Publications by authors named "Gwen Murphy"

71 Publications

A population-based investigation of the association between alcohol intake and serum total ghrelin concentrations among cigarette-smoking, non-alcohol-dependent male individuals.

Drug Alcohol Depend 2021 09 24;226:108835. Epub 2021 Jun 24.

Clinical Psychoneuroendocrinology and Neuropsychopharmacology Section, Translational Addiction Medicine Branch, National Institute on Drug Abuse Intramural Research Program and National Institute on Alcohol Abuse and Alcoholism Division of Intramural Clinical and Biological Research, National Institutes of Health, Baltimore and Bethesda, MD, United States; Medication Development Program, National Institute on Drug Abuse Intramural Research Program, National Institutes of Health, Baltimore, MD, United States; Center for Alcohol and Addiction Studies, Department of Behavioral and Social Sciences, School of Public Health, Brown University, Providence, RI, United States; Division of Addiction Medicine, Department of Medicine, School of Medicine, Johns Hopkins University, Baltimore, MD, United States; Department of Neuroscience, Georgetown University Medical Center, Washington DC, United States. Electronic address:

Background: Ghrelin plays significant roles in regulating appetite, food intake, and metabolism. Furthermore, the ghrelin system is increasingly being studied in relation to alcohol seeking behaviors. To this end, it is important to understand the possible effects of alcohol intake on the ghrelin system. The aim of the present study was to investigate the association between alcohol drinking and circulating ghrelin levels in a large sample of cigarette-smoking, non-alcohol-dependent male individuals.

Methods: We utilized data from two nested case-control studies (study A, n = 807; study B, n = 976) based within the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) trial. Data on alcohol consumption (grams of pure alcohol consumed per day) were obtained via a food frequency questionnaire. Blood samples were also collected (after 12 h of fasting), and serum concentrations of total ghrelin were measured by radioimmunoassay.

Results: Dichotomous comparison between alcohol drinkers (>0 g/day of alcohol intake) and non-drinkers (0 g/day of alcohol intake) found higher total ghrelin levels among individuals who drank alcohol than those who did not, with statistically significant results in study A [F (1, 798) = 4.32, P = 0.03] and less robust results in study B [F (1, 966) = 2.62, P = 0.10], controlling for a list of factors that may influence ghrelin levels and/or differ between drinkers and non-drinkers. Bivariate correlational analysis among drinkers found no association between the quantity of daily alcohol intake and blood total ghrelin concentrations.

Conclusion: These results indicate elevated ghrelin levels among alcohol drinkers and provide additional/relevant information on the complex interaction between alcohol use and the ghrelin system.
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http://dx.doi.org/10.1016/j.drugalcdep.2021.108835DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8355123PMC
September 2021

Indoor wood combustion, carcinogenic exposure and esophageal cancer in southwest Kenya.

Environ Int 2021 07 6;152:106485. Epub 2021 Mar 6.

Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.

Background: Exposure to polycyclic aromatic hydrocarbons (PAHs) is a risk factor for esophageal squamous cell carcinoma (ESCC) in high-incidence areas of China, Iran and Brazil, but PAH assessments have not been conducted in East Africa, another ESCC hot spot.

Objective: To evaluate demographic or lifestyle factors associated with the PAH biomarker concentrations in the study population, and whether PAH metabolite concentrations showed any associations with esophageal precancerous lesions.

Methods: We recruited a community-based sample of 289 asymptomatic adults from a rural area of Kenya and performed Lugol's chromoendoscopy to detect esophageal squamous dysplasia (ESD); participants completed a questionnaire and provided a spot urine specimen. We analyzed urine for seven hydroxylated metabolites of naphthalene, fluorene, phenanthrene, and pyrene at the U.S. National Center for Environmental Health, and compared creatinine-corrected PAH metabolite concentrations with questionnaire data and the presence of ESD.

Results: PAH metabolite concentrations among never tobacco users in these rural Kenya residents were 2.4-28.1 times higher than those reported from never tobacco users in Iran, Brazil and the USA. Female sex, cooking indoors, having no post-primary education, and age <50, but not tobacco use, were positively and significantly associated with PAH metabolite concentrations. Almost all participants used wood as cooking fuel. Nine participants had advanced ESD. Adjusted logistic regression showed a significant association between 2-hydroxynaphthalene (OR = 4.19, 95%CI: 1.01-17.47) and advanced ESD. All other PAH metabolites had positive but non-significant associations with advanced ESD.

Conclusions: Urinary PAH metabolite concentrations among never tobacco users are markedly higher in this group from Kenya than in other populations and are associated with indoor cooking with wood on open, unvented stoves. These metabolite concentrations were also associated with the presence of advanced esophageal dysplasia. Our findings underline the importance of assessing alternative cooking conditions to reduce PAH exposure in this population.
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http://dx.doi.org/10.1016/j.envint.2021.106485DOI Listing
July 2021

Association Between Serological Responses to Two Zoonotic Ruminant Pathogens and Esophageal Squamous Cell Carcinoma.

Vector Borne Zoonotic Dis 2021 Feb 29;21(2):125-127. Epub 2020 Oct 29.

Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland, USA.

Questionnaire data have linked contact with ruminants to the risk of esophageal squamous cell carcinoma (ESCC) in high-risk Asian populations. To better understand this observed association, we investigated exposure to two major zoonotic ruminant pathogens relative to ESCC risk. Using enzyme-linked immunosorbent assay, immunofluorescence assay, and microagglutination test assays, we measured immunoglobulin G anti- and anti- spp. antibodies in patients with ESCC ( = 177) and population-based controls ( = 177) matched by age, gender, and residence area from the Golestan case-control study in Iran. We found a similarly high seroprevalence of in ESCC cases and controls (75% and 80%, respectively), and a similarly low seroprevalence of spp. (0% and 0.6%, respectively). While documenting a high exposure to one of two zoonotic ruminant infections, this exposure failed to explain the observed association of ruminant contact and ESCC risk in this high-risk population.
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http://dx.doi.org/10.1089/vbz.2020.2668DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7876355PMC
February 2021

Seropositivity for Helicobacter pylori and hepatobiliary cancers in the PLCO study.

Br J Cancer 2020 09 29;123(6):909-911. Epub 2020 Jun 29.

Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.

Helicobacter has been suggested to play a possible role in hepatitis, gallstones, and hepatobiliary tumours. We assessed whether seropositivity to 15 H. pylori proteins was associated with subsequent incidence of 74 biliary tract and 105 liver cancer cases vs. 357 matched controls in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial (PLCO). Odds ratios and 95% confidence intervals were computed by conditional logistic regression after adjustment for known hepatobiliary cancer risk factors. H. pylori seropositivity was not associated with either biliary tract (1.76, 0.90-3.46) or liver cancer (0.87, 0.46-1.65). CagA seropositivity was associated with both endpoints, although the latter association was not statistically significant (biliary tract: 2.16, 1.03-4.50; liver cancer: 1.96, 0.98-3.93) and neither association was statistically significant after correcting for multiple comparisons. Together, these results suggest possible associations between H. pylori and hepatobiliary cancer and suggest the value of future studies investigating the association.Trial registration number: NCT00339495.
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http://dx.doi.org/10.1038/s41416-020-0961-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7493958PMC
September 2020

Opiate and Tobacco Use and Exposure to Carcinogens and Toxicants in the Golestan Cohort Study.

