title: Leukocyte telomere length in relation to the risk of Barrett's esophagus and esophageal adenocarcinoma.
abstract: Chronic inflammation and oxidative damage caused by obesity, cigarette smoking, and chronic gastroesophageal reflux disease (GERD) are major risk factors associated with Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC). EAC has been increasing the past few decades, and early discovery and treatment are crucial for survival. Telomere shortening due to cell division and oxidative damage may reflect the impact of chronic inflammation and could possibly be used as predictor for disease development. We examined the prevalence of shorter leukocyte telomere length (LTL) among individuals with GERD, BE, or EAC using a pooled analysis of studies from the Barrett's and Esophageal Adenocarcinoma Consortium (BEACON). Telomere length was measured in leukocyte DNA samples by Q-PCR. Participants included 1173 patients (386 with GERD, 384 with EAC, 403 with BE) and 736 population-based controls. The association of LTL (in tertiles) along the continuum of disease progression from GERD to BE to EAC was calculated using study-specific odds ratios (ORs) and 95% confidence intervals (CIs) from logistic regression models adjusted for potential confounders. Shorter LTL were less prevalent among GERD patients (OR 0.57; 95% CI: 0.35-0.93), compared to population-based controls. No statistically significant increased prevalence of short/long LTL among individuals with BE or EAC was observed. In contrast to some earlier reports, our findings add to the evidence that leukocyte telomere length is not a biomarker of risk related to the etiology of EAC. The findings do not suggest a relationship between LTL and BE or EAC.
authors.affiliation: Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland.|Department of Epidemiology Research, Statens Serum Institut, Copenhagen, Denmark.
authors.forename: E Christina M
authors.initials: EC
authors.lastname: Wennerström
authors.affiliation: Department of Pathology, University of Washington, Seattle, Washington.
authors.forename: Rosa A
authors.initials: RA
authors.lastname: Risques
authors.affiliation: Department of Pathology, University of Washington, Seattle, Washington.
authors.forename: Donna
authors.initials: D
authors.lastname: Prunkard
authors.affiliation: Information Management Services, Bethesda, Maryland.
authors.forename: Carol
authors.initials: C
authors.lastname: Giffen
authors.affiliation: Division of Research and Oakland Medical Center, Kaiser Permanente, Northern California, Oakland, California.
authors.forename: Douglas A
authors.initials: DA
authors.lastname: Corley
authors.affiliation: Centre for Public Health, Queen's University, Belfast, United Kingdom.
authors.forename: Liam J
authors.initials: LJ
authors.lastname: Murray
authors.affiliation: QIMR Berghofer Medical Research Institute, Brisbane, Australia.|School of Population Health, University of Queensland, Brisbane, Australia.
authors.forename: David C
authors.initials: DC
authors.lastname: Whiteman
authors.affiliation: Department of Preventive Medicine, Keck School of Medicine, University of Southern California/Norris Comprehensive Cancer Center, Los Angeles, California.
authors.forename: Anna H
authors.initials: AH
authors.lastname: Wu
authors.affiliation: Division of Cancer Etiology, Department of Population Science, Beckman Research Institute, City of Hope, Duarte, California.
authors.forename: Leslie
authors.initials: L
authors.lastname: Bernstein
authors.affiliation: Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
authors.forename: Weimin
authors.initials: W
authors.lastname: Ye
authors.affiliation: UT MD Anderson Cancer Center, Houston, Texas.
authors.forename: Wong-Ho
authors.initials: WH
authors.lastname: Chow
authors.affiliation: Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington.
authors.forename: Thomas L
authors.initials: TL
authors.lastname: Vaughan
authors.affiliation: Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland. linda.liao@nih.gov.
authors.forename: Linda M
authors.initials: LM
authors.lastname: Liao
mesh_terms: D000230:Adenocarcinoma / Q000453:epidemiology* / Q000209:etiology*; D001471:Barrett Esophagus / Q000453:epidemiology* / Q000209:etiology*; D004938:Esophageal Neoplasms / Q000453:epidemiology* / Q000209:etiology*; D005260:Female; D005764:Gastroesophageal Reflux / Q000150:complications / Q000453:epidemiology / Q000209:etiology; D006801:Humans; D007962:Leukocytes / Q000378:metabolism*; D008297:Male; D016017:Odds Ratio; D011159:Population Surveillance; D015995:Prevalence; D012306:Risk; D016615:Telomere / Q000235:genetics*
keywords: Barrett's esophagus; esophageal Adenocarcinoma, epidemiology; telomere