gastric risk stratification in Asia. Aim: To assess utility of these markers in a Western population. Methods: SPG1 measurements were available for 21 895 Finnish male smokers in the Alpha‐Tocopherol, Beta‐Carotene Cancer Prevention Study. We used Cox proportional hazards models adjusted for potential confounders to estimate gastric cancer hazard ratios (HR) and 95% confidence intervals (95% CI) for low SPG1 (<25 μg/L). In a subset (n = 3555) with anti‐H. pylori serology, these markers jointly defined the following: Group A (H. pylori[−], SPG1[normal]; reference group), Group B (H. pylori[+], SPG1[normal]), Group C (H. pylori[+], SPG1[low]) and Group D (H. pylori[−], SPG1[low]). Odds ratios (ORs) and 95% CI were calculated using multivariate logistic regression. Results: There were 329 gastric cancers diagnosed an average of 13.9 years after baseline. Pre‐diagnostic low SPG1 was significantly associated with increased gastric cancer risk (HR 2.68, 95% CI 1.99‐3.61). Among subjects with both SPG1 and H. pylori serology, groups B, C and D had increased gastric cancer ORs (95% CI) of 1.79 (1.21‐2.64), 3.85 (2.36‐6.28) and 6.35 (2.20‐18.34), respectively. CagA seropositives had significantly higher ORs than CagA seronegatives within group B (Pheterogeneity = 0.01). For groups B and C, repeat SPG1 level at 3 years did not further stratify gastric cancer risk. Conclusions: Low SPG1 was associated with increased gastric cancer risk in our large Finnish cohort. A single measurement of SPG1 along with H. pylori whole cell and CagA serology provides potentially useful prediction of gastric cancer risk. [ABSTRACT FROM AUTHOR]

Published
2018
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30. Hypertension and mortality in the Golestan Cohort Study: A prospective study of 50 000 adults in Iran

Author

Sepanlou, S G, primary, Sharafkhah, M, additional, Poustchi, H, additional, Malekzadeh, M M, additional, Etemadi, A, additional, Khademi, H, additional, Islami, F, additional, Pourshams, A, additional, Pharoah, P D, additional, Abnet, C C, additional, Brennan, P, additional, Boffetta, P, additional, Dawsey, S M, additional, Esteghamati, A, additional, Kamangar, F, additional, and Malekzadeh, R, additional

Published
2015
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31. Pilot study of cytological testing for oesophageal squamous cell dysplasia in a high-risk area in Northern Iran

Author

Roshandel, G, primary, Merat, S, additional, Sotoudeh, M, additional, Khoshnia, M, additional, Poustchi, H, additional, Lao-Sirieix, P, additional, Malhotra, S, additional, O'Donovan, M, additional, Etemadi, A, additional, Nickmanesh, A, additional, Pourshams, A, additional, Norouzi, A, additional, Debiram, I, additional, Semnani, S, additional, Abnet, C C, additional, Dawsey, S M, additional, Fitzgerald, R C, additional, and Malekzadeh, R, additional

Published
2014
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32. Imputation and subset-based association analysis across different cancer types identifies multiple independent risk loci in the TERT-CLPTM1L region on chromosome 5p15.33