Cancer Epidemiol Biomarkers Prev 2020 03 8;29(3):650-658. Epub 2020 Jan 8.

Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland.

Background: There is little information on human exposure to carcinogens and other toxicants related to opiate use, alone or in combination with tobacco.

Methods: Among male participants of the Golestan Cohort Study in Northeast Iran, we studied 28 never users of either opiates or tobacco, 33 exclusive cigarette smokers, 23 exclusive users of smoked opiates, and 30 opiate users who also smoked cigarettes (dual users; 21 smoked opiates and 9 ingested them). We quantified urinary concentrations of 39 exposure biomarkers, including tobacco alkaloids, tobacco-specific nitrosamines, polycyclic aromatic hydrocarbons (PAH), and volatile organic compounds (VOC), and used decomposition to parse out the share of the biomarker concentrations explained by opiate use and nicotine dose.

Results: Dual users had the highest concentrations of all biomarkers, but exclusive cigarette smokers and exclusive opiate users had substantially higher concentrations of PAH and VOC biomarkers than never users of either product. Decomposition analysis showed that opiate use contributed a larger part of the PAH concentrations than nicotine dose, and the sum of 2- and 3-hydroxyphenanthrene (∑-phe) resulted almost completely from opiate use. Concentrations of most VOC biomarkers were explained by both nicotine dose and opiate use. Two acrylamide metabolites, a 1,3-butadiene metabolite and a dimethylformamide metabolite, were more strongly explained by opiate use. Acrylamide metabolites and ∑-phe were significantly higher in opiate smokers than opiate eaters; other biomarkers did not vary by the route of opiate intake.

Conclusions: Both cigarette smokers and opiate users (by smoking or ingestion) were exposed to many toxicants and carcinogens.

Impact: This high exposure, particularly among dual opiate and cigarette users, can have a substantial global public health impact.
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http://dx.doi.org/10.1158/1055-9965.EPI-19-1212DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7839071PMC
March 2020

The U-shaped association between body mass index and gastric cancer risk in the Helicobacter pylori Biomarker Cohort Consortium: A nested case-control study from eight East Asian cohort studies.

Int J Cancer 2020 08 12;147(3):777-784. Epub 2019 Dec 12.

Cancer Control and Population Sciences Program, Duke Cancer Institute, Durham, NC.

The association between body mass index (BMI) and noncardia gastric cancer (NCGC) risk remains controversial. The purpose of our study was to examine the association of BMI with NCGC risk with consideration of Helicobacter pylori (HP) biomarkers. This international nested case-control study, composed of 1,591 incident NCGC cases and 1,953 matched controls, was established from eight cohorts in China, Japan and Korea, where the majority of NCGCs are diagnosed worldwide. HP antibody biomarkers were measured in blood collected at cohort enrollment by multiplex serology. The NCGC risk according to baseline BMI was estimated using logistic regression to produce odds ratios (ORs) and 95% confidence intervals (CIs). We found a U-shaped association between BMI category and NCGC risk. Compared to those with reference BMI (22.6-25.0 kg/m ), those with lower and higher BMI had an increased NCGC risk (BMI <18.5 kg/m , OR = 1.56, 95% CI = 1.04-2.34; BMI >27.5 kg/m , OR = 1.48, 95% CI = 1.15-1.91; adjusted for age, sex and smoking). The U-shaped association was persistent among subjects with HP infection and high-risk biomarkers (HP+ CagA+: BMI <18.5 kg/m , OR = 1.60, 95% CI = 1.00-2.55; BMI >27.5 kg/m , OR = 1.59, 95% CI = 1.21-2.11; and Omp+ HP0305+: BMI <18.5 kg/m , OR = 1.88, 95% CI = 1.04-3.42; BMI >27.5 kg/m , OR = 1.70, 95% CI = 1.20-2.42, respectively). Our study provides evidence of significantly increased NCGC risk among individuals with low or high BMI, including in subjects with high-risk HP biomarkers (HP+ CagA+, Omp+ HP0305+) in the high-risk area of East Asia.
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http://dx.doi.org/10.1002/ijc.32790DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7234914PMC
August 2020

Serologic Profile of Antiparietal Cell Antibodies, Pepsinogens, and and Risk of Upper Gastrointestinal Cancer: A Nested Case-Control Study in China.

Cancer Epidemiol Biomarkers Prev 2019 12 9;28(12):2022-2029. Epub 2019 Sep 9.

Metabolic Epidemiology Branch, Division of Cancer Epidemiology & Genetics, National Cancer Institute, National Institutes of Health, Rockville, Maryland.

Background: Autoimmune gastritis is understudied and possibly associated with gastric noncardia adenocarcinoma (GNCA) and esophageal squamous cell carcinoma (ESCC) in Western populations when it presents as pernicious anemia.

Methods: A nested case-control study within a Chinese cohort included 100 ESCC, 200 gastric cardia adenocarcinoma (GCA), and 200 GNCA cases diagnosed between 1986 and 2001 and 400 controls. Serostatus of antiparietal cell antibodies (APCA), antibodies, and pepsinogens were measured using commercial kits and serum collected at baseline. We used logistic regression to calculate odds ratios (OR) and 95% confidence interval (CI) for associations between serologic biomarkers and cancer risk adjusted for numerous potential confounders.

Results: There was an average interval of 8 years between baseline blood draw and cancer diagnosis. The baseline prevalence of APCA seropositivity was 10.0% and 14.5% in subjects who developed GCA and GNCA, respectively. APCA seropositivity was inversely associated with later development of GCA (OR = 0.42; 95% CI, 0.24-0.75), but not significantly associated with later development of GNCA (OR = 0.82; 95% CI, 0.50-1.36) or ESCC (OR = 1.05; 95% CI, 0.58-1.88). APCA seropositivity was significantly associated with low pepsinogen I/II ratios (OR = 3.69; 95% CI, 1.66-8.21), and individuals with low pepsinogen I/II ratios who were seronegative for APCA had the highest risk of both GCA and GNCA.

Conclusions: APCA seropositivity measured years prior to diagnosis was associated with prevalent atrophic gastritis but inversely associated with incident GCA in this Chinese population.

Impact: APCA may contribute to a growing list of serologic markers that can improve risk stratification for gastric cancer.
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http://dx.doi.org/10.1158/1055-9965.EPI-19-0512DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6891191PMC
December 2019

Serum ghrelin and esophageal and gastric cancer in two cohorts in China.

Int J Cancer 2020 05 12;146(10):2728-2735. Epub 2019 Aug 12.

Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD.

