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Published in: Digestive Diseases and Sciences 6/2011

01-06-2011 | Editorial

Familial Barrett’s Esophagus: Clues to Genetic Risks for Esophageal Adenocarcinoma

Author: Joel H. Rubenstein

Published in: Digestive Diseases and Sciences | Issue 6/2011

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Excerpt

Esophageal adenocarcinoma is a particularly deadly neoplasm, and the incidence of it has been rising at an alarming rate in recent decades in Western countries [1, 2]. Barrett’s esophagus has been recognized as a precursor lesion for cancer, and screening and subsequent surveillance or other intervention for this lesion is an attractive proposition. Despite the rising incidence, the cancer still remains relatively uncommon. Therefore, selecting high-risk patients for screening, surveillance, or intervention is important in order to make the practice economically reasonable. Risk factors have been established for the cancer and for Barrett’s esophagus, including male gender, white race, older age, symptoms of gastroesophageal reflux, obesity, tobacco use, and absence of infection with Helicobacter pylori. However, most of these factors are highly prevalent in Western societies, so more specific risk factors would improve the efficiency of clinical practice. The association with white race might be because of environmental differences among races, but also suggests that genetic factors play an important role. …
Literature
1.
go back to reference Pohl H, Welch HG. The role of overdiagnosis and reclassification in the marked increase of esophageal adenocarcinoma incidence. J Natl Cancer Inst. 2005;97:142–146.PubMedCrossRef Pohl H, Welch HG. The role of overdiagnosis and reclassification in the marked increase of esophageal adenocarcinoma incidence. J Natl Cancer Inst. 2005;97:142–146.PubMedCrossRef
2.
go back to reference Bollschweiler E, Wolfgarten E, Gutschow C, Holscher AH. Demographic variations in the rising incidence of esophageal adenocarcinoma in white males. Cancer. 2001;92:549–555.PubMedCrossRef Bollschweiler E, Wolfgarten E, Gutschow C, Holscher AH. Demographic variations in the rising incidence of esophageal adenocarcinoma in white males. Cancer. 2001;92:549–555.PubMedCrossRef
3.
go back to reference Chak A, Lee T, Kinnard MF, et al. Familial aggregation of Barrett’s oesophagus, oesophageal adenocarcinoma, and oesophagogastric junctional adenocarcinoma in Caucasian adults. Gut. 2002;51:323–328.PubMedCrossRef Chak A, Lee T, Kinnard MF, et al. Familial aggregation of Barrett’s oesophagus, oesophageal adenocarcinoma, and oesophagogastric junctional adenocarcinoma in Caucasian adults. Gut. 2002;51:323–328.PubMedCrossRef
4.
go back to reference Munitiz V, Parrilla P, Ortiz A, Martinez-de-Haro LF, Yelamos J, Molina J. High risk of malignancy in familial Barrett’s esophagus: presentation of one family. J Clin Gastroenterol. 2008;42:806–809.PubMedCrossRef Munitiz V, Parrilla P, Ortiz A, Martinez-de-Haro LF, Yelamos J, Molina J. High risk of malignancy in familial Barrett’s esophagus: presentation of one family. J Clin Gastroenterol. 2008;42:806–809.PubMedCrossRef
5.
go back to reference Jochem VJ, Fuerst PA, Fromkes JJ. Familial Barrett’s esophagus associated with adenocarcinoma. Gastroenterology. 1992;102:1400–1402.PubMed Jochem VJ, Fuerst PA, Fromkes JJ. Familial Barrett’s esophagus associated with adenocarcinoma. Gastroenterology. 1992;102:1400–1402.PubMed