Author

Wang, Z., primary, Zhu, B., additional, Zhang, M., additional, Parikh, H., additional, Jia, J., additional, Chung, C. C., additional, Sampson, J. N., additional, Hoskins, J. W., additional, Hutchinson, A., additional, Burdette, L., additional, Ibrahim, A., additional, Hautman, C., additional, Raj, P. S., additional, Abnet, C. C., additional, Adjei, A. A., additional, Ahlbom, A., additional, Albanes, D., additional, Allen, N. E., additional, Ambrosone, C. B., additional, Aldrich, M., additional, Amiano, P., additional, Amos, C., additional, Andersson, U., additional, Andriole, G., additional, Andrulis, I. L., additional, Arici, C., additional, Arslan, A. A., additional, Austin, M. A., additional, Baris, D., additional, Barkauskas, D. A., additional, Bassig, B. A., additional, Beane Freeman, L. E., additional, Berg, C. D., additional, Berndt, S. I., additional, Bertazzi, P. A., additional, Biritwum, R. B., additional, Black, A., additional, Blot, W., additional, Boeing, H., additional, Boffetta, P., additional, Bolton, K., additional, Boutron-Ruault, M.-C., additional, Bracci, P. M., additional, Brennan, P., additional, Brinton, L. A., additional, Brotzman, M., additional, Bueno-de-Mesquita, H. B., additional, Buring, J. E., additional, Butler, M. A., additional, Cai, Q., additional, Cancel-Tassin, G., additional, Canzian, F., additional, Cao, G., additional, Caporaso, N. E., additional, Carrato, A., additional, Carreon, T., additional, Carta, A., additional, Chang, G.-C., additional, Chang, I.-S., additional, Chang-Claude, J., additional, Che, X., additional, Chen, C.-J., additional, Chen, C.-Y., additional, Chen, C.-H., additional, Chen, C., additional, Chen, K.-Y., additional, Chen, Y.-M., additional, Chokkalingam, A. P., additional, Chu, L. W., additional, Clavel-Chapelon, F., additional, Colditz, G. A., additional, Colt, J. S., additional, Conti, D., additional, Cook, M. B., additional, Cortessis, V. K., additional, Crawford, E. D., additional, Cussenot, O., additional, Davis, F. G., additional, De Vivo, I., additional, Deng, X., additional, Ding, T., additional, Dinney, C. P., additional, Di Stefano, A. L., additional, Diver, W. R., additional, Duell, E. J., additional, Elena, J. W., additional, Fan, J.-H., additional, Feigelson, H. S., additional, Feychting, M., additional, Figueroa, J. D., additional, Flanagan, A. M., additional, Fraumeni, J. F., additional, Freedman, N. D., additional, Fridley, B. L., additional, Fuchs, C. S., additional, Gago-Dominguez, M., additional, Gallinger, S., additional, Gao, Y.-T., additional, Gapstur, S. M., additional, Garcia-Closas, M., additional, Garcia-Closas, R., additional, Gastier-Foster, J. M., additional, Gaziano, J. M., additional, Gerhard, D. S., additional, Giffen, C. A., additional, Giles, G. G., additional, Gillanders, E. M., additional, Giovannucci, E. L., additional, Goggins, M., additional, Gokgoz, N., additional, Goldstein, A. M., additional, Gonzalez, C., additional, Gorlick, R., additional, Greene, M. H., additional, Gross, M., additional, Grossman, H. B., additional, Grubb, R., additional, Gu, J., additional, Guan, P., additional, Haiman, C. A., additional, Hallmans, G., additional, Hankinson, S. E., additional, Harris, C. C., additional, Hartge, P., additional, Hattinger, C., additional, Hayes, R. B., additional, He, Q., additional, Helman, L., additional, Henderson, B. E., additional, Henriksson, R., additional, Hoffman-Bolton, J., additional, Hohensee, C., additional, Holly, E. A., additional, Hong, Y.-C., additional, Hoover, R. N., additional, Hosgood, H. D., additional, Hsiao, C.-F., additional, Hsing, A. W., additional, Hsiung, C. A., additional, Hu, N., additional, Hu, W., additional, Hu, Z., additional, Huang, M.-S., additional, Hunter, D. J., additional, Inskip, P. D., additional, Ito, H., additional, Jacobs, E. J., additional, Jacobs, K. B., additional, Jenab, M., additional, Ji, B.-T., additional, Johansen, C., additional, Johansson, M., additional, Johnson, A., additional, Kaaks, R., additional, Kamat, A. M., additional, Kamineni, A., additional, Karagas, M., additional, Khanna, C., additional, Khaw, K.-T., additional, Kim, C., additional, Kim, I.-S., additional, Kim, J. H., additional, Kim, Y. H., additional, Kim, Y.-C., additional, Kim, Y. T., additional, Kang, C. H., additional, Jung, Y. J., additional, Kitahara, C. M., additional, Klein, A. P., additional, Klein, R., additional, Kogevinas, M., additional, Koh, W.