Ghrelin is a hormone produced in the oxyntic glands of the stomach. Previous work by our group has suggested that serum ghrelin concentrations are inversely associated with gastric and esophageal cancer risk. We measured ghrelin concentrations in the Linxian General Population Nutrition Intervention Trial (NIT), and the Shanghai Women's Health Study (SWHS). In NIT, we analyzed serum samples from 298 esophageal squamous cell carcinoma (ESCC) cases, 518 gastric cardia adenocarcinoma (GCA) cases, 258 gastric noncardia adenocarcinoma (GNCA) cases and 770 subcohort controls (case-cohort). In SWHS, we measured ghrelin in plasma samples from 249 GNCA cases and 498 matched controls (nested case-control). Ghrelin was measured using radioimmunoassay. In NIT and SWHS, low ghrelin concentrations were associated with an increased risk of developing GNCA and GCA. The hazard ratio (HR ) for GNCA in NIT was 1.35 (95% CI: 0.89-2.05; p-trend = 0.02); the odds ratio in SWHS was 1.66 (95% CI: 1.02-2.70; p-trend = 0.06). Low ghrelin was associated with a twofold increase of GCA (HR = 2.00, 95% CI: 1.45-2.77; p-trend<0.001). In contrast, a lower risk of ESCC (NIT ESCC HR = 0.65, 95% CI: 0.45-0.92; p-trend = 0.02) was found in NIT. Low baseline ghrelin concentrations were associated with an increased risk for GNCA and GCA in the NIT and the SWHS. In contrast, low ghrelin concentrations at baseline were associated with a reduced risk of developing ESCC in the NIT. Ghrelin may be an early marker of future cancer risk for developing upper gastrointestinal cancer in regions of high incidence.
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http://dx.doi.org/10.1002/ijc.32597DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7477842PMC
May 2020

Nut and Peanut Butter Consumption and Mortality in the National Institutes of Health-AARP Diet and Health Study.

Nutrients 2019 Jul 2;11(7). Epub 2019 Jul 2.

Metabolic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD 20850, USA.

Although previous studies have shown inverse associations between nut consumption and mortality, the associations between nut consumption and less common causes of mortality have not been investigated. Additionally, about 50% of peanut consumption in the US is through peanut butter but the association between peanut butter consumption and mortality has not been thoroughly evaluated. The National Institutes of Health-AARP (NIH-AARP) Diet and Health Study recruited 566,398 individuals aged 50-71 at baseline in 1995-1996. A food-frequency questionnaire was used to evaluate nut and peanut butter consumption. Cox proportional hazard models were used to estimate hazard ratios and 95% confidence intervals for mortality using the non-consumers as reference groups and three categories of consumption. After excluding subjects with chronic diseases at baseline, there were 64,464 deaths with a median follow-up time of 15.5 years. We observed a significant inverse association between nut consumption and overall mortality (HR = 0.78, 95% CI = 0.76, 0.81, ≤ 0.001). Nut consumption was significantly associated with reduced risk of cancer, cardiovascular, respiratory, infectious, renal and liver disease mortality but not with diabetes or Alzheimer's disease mortality. We observed no significant associations between peanut butter consumption and all-cause (HR = 1.00, 95% CI = 0.98, 1.04, = 0.001) and cause-specific mortality. In a middle-aged US population, nut intake was inversely associated with all-cause mortality and certain types of cause-specific mortality. However, peanut butter consumption was not associated with differential mortality.
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http://dx.doi.org/10.3390/nu11071508DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6682967PMC
July 2019

Potato consumption and the risk of overall and cause specific mortality in the NIH-AARP study.

PLoS One 2019 7;14(5):e0216348. Epub 2019 May 7.

Metabolic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, United States of America.

Background: Potato consumption has been hypothesized to be associated with higher risk of hypertension, diabetes, and colorectal cancer.

Objective: The aim of this study was to examine the association between potato consumption and the risk of overall and cause specific mortality in the large prospective National Institutes of Health-AARP (NIH-AARP) Study.

Design: The NIH-AARP study recruited 566,407 persons, aged 50-72 years in 1995-1996. We excluded subjects that reported a history of chronic disease at baseline. Potato consumption data from a validated food frequency questionnaire completed at baseline was used in Cox proportional hazard models to estimate hazard ratios (HR) and 95% confidence intervals (95% CI) for overall and cause specific mortality. Final models were adjusted for potential risk factors for mortality.

Results: Among 410,701 participants included in this analysis, 76,921 persons died during the 15.6 years of follow-up. Eating baked, boiled, or mashed potatoes, French fries or potato salad seven or more times per week was associated with higher risk of overall mortality, in models adjusted only for age and sex (HR C4 vs C1 = 1.17, 95%CI = 1.13, 1.21). These results were attenuated in fully adjusted models (HR C4 vs C1 = 1.02, 95%CI = 0.97, 1.06). Potato consumption was not associated with risk of mortality caused by cancer (HR C4 vs C1 = 1.04, 95%CI = 0.97, 1.11), heart disease (HR C4 vs C1 = 1.00, 95%CI = 0.93, 1.09), respiratory disease (HR C4 vs C1 = 1.16, 95%CI = 0.99, 1.37), or diabetes (HR C4 vs C1 = 0.91, 95%CI = 0.71, 1.19). We tested for an association with different preparation methods and found limited evidence for differences by preparation method. The only statistically significant association was that for French fry consumption with cancer-related mortality (HR C4 vs C1 = 1.27, 95%CI = 1.02, 1.59), a finding for which uncontrolled confounding could not be ruled out.

Conclusion: We find little evidence that potato consumption is associated with all-cause or cause-specific mortality.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0216348PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6504095PMC
January 2020

Coffee and tea drinking and risk of cancer of the urinary tract in male smokers.

Ann Epidemiol 2019 06 3;34:33-39. Epub 2019 Apr 3.

Metabolic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD.

Purpose: We evaluated the association of coffee and tea drinking with risk of the urinary tract cancer in Finnish men, with high coffee consumption, using data from the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study.

Methods: The ATBC trial conducted from 1985 to 1993 enrolled 29,133 male smokers. We used Cox proportional hazards regression models to estimate hazard ratios (HRs) and confidence intervals (CIs), using men who drank more than 0 but less than 1 cup coffee/d and tea nondrinkers as our referent group for coffee and tea analyses, respectively.

Results: During 472,402 person-years of follow-up, 835 incident cases of bladder cancer and 366 cases of renal cell carcinoma were ascertained. For bladder cancer, we observed no association for coffee consumption (HR ≥4 vs. >0 to <1 cups/d = 1.16, 95% CI = 0.86-1.56) and a borderline statistically significant inverse association for tea consumption (HR ≥1 vs. 0 cup/d = 0.77, 95% CI = 0.58-1.00). For renal cell carcinoma, we observed no association for coffee (HR ≥4 vs. >0 to <1 cups/d = 0.85, 95% CI = 0.55-1.32) or tea consumption (HR ≥1 vs. 0 cup/d = 1.00, 95% CI = 0.68-1.46). We found no impact of coffee preparation on coffee-cancer associations.

Conclusions: Coffee drinking was not associated with urinary tract cancers risk. Further research on tea and bladder cancer is warranted.
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http://dx.doi.org/10.1016/j.annepidem.2019.03.014DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6684125PMC
June 2019

Investigating tea temperature and content as risk factors for esophageal cancer in an endemic region of Western Kenya: Validation of a questionnaire and analysis of polycyclic aromatic hydrocarbon content.

Cancer Epidemiol 2019 06 26;60:60-66. Epub 2019 Mar 26.