6.
go back to reference Crabb DW, Berk MA, Hall TR, Conneally PM, Biegel AA, Lehman GA. Familial gastroesophageal reflux and development of Barrett’s esophagus. Ann Intern Med. 1985;103:52–54.PubMed Crabb DW, Berk MA, Hall TR, Conneally PM, Biegel AA, Lehman GA. Familial gastroesophageal reflux and development of Barrett’s esophagus. Ann Intern Med. 1985;103:52–54.PubMed
7.
go back to reference Ash S, Vaccaro BJ, Dabney MK, Chung WK, Lightdale CJ, Abrams JA. Comparison of endoscopic and clinical characteristics of patients with familial and sporadic Barrett’s esophagus. Dig Dis Sci. 2011 (Epub ahead of print). doi:10.1007/s10620-011-1620-3. Ash S, Vaccaro BJ, Dabney MK, Chung WK, Lightdale CJ, Abrams JA. Comparison of endoscopic and clinical characteristics of patients with familial and sporadic Barrett’s esophagus. Dig Dis Sci. 2011 (Epub ahead of print). doi:10.​1007/​s10620-011-1620-3.
8.
go back to reference di Martino E, Hardie LJ, Wild CP, et al. The NAD(P)H:quinone oxidoreductase I C609T polymorphism modifies the risk of Barrett esophagus and esophageal adenocarcinoma. Genet Med. 2007;9:341–347.PubMedCrossRef di Martino E, Hardie LJ, Wild CP, et al. The NAD(P)H:quinone oxidoreductase I C609T polymorphism modifies the risk of Barrett esophagus and esophageal adenocarcinoma. Genet Med. 2007;9:341–347.PubMedCrossRef
9.
go back to reference McElholm AR, McKnight A-J, Patterson CC, Johnston BT, Hardie LJ, Murray LJ, et al. A population-based study of IGF axis polymorphisms and the esophageal inflammation, metaplasia, adenocarcinoma sequence. Gastroenterology. 2010;139:204-212.e3. McElholm AR, McKnight A-J, Patterson CC, Johnston BT, Hardie LJ, Murray LJ, et al. A population-based study of IGF axis polymorphisms and the esophageal inflammation, metaplasia, adenocarcinoma sequence. Gastroenterology. 2010;139:204-212.e3.
10.
go back to reference Zhai R, Chen F, Liu G, et al. Interactions among genetic variants in apoptosis pathway genes, reflux symptoms, body mass index, and smoking indicate two distinct etiologic patterns of esophageal adenocarcinoma. J Clin Oncol. 2010;28:2445–2451.PubMedCrossRef Zhai R, Chen F, Liu G, et al. Interactions among genetic variants in apoptosis pathway genes, reflux symptoms, body mass index, and smoking indicate two distinct etiologic patterns of esophageal adenocarcinoma. J Clin Oncol. 2010;28:2445–2451.PubMedCrossRef
11.
go back to reference Doecke J, Zhao ZZ, Pandeya N, et al. Polymorphisms in MGMT and DNA repair genes and the risk of esophageal adenocarcinoma. Int J Cancer. 2008;123:174–180.PubMedCrossRef Doecke J, Zhao ZZ, Pandeya N, et al. Polymorphisms in MGMT and DNA repair genes and the risk of esophageal adenocarcinoma. Int J Cancer. 2008;123:174–180.PubMedCrossRef
12.
go back to reference Feero WG, Guttmacher AE, Manolio TA. Genomewide association studies and assessment of the risk of disease. N Engl J Med. 2010;363:166–176.CrossRef Feero WG, Guttmacher AE, Manolio TA. Genomewide association studies and assessment of the risk of disease. N Engl J Med. 2010;363:166–176.CrossRef
Metadata
Title
Familial Barrett’s Esophagus: Clues to Genetic Risks for Esophageal Adenocarcinoma
Author
Joel H. Rubenstein
Publication date
01-06-2011
Publisher
Springer US
Published in
Digestive Diseases and Sciences / Issue 6/2011
Print ISSN: 0163-2116
Electronic ISSN: 1573-2568
DOI
https://doi.org/10.1007/s10620-011-1676-0

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