-P., additional, Kohno, T., additional, Kolonel, L. N., additional, Kooperberg, C., additional, Kratz, C. P., additional, Krogh, V., additional, Kunitoh, H., additional, Kurtz, R. C., additional, Kurucu, N., additional, Lan, Q., additional, Lathrop, M., additional, Lau, C. C., additional, Lecanda, F., additional, Lee, K.-M., additional, Lee, M. P., additional, Le Marchand, L., additional, Lerner, S. P., additional, Li, D., additional, Liao, L. M., additional, Lim, W.-Y., additional, Lin, D., additional, Lin, J., additional, Lindstrom, S., additional, Linet, M. S., additional, Lissowska, J., additional, Liu, J., additional, Ljungberg, B., additional, Lloreta, J., additional, Lu, D., additional, Ma, J., additional, Malats, N., additional, Mannisto, S., additional, Marina, N., additional, Mastrangelo, G., additional, Matsuo, K., additional, McGlynn, K. A., additional, McKean-Cowdin, R., additional, McNeill, L. H., additional, McWilliams, R. R., additional, Melin, B. S., additional, Meltzer, P. S., additional, Mensah, J. E., additional, Miao, X., additional, Michaud, D. S., additional, Mondul, A. M., additional, Moore, L. E., additional, Muir, K., additional, Niwa, S., additional, Olson, S. H., additional, Orr, N., additional, Panico, S., additional, Park, J. Y., additional, Patel, A. V., additional, Patino-Garcia, A., additional, Pavanello, S., additional, Peeters, P. H. M., additional, Peplonska, B., additional, Peters, U., additional, Petersen, G. M., additional, Picci, P., additional, Pike, M. C., additional, Porru, S., additional, Prescott, J., additional, Pu, X., additional, Purdue, M. P., additional, Qiao, Y.-L., additional, Rajaraman, P., additional, Riboli, E., additional, Risch, H. A., additional, Rodabough, R. J., additional, Rothman, N., additional, Ruder, A. M., additional, Ryu, J.-S., additional, Sanson, M., additional, Schned, A., additional, Schumacher, F. R., additional, Schwartz, A. G., additional, Schwartz, K. L., additional, Schwenn, M., additional, Scotlandi, K., additional, Seow, A., additional, Serra, C., additional, Serra, M., additional, Sesso, H. D., additional, Severi, G., additional, Shen, H., additional, Shen, M., additional, Shete, S., additional, Shiraishi, K., additional, Shu, X.-O., additional, Siddiq, A., additional, Sierrasesumaga, L., additional, Sierri, S., additional, Loon Sihoe, A. D., additional, Silverman, D. T., additional, Simon, M., additional, Southey, M. C., additional, Spector, L., additional, Spitz, M., additional, Stampfer, M., additional, Stattin, P., additional, Stern, M. C., additional, Stevens, V. L., additional, Stolzenberg-Solomon, R. Z., additional, Stram, D. O., additional, Strom, S. S., additional, Su, W.-C., additional, Sund, M., additional, Sung, S. W., additional, Swerdlow, A., additional, Tan, W., additional, Tanaka, H., additional, Tang, W., additional, Tang, Z.-Z., additional, Tardon, A., additional, Tay, E., additional, Taylor, P. R., additional, Tettey, Y., additional, Thomas, D. M., additional, Tirabosco, R., additional, Tjonneland, A., additional, Tobias, G. S., additional, Toro, J. R., additional, Travis, R. C., additional, Trichopoulos, D., additional, Troisi, R., additional, Truelove, A., additional, Tsai, Y.-H., additional, Tucker, M. A., additional, Tumino, R., additional, Van Den Berg, D., additional, Van Den Eeden, S. K., additional, Vermeulen, R., additional, Vineis, P., additional, Visvanathan, K., additional, Vogel, U., additional, Wang, C., additional, Wang, J., additional, Wang, S. S., additional, Weiderpass, E., additional, Weinstein, S. J., additional, Wentzensen, N., additional, Wheeler, W., additional, White, E., additional, Wiencke, J. K., additional, Wolk, A., additional, Wolpin, B. M., additional, Wong, M. P., additional, Wrensch, M., additional, Wu, C., additional, Wu, T., additional, Wu, X., additional, Wu, Y.-L., additional, Wunder, J. S., additional, Xiang, Y.-B., additional, Xu, J., additional, Yang, H. P., additional, Yang, P.-C., additional, Yatabe, Y., additional, Ye, Y., additional, Yeboah, E. D., additional, Yin, Z., additional, Ying, C., additional, Yu, C.-J., additional, Yu, K., additional, Yuan, J.-M., additional, Zanetti, K. A., additional, Zeleniuch-Jacquotte, A., additional, Zheng, W., additional, Zhou, B., additional, Mirabello, L., additional, Savage, S. A., additional, Kraft, P., additional, Chanock, S. J., additional, Yeager, M., additional, Landi, M. T., additional, Shi, J., additional, Chatterjee, N., additional, and Amundadottir, L. T., additional