Departments of Surgery and Endoscopy, Tenwek Hospital, Bomet, Kenya; Department of Surgery, Alpert Medical School of Brown University, Providence, RI, USA.

Background: Esophageal squamous cell carcinoma (ESCC) is common in certain areas worldwide. One area, western Kenya, has a high risk of ESCC, including many young cases (<30 years old), but has limited prior study of potential risk factors. Thermal injury from hot food and beverages and exposure to polycyclic aromatic hydrocarbons (PAHs) have been proposed as important risk factors for ESCC in other settings. The beverage of choice in western Kenya is milky tea (chai).

Methods: Healthy individuals >18 years of age who were accompanying relatives to an endoscopy unit were recruited to participate. The preferred initial temperature of chai consumption in these adults was measured by questionnaire and digital thermometer. Comparisons of these results were assessed by kappa statistics. Concentrations of 26 selected PAHs were determined by gas chromatography/mass spectrometry in samples of 11 brands of commercial tea leaves commonly consumed in Kenya.

Results: Kappa values demonstrated moderate agreement between questionnaire responses and measured temperatures. The mean preferred chai temperatures were 72.1 °C overall, 72.6 °C in men (n = 78), and 70.2 °C in women (n = 22; p < 0.05). Chai temperature did not significantly differ by age or ethnic group. The PAH levels in the commercial Kenyan tea leaves were uniformly low (total PAH < 300 ng/g of leaves).

Conclusions: Study participants drink chai at higher temperatures than previously reported in other high-risk ESCC regions. Chai is not, however, a source of significant PAH exposure. Very hot chai consumption should be further evaluated as a risk factor for ESCC in Kenya with the proposed questionnaire.
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http://dx.doi.org/10.1016/j.canep.2019.03.010DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6559237PMC
June 2019

The application of six dietary scores to a Middle Eastern population: a comparative analysis of mortality in a prospective study.

Eur J Epidemiol 2019 Apr 18;34(4):371-382. Epub 2019 Mar 18.

Digestive Oncology Research Center, Digestive Diseases Research Institute, Tehran University of Medical Sciences, Tehran, Iran.

Background The associations between dietary indices and mortality have not been evaluated in populations from the Middle East, which have different dietary patterns compared to the US and Europe. In this study, we evaluated the association between six dietary indices and mortality in the Golestan Cohort Study (GCS) in Iran, which is the largest prospective study in the Middle East with 50,045 participants. Methods The six dietary indices, namely the Healthy Eating Index (HEI-2015), Alternative Healthy Eating Index (AHEI-2010), Alternative Mediterranean Diet (AMED), Dietary Approach to Stop Hypertension created by Fung (DASH-Fung) and Mellen (DASH-Mellen), and the World Cancer Research Fund (WCRF/AICR) index, were applied to data from a food frequency questionnaire, computed and divided into quintiles. Adjusted Cox models were used to estimate hazards ratio (HR) and 95% confidence intervals (CI) for overall and cause-specific mortality, using the lowest quintile as a reference group. Results Among 42,373 participants included in the current analyses, 4424 subjects died during 10.6 years of follow-up. Participants with the highest quintile dietary scores, compared with the lowest quintile dietary scores, had significantly decreased overall mortality in the AHEI-2010, AMED, DASH-Fung, and WCRF/AICR indices (HR 0.88, 95% CI = 0.80-0.97; 0.80, 0.70-0.91; 0.77, 0.70-0.86; and 0.79, 0.70-0.90, respectively). A reduced cardiovascular mortality was found for high AHEI-2010 and DASH-Fung scores (17% and 23%, respectively), and a reduced cancer mortality for high HEI-2015, AMED, and DASH-Fung scores (21, 37 and 25%, respectively). Conclusion Various indices of dietary quality are inversely associated with overall mortality, and selectively with cancer and cardiovascular mortality in the GCS, which contribute to the generalizability and validity of dietary guidelines.
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http://dx.doi.org/10.1007/s10654-019-00508-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6707799PMC
April 2019

Urinary Biomarkers of Carcinogenic Exposure among Cigarette, Waterpipe, and Smokeless Tobacco Users and Never Users of Tobacco in the Golestan Cohort Study.

Cancer Epidemiol Biomarkers Prev 2019 02 8;28(2):337-347. Epub 2019 Jan 8.

Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, Maryland.

Background: How carcinogen exposure varies across users of different, particularly noncigarette, tobacco products remains poorly understood.

Methods: We randomly selected 165 participants of the Golestan Cohort Study from northeastern Iran: 60 never users of any tobacco, 35 exclusive cigarette, 40 exclusive (78% daily) waterpipe, and 30 exclusive smokeless tobacco (nass) users. We measured concentrations of 39 biomarkers of exposure in 4 chemical classes in baseline urine samples: tobacco alkaloids, tobacco-specific nitrosamines (TSNA), polycyclic aromatic hydrocarbons (PAH), and volatile organic compounds (VOC). We also quantified the same biomarkers in a second urine sample, obtained 5 years later, among continuing cigarette smokers and never tobacco users.

Results: Nass users had the highest concentrations of tobacco alkaloids. All tobacco users had elevated TSNA concentrations, which correlated with nicotine dose. In both cigarette and waterpipe smokers, PAH and VOC biomarkers were higher than never tobacco users and nass users, and highly correlated with nicotine dose. PAH biomarkers of phenanthrene and pyrene and two VOC metabolites (phenylmercapturic acid and phenylglyoxylic acid) were higher in waterpipe smokers than in all other groups. PAH biomarkers among Golestan never tobacco users were comparable to those in U.S. cigarette smokers. All biomarkers had moderate to good correlations over 5 years, particularly in continuing cigarette smokers.

Conclusions: We observed two patterns of exposure biomarkers that differentiated the use of the combustible products (cigarettes and waterpipe) from the smokeless product. Environmental exposure from nontobacco sources appeared to contribute to the presence of high levels of PAH metabolites in the Golestan Cohort.

Impact: Most of these biomarkers would be useful for exposure assessment in a longitudinal study.
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http://dx.doi.org/10.1158/1055-9965.EPI-18-0743DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6935158PMC
February 2019

The African Esophageal Cancer Consortium: A Call to Action.