Published
2014
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34. Signal Transmission in the Auditory System

Author

Frishkopf, Lawrence S., Kiang, Nelson Y-S., Peake, William T., Siebert, William M., Weiss, Thomas F., Freeman, Dennis M., Delgutte, Bertrand, Eddington, Donald K., Guinan, John J., Jr., Rosowski, John J., Puria, Sunil, Huang, Gregory T., Ravicz, Michael E., Teoh, Su W., Voss, Susan E., Abnet, C. Cameron, Aranyosi, Alexander J., Davis, Charles Quentin, Hattangadi, Shilpa M., Johnson, Laura K., Karu, Zoher Z., Rouf, Rosanne, Shatz, Lisa F., Slifka, Janet L., Cariani, Peter A., Hammond, Benjamin M., Kalluri, Sridhar, McKinney, Martin F., Litovsky, Ruth Y., Dynes, Scott B. C., Shera, Christopher A., Stankovic, Konstantina M., Hall, Robert D., Lighvani, Arash, McKinney, Christopher, Frishkopf, Lawrence S., Kiang, Nelson Y-S., Peake, William T., Siebert, William M., Weiss, Thomas F., Freeman, Dennis M., Delgutte, Bertrand, Eddington, Donald K., Guinan, John J., Jr., Rosowski, John J., Puria, Sunil, Huang, Gregory T., Ravicz, Michael E., Teoh, Su W., Voss, Susan E., Abnet, C. Cameron, Aranyosi, Alexander J., Davis, Charles Quentin, Hattangadi, Shilpa M., Johnson, Laura K., Karu, Zoher Z., Rouf, Rosanne, Shatz, Lisa F., Slifka, Janet L., Cariani, Peter A., Hammond, Benjamin M., Kalluri, Sridhar, McKinney, Martin F., Litovsky, Ruth Y., Dynes, Scott B. C., Shera, Christopher A., Stankovic, Konstantina M., Hall, Robert D., Lighvani, Arash, and McKinney, Christopher

Abstract

Contains table of contents for Section 3, an introduction and reports on seven research projects., National Institutes of Health Grant P01-DC-00119, National Institutes of Health Grant R01-DC-00194, National Institutes of Health Grant R01 DC00238, National Institutes of Health Grant R01-DC02258, National Institutes of Health Grant T32-DC00038, National Institutes of Health Grant P01-DC00361, National Institutes of Health Grant 2RO1 DC00235, National Institutes of Health Contract N01-DC22402

Published
2010

38. Common genetic variants in the 9p21 region and their associations with multiple tumours

Author

Gu, F, primary, Pfeiffer, R M, additional, Bhattacharjee, S, additional, Han, S S, additional, Taylor, P R, additional, Berndt, S, additional, Yang, H, additional, Sigurdson, A J, additional, Toro, J, additional, Mirabello, L, additional, Greene, M H, additional, Freedman, N D, additional, Abnet, C C, additional, Dawsey, S M, additional, Hu, N, additional, Qiao, Y-L, additional, Ding, T, additional, Brenner, A V, additional, Garcia-Closas, M, additional, Hayes, R, additional, Brinton, L A, additional, Lissowska, J, additional, Wentzensen, N, additional, Kratz, C, additional, Moore, L E, additional, Ziegler, R G, additional, Chow, W-H, additional, Savage, S A, additional, Burdette, L, additional, Yeager, M, additional, Chanock, S J, additional, Chatterjee, N, additional, Tucker, M A, additional, Goldstein, A M, additional, and Yang, X R, additional