J Glob Oncol 2018 09;4:1-9

Katherine Van Loon, University of California, San Francisco, San Francisco, CA; Michael M. Mwachiro, Stephen L. Burgert, and Russell E. White, Tenwek Hospital, Bomet; Diana Menya, Moi University, Eldoret, Kenya; Christian C. Abnet, Gwen Murphy, Natalie Pritchett, and Sanford M. Dawsey, National Cancer Institute, Bethesda, MD; Larry Akoko, Elia Mmbaga, Beatrice Mushi, and Ally Mwanga, Muhimbili University of Health and Allied Sciences, Dar es Salaam; Blandina T. Mmbaga and Amos Mwasamwaja, Kilimanjaro Clinical Research Institute, Moshi, Tanzania; Mathewos Assefa, Addis Ababa University, Addis Ababa, Ethiopia; Steady Chasimpha and Charles Dzamalala, Queen Elizabeth Central Hospital; Charles Dzamalala, Satish Gopal, Bongani Kaimila, and Yohannie Mlombe, University of Malawi College of Medicine, Blantyre; Gift Mulima, Kamuzu Central Hospital, Lilongwe, Malawi; David E. Fleischer, Mayo Clinic, Phoenix, AZ; Satish Gopal, University of North Carolina, Chapel Hill, NC; Prasad G. Iyer and Mark D. Topazian, Mayo Clinic, Rochester, MN; Violet Kayamba and Paul Kelly, University of Zambia, Lusaka, Zambia; Paul Kelly, Queen Mary University of London; Christopher G. Mathew, King's College London, London, United Kingdom; Maria E. Leon, Daniel Middleton, Joachim Schüz, and Valerie McCormack, International Agency for Research on Cancer, Lyon, France; Christopher G. Mathew, University of the Witwatersrand, Johannesburg; and M. Iqbal Parker, University of Cape Town, Cape Town, South Africa.

Esophageal cancer is the eighth most common cancer worldwide and the sixth most common cause of cancer-related death; however, worldwide incidence and mortality rates do not reflect the geographic variations in the occurrence of this disease. In recent years, increased attention has been focused on the high incidence of esophageal squamous cell carcinoma (ESCC) throughout the eastern corridor of Africa, extending from Ethiopia to South Africa. Nascent investigations are underway at a number of sites throughout the region in an effort to improve our understanding of the etiology behind the high incidence of ESCC in this region. In 2017, these sites established the African Esophageal Cancer Consortium. Here, we summarize the priorities of this newly established consortium: to implement coordinated multisite investigations into etiology and identify targets for primary prevention; to address the impact of the clinical burden of ESCC via capacity building and shared resources in treatment and palliative care; and to heighten awareness of ESCC among physicians, at-risk populations, policy makers, and funding agencies.
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http://dx.doi.org/10.1200/JGO.17.00163DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6223465PMC
September 2018

Validation of a Blood Biomarker for Identification of Individuals at High Risk for Gastric Cancer.

Cancer Epidemiol Biomarkers Prev 2018 12 29;27(12):1472-1479. Epub 2018 Aug 29.

Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital and Institute, Beijing, China.

Background: is the leading cause of gastric cancer, yet the majority of infected individuals will not develop neoplasia. Previously, we developed and replicated serologic biomarkers for gastric cancer risk among prospective cohorts in East Asia and now seek to validate the performance of these biomarkers in identifying individuals with premalignant lesions.

Methods: This cross-sectional study included 1,402 individuals from Linqu County screened by upper endoscopy. protein-specific antibody levels were assessed using multiplex serology. Multivariable-adjusted logistic regression models were used to calculate odds ratios (ORs) and 95% confidence intervals (CIs) for prevalent intestinal metaplasia, indefinite dysplasia, or dysplasia, compared with superficial or mild atrophic gastritis.

Results: Compared with individuals seronegative to Omp and HP0305, individuals seropositive to both were seven times more likely to have precancerous lesions (OR, 7.43; 95% CI, 5.59-9.88). A classification model for precancerous lesions that includes age, smoking, and seropositivity to , Omp, and HP0305 resulted in an area under the curve (AUC) of 0.751 (95% CI, 0.725-0.777), which is significantly better than the same model, including the established gastric cancer risk factor CagA (AUC, 0.718; 95% CI, 0.691-0.746, = 0.0002).

Conclusions: The present study of prevalent precancerous gastric lesions provides support for two new serum biomarkers of gastric cancer risk, Omp and HP 0305.

Impact: Our results support further research into the serological biomarkers Omp and HP0305 as possible improvements over the established virulence marker CagA for identifying individuals with precancerous lesions in East Asia.
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http://dx.doi.org/10.1158/1055-9965.EPI-18-0582DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6279536PMC
December 2018

Nut consumption and the risk of oesophageal squamous cell carcinoma in the Golestan Cohort Study.

Br J Cancer 2018 07 28;119(2):176-181. Epub 2018 Jun 28.

Digestive Oncology Research Center, Digestive Diseases Research Institute, Tehran University of Medical Sciences, Tehran, Iran.

Background: Nut consumption has been inversely associated with gastric cancer incidence in US-based studies, but not with oesophageal cancer. However, there is aetiologic heterogeneity, among oesophageal squamous cell carcinoma (ESCC) cases in low-risk vs. high-risk populations. The objective of this study was to evaluate the association between nut consumption and risk of ESCC in a high-risk population.

Methods: The Golestan Cohort Study enroled 50,045 participants in Northeastern Iran, between 2004 and 2008. Intake of peanuts, walnuts and mixed nuts (including seeds) were assessed using a validated food frequency questionnaire at baseline. Cox proportional hazard models were used to estimate hazard ratios (HR) and 95% confidence intervals for subsequent ESCC adjusted for potential confounders. Non-consumers of nuts were used as the reference category and the consumers were categorised into tertiles.

Results: We accrued 280 incident ESCC cases during 337,983 person-years of follow up. Individuals in the highest tertiles of total nut consumption, and mixed nut consumption were significantly associated with lower risk of developing ESCC compared to non-consumers (HR = 0.60, 95% CI = 0.39-0.93, p-trend = 0.02, and HR = 0.52, 95% CI = 0.32-0.84, p trend = 0.002, respectively).

Conclusions: We found a statistically significant inverse association between total nut consumption and the risk of ESCC in this high-risk population.
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http://dx.doi.org/10.1038/s41416-018-0148-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6048068PMC
July 2018

Epstein-Barr Virus Antibody Titers Are Not Associated with Gastric Cancer Risk in East Asia.

Dig Dis Sci 2018 10 8;63(10):2765-2772. Epub 2018 Jun 8.

Division of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center and Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, TN, 37203, USA.

Background: Epstein-Barr virus (EBV)-positive gastric cancers represent a distinct subtype of gastric cancers and account for nearly 10% of the gastric cancer burden, yet risk detection strategies for this cancer subtype are lacking.

Methods: We conducted a nested case-control study where we assayed 4 EBV antigens [viral capsid antigen (VCA), early antigen (EA), Epstein-Barr nuclear antigen (EBNA), and BZLF1-encoded replication activator protein (ZEBRA)] in either sera or plasma from 1447 gastric cancer cases and 1797 controls obtained from seven prospective cohorts representing individuals from the high gastric cancer-risk countries of China, Japan, and Korea.

Results: The prevalence of EBV sero-positivity was universal with the exception of one sero-negative individual, and the highest titers of the EBV antigens VCA (OR 0.95, 95% CI 0.78-1.17), EBNA (OR 0.88, 95% CI 0.72-1.08), EA (OR 0.97, 95% CI 0.79-1.19), and ZEBRA (OR 0.87, 95% CI 0.71-1.07) were not associated with risk of incident gastric cancer. When we stratified these data by H. pylori status, there was no change in the association.

Conclusions: Multiplex serology of the aforementioned EBV antigens in serum may not be a suitable biomarker for predicting gastric cancer risk in East Asian populations.
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http://dx.doi.org/10.1007/s10620-018-5154-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6139270PMC
October 2018

Effects of Nutrition Intervention on Total and Cancer Mortality: 25-Year Post-trial Follow-up of the 5.25-Year Linxian Nutrition Intervention Trial.

J Natl Cancer Inst 2018 11;110(11):1229-1238

Metabolic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD.

Background: A beneficial effect of supplementation with selenium, vitamin E, and beta-carotene was observed on total and cancer mortality in a Chinese population, and it endured for 10 years postintervention, but longer durability is unknown.

Methods: A randomized, double-blind, placebo-controlled trial was conducted in Linxian, China, from 1986 to 1991; 29 584 residents age 40 to 69 years received daily supplementations based on a factorial design: Factors A (retinol/zinc), B (riboflavin/niacin), C (vitamin C/molybdenum), and/or D (selenium/vitamin E/beta-carotene), or placebo for 5.25 years, and followed for up 25 years. Hazard ratios (HRs) and 95% confidence intervals (CIs) for the intervention effects on mortalities were estimated using Cox proportional hazards models.

Results: Through 2016, the interventions showed no effect on total mortality. The previously reported protective effect of Factor D against total mortality was lost 10 years postintervention. The protective effect of Factor D for gastric cancer was attenuated (HR = 0.93, 95% CI = 0.85 to 1.01), but a newly apparent protective effect against esophageal cancer was found for Factor B (HR = 0.92, 95% CI = 0.85 to 1.00, two-sided P = .04). Other protective/adverse associations were observed for cause-specific mortalities. Protective effects were found in people younger than age 55 years at baseline against non-upper gastrointestinal cancer death for Factor A (HR = 0.80, 95% CI = 0.69 to 0.92) and against death from stroke for Factor C (HR = 0.89, 95% CI = 0.82 to 0.96). In contrast, increased risk of esophageal cancer was found when the intervention began after age 55 years for Factors C (HR = 1.16, 95% CI = 1.04 to 1.30) and D (HR = 1.20, 95% CI = 1.07 to 1.34).

Conclusions: Multiyear nutrition intervention is unlikely to have a meaningful effect on mortality more than a decade after supplementation ends, even in a nutritionally deprived population. Whether sustained or repeat intervention would provide longer effects needs further investigation.
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http://dx.doi.org/10.1093/jnci/djy043DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6235687PMC
November 2018

Family history of colorectal cancer in first-degree relatives and metachronous colorectal adenoma.

Am J Gastroenterol 2018 06 20;113(6):899-905. Epub 2018 Feb 20.

University of Arizona Cancer Center, Tucson, AZ, USA. Mel and Enid Zuckerman College of Public Health, University of Arizona, Tucson, AZ, USA. Veteran Affairs San Diego System, San Diego, CA, USA. Department of Internal Medicine, Division of Gastroenterology, and the Moores Cancer Center, University of California San Diego, La Jolla, CA, USA. Department of Medicine, University of North Carolina School of Medicine, Chapel Hill, NC, USA. Imperial College London, London, UK. Division of Gastroenterology and Hepatology, Veterans Affairs Medical Center and Oregon Health and Science University, Portland, OR, USA. Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. Department of Family Medicine and Public Health and Moores Cancer Center, University of California San Diego, La Jolla, CA, USA.

Objectives: Little is known about the relationship between having a first-degree relative (FDR) with colorectal cancer (CRC) and risk for metachronous colorectal adenoma (CRA) following polypectomy.

Methods: We pooled data from seven prospective studies of 7697 patients with previously resected CRAs to quantify the relationship between having a FDR with CRC and risk for metachronous adenoma.

Results: Compared with having no family history of CRC, a positive family history in any FDR was significantly associated with increased odds of developing any metachronous CRA (OR = 1.14; 95% CI = 1.01-1.29). Higher odds of CRA were observed among individuals with an affected mother (OR = 1.27; 95% CI = 1.05-1.53) or sibling (OR = 1.34; 95% CI = 1.11-1.62) as compared with those without, whereas no association was shown for individuals with an affected father. Odds of having a metachronous CRA increased with number of affected FDRs, with ORs (95% CIs) of 1.07 (0.93-1.23) for one relative and 1.39 (1.02-1.91) for two or more. Younger age of diagnosis of a sibling was associated with higher odds of metachronous CRA, with ORs (95% CIs) of 1.66 (1.08-2.56) for diagnosis at <54 years; 1.34 (0.89-2.03) for 55-64 years; and 1.10 (0.70-1.72) for >65 years (p-trend = 0.008). Although limited by sample size, results for advanced metachronous CRA were similar to those for any metachronous CRA.

Conclusions: A family history of CRC is related to a modestly increased odds of metachronous CRA. Future research should explore whether having a FDR with CRC, particularly at a young age, should have a role in risk stratification for surveillance colonoscopy.
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http://dx.doi.org/10.1038/s41395-018-0007-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8283793PMC
June 2018

Urinary Concentrations of Polycyclic Aromatic Hydrocarbon Metabolites in Drinkers in Rio Grande do Sul, Brazil.

Cancer Epidemiol Biomarkers Prev 2018 03 20;27(3):331-337. Epub 2017 Dec 20.

Programa de Pós Graduação Ciências em Gastroenterologia e Hepatologia, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.

Consumption of , an infusion of the herb , is associated with increased risk of esophageal squamous cell carcinoma (ESCC), but the carcinogenic mechanism is unclear. Commercial brands of contain high levels of carcinogenic polycyclic aromatic hydrocarbons (PAHs), which are acquired during the traditional drying process. The purpose of this study was to characterize exposure to PAHs in drinkers over a wide range of consumption. We recruited 244 adults who answered a questionnaire and collected a fasting spot urine specimen. We quantified urinary concentrations of seven PAH metabolites and assessed associations between self-reported recent consumption and urinary PAH metabolites by multivariate regression. Recent consumption showed a significant dose-response association with 6 of 7 PAH metabolites in unadjusted models ( < 0.05). After adjustment for creatinine and potential confounders, concentrations of 2-naphthol, 1-hydroxyphenanthrene, and the sum of 2- and 3-hydroxyphenanthrene remained significantly associated with recent intake. The sum of the urinary concentrations of the phenanthrene metabolites was similar or higher among drinkers who did not smoke than among smokers who did not drink Urinary concentrations of PAH metabolites were significantly associated with self-reported amounts of recent intake, and drinking increased urinary concentrations of some PAH metabolites as much as smoking cigarettes. Drinking is a source of exposure to potentially carcinogenic PAHs, consistent with the hypothesis that the PAH content of may contribute to the increased risk of ESCC in drinkers. .
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http://dx.doi.org/10.1158/1055-9965.EPI-17-0773DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5835188PMC
March 2018

Cross sectional study of serum selenium concentration and esophageal squamous dysplasia in western Kenya.

BMC Cancer 2017 12 8;17(1):835. Epub 2017 Dec 8.

Tenwek Hospital, Bomet, Kenya.

Background: Low serum selenium status has been associated with increased risk of esophageal squamous cell carcinoma (ESCC). East Africa is a region of high ESCC incidence and is known to have low soil selenium levels, but this association has not previously been evaluated. In this study we assessed the association of serum selenium concentration and the prevalence of esophageal squamous dysplasia (ESD), the precursor lesion of ESCC, in a cross-sectional study of subjects from Bomet, Kenya.