Published
2013
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40. Gastric atrophy and oesophageal squamous cell carcinoma: possible interaction with dental health and oral hygiene habit

Author

Nasrollahzadeh, D, primary, Malekzadeh, R, additional, Aghcheli, K, additional, Sotoudeh, M, additional, Merat, S, additional, Islami, F, additional, Kamangar, F, additional, Abnet, C C, additional, Shakeri, R, additional, Pourshams, A, additional, Semnani, S, additional, Boffetta, P, additional, Dawsey, S M, additional, and Ye, W, additional

Published
2012
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41. Opium use and mortality in Golestan Cohort Study: prospective cohort study of 50 000 adults in Iran

Author

Khademi, H., primary, Malekzadeh, R., additional, Pourshams, A., additional, Jafari, E., additional, Salahi, R., additional, Semnani, S., additional, Abaie, B., additional, Islami, F., additional, Nasseri-Moghaddam, S., additional, Etemadi, A., additional, Byrnes, G., additional, Abnet, C. C., additional, Dawsey, S. M., additional, Day, N. E., additional, Pharoah, P. D., additional, Boffetta, P., additional, Brennan, P., additional, and Kamangar, F., additional

Published
2012
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45. Alcohol intake and risk of oesophageal adenocarcinoma: a pooled analysis from the BEACON Consortium

Author

Freedman, N. D., primary, Murray, L. J., additional, Kamangar, F., additional, Abnet, C. C., additional, Cook, M. B., additional, Nyren, O., additional, Ye, W., additional, Wu, A. H., additional, Bernstein, L., additional, Brown, L. M., additional, Ward, M. H., additional, Pandeya, N., additional, Green, A. C., additional, Casson, A. G., additional, Giffen, C., additional, Risch, H. A., additional, Gammon, M. D., additional, Chow, W.-H., additional, Vaughan, T. L., additional, Corley, D. A., additional, and Whiteman, D. C., additional

Published
2011
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49. Circulating 25-Hydroxyvitamin D and Risk of Esophageal and Gastric Cancer: Cohort Consortium Vitamin D Pooling Project of Rarer Cancers

Author

Abnet, C. C., primary, Chen, Y., additional, Chow, W.-H., additional, Gao, Y.-T., additional, Helzlsouer, K. J., additional, Le Marchand, L., additional, McCullough, M. L., additional, Shikany, J. M., additional, Virtamo, J., additional, Weinstein, S. J., additional, Xiang, Y.-B., additional, Yu, K., additional, Zheng, W., additional, Albanes, D., additional, Arslan, A. A., additional, Campbell, D. S., additional, Campbell, P. T., additional, Hayes, R. B., additional, Horst, R. L., additional, Kolonel, L. N., additional, Nomura, A. M. Y., additional, Purdue, M. P., additional, Snyder, K., additional, and Shu, X.-O., additional

Published
2010
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50. Circulating 25-Hydroxyvitamin D and the Risk of Rarer Cancers: Design and Methods of the Cohort Consortium Vitamin D Pooling Project of Rarer Cancers

Author

Gallicchio, L., primary, Helzlsouer, K. J., additional, Chow, W.-H., additional, Freedman, D. M., additional, Hankinson, S. E., additional, Hartge, P., additional, Hartmuller, V., additional, Harvey, C., additional, Hayes, R. B., additional, Horst, R. L., additional, Koenig, K. L., additional, Kolonel, L. N., additional, Laden, F., additional, McCullough, M. L., additional, Parisi, D., additional, Purdue, M. P., additional, Shu, X.-O., additional, Snyder, K., additional, Stolzenberg-Solomon, R. Z., additional, Tworoger, S. S., additional, Varanasi, A., additional, Virtamo, J., additional, Wilkens, L. R., additional, Xiang, Y.-B., additional, Yu, K., additional, Zeleniuch-Jacquotte, A., additional, Zheng, W., additional, Abnet, C. C., additional, Albanes, D., additional, Bertrand, K., additional, and Weinstein, S. J., additional

Published
2010
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