Methods: 294 asymptomatic adult residents of Bomet, Kenya completed questionnaires and underwent endoscopy with Lugol's iodine staining and biopsy for detection of ESD. Serum selenium concentrations were measured by instrumental neutron activation analysis. Odds ratios (OR) and confidence intervals (95% CI) for associations between serum selenium and ESD were calculated using unconditional logistic regression.

Results: The mean serum selenium concentration was 85.5 (±28.3) μg/L. Forty-two ESD cases were identified (14% of those screened), including 5 (12%) in selenium quartile 1 (Q1), 5 (12%) in Q2, 15 (36%) in Q3, and 17 (40%) in Q4. Higher serum selenium was associated with prevalence of ESD (Q4 vs Q1: OR: 3.03; 95% CI: 1.05-8.74) and this association remained after adjusting for potential confounders (Q4 vs Q1: OR: 3.87; 95% CI: 1.06-14.19).

Conclusion: This is the first study to evaluate the association of serum selenium concentration and esophageal squamous dysplasia in an African population at high risk for ESCC. We found a positive association between higher serum selenium concentration and prevalence of ESD, an association contrary to our original hypothesis. Further work is needed to better understand the role of selenium in the etiology of ESCC in this region, and to develop effective ESCC prevention and control strategies.
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http://dx.doi.org/10.1186/s12885-017-3837-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5721656PMC
December 2017

Toenail mineral concentration and risk of esophageal squamous cell carcinoma, results from the Golestan Cohort Study.

Cancer Med 2017 Dec 10;6(12):3052-3059. Epub 2017 Nov 10.

Metabolic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland.

Studies conducted in China linked selenium deficiency to higher risk of esophageal squamous cell carcinoma (ESCC), but this has not been widely tested outside that selenium-deficient region. The aim of this study was to investigate the association between selenium and other mineral concentrations in toenails and risk of ESCC in a region with high incidence rates. In this nested case-control study, we identified 222 cases of ESCC from the Golestan Cohort Study, Iran, which has followed up 50,045 participants since enrollment (2004-2008). We randomly selected one control for each case matched by age and sex, using incidence density sampling. We used toenail samples collected at baseline to measure the concentration of selenium, zinc, chromium, mercury, and scandium using instrumental neutron activation analysis. Multivariate adjusted logistic regression models were used to estimate odds ratios (OR) and 95% confidence intervals. Median nail selenium, zinc, chromium, and mercury levels were 1.01, 74.59, 0.77, and 0.018 μg/g in cases and 1.02, 75.71, 0.71, and 0.023 μg/g in controls, respectively. The adjusted odds ratios comparing each fourth quartile of mineral status versus the first quartile were as follows: selenium = 0.78 (95% CI, 0.41-1.49); zinc=0.80 (95% CI, 0.42-1.53); chromium = 0.91 (95% CI, 0.46-1.80); and mercury=0.61 (95% CI, 0.27-1.38), and all trend tests were non-significant. The nail selenium concentration in our controls reflects relatively high selenium status. No evidence of association between selenium or chromium concentrations in toenails and the risk of ESCC was detected in this population.
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http://dx.doi.org/10.1002/cam4.1247DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5727321PMC
December 2017

Serum ghrelin is associated with risk of colorectal adenocarcinomas in the ATBC study.

Gut 2018 09 16;67(9):1646-1651. Epub 2017 Aug 16.

Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.

Background: Colorectal cancers are the third most common cancers in women and men in the USA. While dietary and lifestyle factors such as Western diet, physical inactivity and obesity have been linked to an increased risk of this malignancy, the mechanisms for these associations are unclear. GI hormones, including ghrelin, are involved in energy balance by mediating appetite and metabolism; however, the association between ghrelin and colorectal cancer has not been studied.

Methods: We conducted a case-control study nested within the all-male Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study of Finnish smokers (aged 50-69 years) to examine serum ghrelin concentration and colorectal cancer risk. Data from 284 colon and 239 rectal cancers and 523 controls (matched on age, date of blood draw and serum availability) were analysed. ORs and 95% CIs were calculated using multivariable (conditional) logistic regression.

Results: Overall, low-serum ghrelin was significantly associated with increased risk of colorectal cancer (Q1 vs Q4: OR:1.57, 95% CI 1.05 to 2.34). For individuals developing tumours within 10 years of blood draw, those in the lowest quartile of serum ghrelin concentrations were statistically significantly more likely to develop colorectal cancers than those with higher serum ghrelin concentrations (OR: 10.86, 95% CI 5.01 to 23.55). However, for individuals with tumours developing more than 20 years after blood draw, low-serum ghrelin concentrations were associated with a decreased risk of colorectal cancer relative to those with the highest serum ghrelin concentrations (OR: 0.26, 95% CI 0.11 to 0.64).

Conclusion: Low-serum ghrelin was associated with an increased colorectal cancer risk within 10 years of blood draw with a decreased risk for developing colorectal cancer more than 20 years after blood draw. These results suggest that ghrelin concentrations may vary across the carcinogenic process.
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http://dx.doi.org/10.1136/gutjnl-2016-313157DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5815951PMC
September 2018

Nut and peanut butter consumption and the risk of esophageal and gastric cancer subtypes.

Am J Clin Nutr 2017 Sep 2;106(3):858-864. Epub 2017 Aug 2.

Metabolic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD;

Nut consumption has been associated with decreased risk of colorectal, endometrial, lung, and pancreatic cancers. Polyphenols, fiber, vitamins, and minerals in nuts may confer this observed protective effect. To our knowledge, no prospective study has evaluated the effect of nut consumption on esophageal and gastric cancers. The objective was to evaluate the associations between nut and peanut butter consumption and the risk of esophageal and gastric cancers and their different subtypes. In this study we used data from the NIH-AARP Diet and Health Study, which enrolled 566,407 persons who were 50-71 y old at baseline (1995-1996). The median follow-up time was 15.5 y. Intakes of nuts and peanut butter were assessed through the use of a validated food-frequency questionnaire. We used Cox proportional hazard models to estimate HRs and 95% CIs for esophageal and gastric cancers and their subtypes. We identified 966 incident cases of esophageal adenocarcinomas, 323 cases of esophageal squamous cell carcinoma, 698 cases of gastric cardia adenocarcinoma, and 732 cases of gastric noncardia adenocarcinoma. Compared with those who did not consume nuts or peanut butter [lowest category of consumption (C0)], participants in the highest category of nut consumption (C3) had a lower risk of developing gastric noncardia adenocarcinoma [C3 compared with C0, HR: 0.73 (95% CI: 0.57, 0.94)]. This inverse association was also seen for peanut butter consumption [C3 compared with C0, HR: 0.75 (95% CI: 0.60, 0.94)]. We observed no significant associations between the highest and lowest intakes of nuts or peanut butter and the risk of gastric cardia adenocarcinoma, esophageal adenocarcinoma, or esophageal squamous cell carcinoma. Among older American adults, both nut and peanut butter consumption were inversely associated with the risk of gastric noncardia adenocarcinoma. This trial was registered at clinicaltrials.gov as NCT00340015.
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http://dx.doi.org/10.3945/ajcn.117.159467DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5573026PMC
September 2017

Low vitamin B increases risk of gastric cancer: A prospective study of one-carbon metabolism nutrients and risk of upper gastrointestinal tract cancer.

Int J Cancer 2017 09 21;141(6):1120-1129. Epub 2017 Jun 21.

Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland.

Previous studies have found associations between one-carbon metabolism nutrients and risk of several cancers, but little is known regarding upper gastrointestinal tract (UGI) cancer. We analyzed prediagnostic serum concentrations of several one-carbon metabolism nutrients (vitamin B12, folate, vitamin B6, riboflavin and homocysteine) in a nested case-control study within the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study of male smokers, which was undertaken in Finland between 1985 and 1988. We conducted a nested case-control study including 127 noncardia gastric adenocarcinoma (NCGA), 41 esophagogastric junctional adenocarcinoma and 60 esophageal squamous cell carcinoma incident cases identified within ATBC. Controls were matched to cases on age, date of serum collection and follow-up time. One-carbon nutrient concentrations were measured in fasting serum samples collected at baseline (up to 17 years prior to cancer diagnosis). Odds ratios and 95% confidence intervals (CI) were calculated using conditional logistic regression. Lower prediagnostic vitamin B12 concentrations at baseline were associated with a 5.8-fold increased risk of NCGA (95% CI = 2.7-12.6 for lowest compared to highest quartile, p-trend <0.001). This association remained in participants who developed cancer more than 10 years after blood collection, and after restricting the analysis to participants with clinically normal serum vitamin B12 (>300 pmol/L). In contrast, pepsinogen I, a known serologic marker of gastric atrophy, was not associated with NCGA in this population. As vitamin B12 absorption requires intact gastric mucosa to produce acid and intrinsic factor, our findings suggest vitamin B12 as a possible serologic marker for the atrophic gastritis that precedes NCGA, one more strongly associated with subsequent NCGA than pepsinogen.
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http://dx.doi.org/10.1002/ijc.30809DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5550828PMC
September 2017

Tooth loss and liver cancer incidence in a Finnish cohort.

Cancer Causes Control 2017 Aug 22;28(8):899-904. Epub 2017 May 22.

Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, USA, 20892-9774.

Purpose: Periodontal disease, a major cause of tooth loss in adults, may have systemic effects and has been associated with higher risk of several cancer types. However, the associations of periodontal disease or tooth loss with liver cancer have only been examined prospectively in two studies, neither of which had sufficient statistical power. In addition, no studies assessed the potential confounding by viral hepatitis or Helicobacter pylori infection status.

Methods: In this study, we examined the association between tooth loss and primary liver cancer incidence in a prospective cohort of Finnish male smokers (n = 29,096). We used Cox proportional hazards models to calculate multivariable-adjusted hazard ratios (HRs) and 95% CIs. As a sensitivity analysis, we conducted a nested case-control study within the original cohort to assess confounding by hepatitis B or C virus infection and seropositivity of H. pylori.

Results: A total of 213 incident primary liver cancers occurred during a mean follow-up of 17 years. Among these cases, having 11-31 permanent teeth lost (HR 1.42, 95% CI 1.01-1.98) or all 32 teeth lost (HR 1.45, 95% CI 1.00-2.10) was each associated with higher risk of liver cancer, compared to those having 0-10 teeth lost. Adjusting for H. pylori seropositivity yielded a small attenuation of the effect estimate.

Conclusions: Greater number of teeth lost was associated with higher risk of primary liver cancer in our study. The role of periodontal infection in the development of liver cancer warrants further investigation.
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http://dx.doi.org/10.1007/s10552-017-0906-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5639923PMC
August 2017

Serum gastrin and cholecystokinin are associated with subsequent development of gastric cancer in a prospective cohort of Finnish smokers.

Int J Epidemiol 2017 06;46(3):914-923

Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, USA.

Background: Gastrin, which induces gastric acid secretion, and a structurally similar hormone, cholecystokinin (CCK)-a potent acid inhibitor, may each play a role in gastric cancer. However, few studies have investigated this hypothesis in humans. We therefore investigated whether serum gastrin or CCK concentrations at baseline were associated with the incidence of gastric non-cardia adenocarcinomas (GNCA), oesophagogastric junctional adenocarcinomas (EGJA) or gastric carcinoid tumours over 24 years of follow-up in a study nested within the all-male Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study of Finnish smokers.

Methods: Totals of 283 incident GNCA, 96 EGJA and 10 gastric carcinoid cases, and 778 matched controls, were included in our analysis. Gastrin and CCK were measured using specific radioimmunoassays. Odds ratios (OR) and 95% confidence intervals (95% CI) were estimated by multivariable logistic regression with adjustment for all known or suspected confounding factors, including Helicobacter pylori seropositivity.

Results: Those with high gastrin (Q4 vs Q1), had an increased risk of GNCA (fully adjusted OR: 1.92; 95% CI: 1.21, 3.05) and gastric carcinoids, though the small number of carcinoid cases meant the fully adjusted model was unstable (age-adjusted continuous model OR: 4.67; 95% CI: 2.67, 8.15). CCK was associated with risk of GNCA only for those in Q3 relative to Q1 (OR: 0.56; 95% CI: 0.33, 0.96), and no significant trend was observed.

Conclusions: Our data suggest that high serum concentrations of gastrin may be associated independently with an increased risk of gastric cancer; the role of CCK in cancer risk is less clear.
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http://dx.doi.org/10.1093/ije/dyx030DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5837256PMC
June 2017

Prospective study of serum B vitamins levels and oesophageal and gastric cancers in China.

Sci Rep 2016 10 17;6:35281. Epub 2016 Oct 17.

Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.

B vitamins play an essential role in DNA synthesis and methylation, and may protect against oesophageal and gastric cancers. In this case-cohort study, subjects were enrolled from the General Population Nutrition Intervention Trial in Linxian, China. Subjects included 498 oesophageal squamous cell carcinomas (OSCCs), 255 gastric cardia adenocarcinomas (GCAs), and an age- and sex-matched sub-cohort of 947 individuals. Baseline serum riboflavin, pyridoxal phosphate (PLP), folate, vitamin B12, and flavin mononucleotide (FMN) were measured for all subjects. We estimated the associations with Cox proportional hazard models, with adjustment for potential confounders. Compared to those in the lowest quartile of serum riboflavin, those in the highest had a 44% lower risk of OSCC (HR: 0.56, 95% CI: 0.41 to 0.75). Serum vitamin B12 as a continuous variable was observed to be significantly inversely associated with OSCC (HR: 0.95, 95% CI: 0.89 to 1.01, P for score test = 0.041). Higher serum FMN levels were significantly associated with increased risk of OSCC (HR: 1.08, 95% CI: 1.01 to 1.16) and GCA (HR: 1.09, 95% CI: 1.00 to 1.20). Our study prompted that B vitamins have the potential role as chemopreventive agents for upper gastrointestinal cancers.
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http://dx.doi.org/10.1038/srep35281DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5066215PMC
October 2016
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