Association Between Markers of Obesity and Progression From Barrett's Esophagus to Esophageal Adenocarcinoma

Duggan, Catherine; Onstad, Lynn; Hardikar, Sheetal; Blount, Patricia L.; Reid, Brian J.; Vaughan, Thomas L.

doi:10.1016/j.cgh.2013.02.017

Cited by 122 publications

(106 citation statements)

References 75 publications

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“…As discussed previously, obesity seems to promote the development of BO and OAC through reflux-dependent and -independent means, and epidemiologically the combination of obesity and reflux is a significantly greater risk than either alone or the additive effect [Duggan et al 2013;El-Serag et al 2014;Garcia et al 2014;Lagergren et al 1999]. This is reflected in further experimental data.…”

Section: The Role Of Adipokinessupporting

confidence: 54%

The role of obesity in oesophageal cancer development

Long

Beales

2014

Therap Adv Gastroenterol

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Abstract:The incidence of oesophageal adenocarcinoma has increased dramatically in the developed world in the last half century. Over approximately the same period there has been an increase in the prevalence of obesity. Multiple epidemiological studies and metaanalyses have confirmed that obesity, especially abdominal, visceral obesity, is a risk factor for gastro-oesophageal reflux, Barrett's oesophagus and oesophageal adenocarcinoma. Although visceral obesity enhances gastro-oesophageal reflux, the available data also show that visceral obesity increases the risk of Barrett's oesophagus and adenocarcinoma via reflux-independent mechanisms. Several possible mechanisms could link obesity with the risk of oesophageal adenocarcinoma in addition to mechanical effects increasing reflux. These include reduced gastric Helicobacter pylori infection, altered intestinal microbiome, factors related to lifestyle, the metabolic syndrome and associated low-grade inflammation induced by obesity and the secretion of mediators by adipocytes which may directly influence the oesophageal epithelium. Of these adipocyte-derived mediators, increased leptin levels have been independently associated with progression to oesophageal adenocarcinoma and in laboratory studies leptin enhances malignant behaviours in cell lines. Adiponectin is also secreted by adipocytes and levels decline with obesity: decreased serum adiponectin levels are associated with malignant progression in Barrett's oesophagus and experimentally adiponectin exerts anticancer effects in Barrett's cell lines and inhibits growth factor signalling. At present there are no proven chemopreventative interventions that may reduce the incidence of obesity-associated oesophageal cancer: observational studies suggest that the combined use of a statin and aspirin or another cyclo-oxygenase inhibitor is associated with a significantly reduced cancer incidence in patients with Barrett's oesophagus.

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Section: The Role Of Adipokinessupporting

confidence: 54%

The role of obesity in oesophageal cancer development

Long

Beales

2014

Therap Adv Gastroenterol

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“…More specifically, it has been postulated that obesity increases intraabdominal pressure and gastroesophageal reflux by a specific mechanism, although some studies provided contradictory results. On the other hand, adipose tissue itself influences tumor development [50][51][52][53][54] . Adipocytes and inflammatory cells secrete adipokines and cytokines which are known to promote tumor development.…”

Section: Obesitymentioning

confidence: 99%

Epidemiology of esophageal cancer

Zhang¹

2013

WJG

892

749

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Esophageal cancer (EsC) is one of the least studied and deadliest cancers worldwide because of its extremely aggressive nature and poor survival rate. It ranks sixth among all cancers in mortality. In retrospective studies of EsC, smoking, hot tea drinking, red meat consumption, poor oral health, low intake of fresh fruit and vegetables, and low socioeconomic status have been associated with a higher risk of esophageal squamous cell carcinoma. Barrett's esophagus is clearly recognized as a risk factor for EsC, and dysplasia remains the only factor useful for identifying patients at increased risk, for the development of esophageal adenocarcinoma in clinical practice. Here, we investigated the epidemiologic patterns and causes of EsC. Using population based cancer data from the Surveillance, Epidemiology and End Results Program of the United States; we generated the most up-to-date stage distribution and 5-year relative survival by stage at diagnosis for 1998-2009. Special note should be given to the fact that esophageal cancer, mainly adenocarcinoma, is one of the very few cancers that is contributing to increasing death rates (20%) among males in the United States. To further explore the mechanism of development of EsC will hopefully decrease the incidence of EsC and improve outcomes.© 2013 Baishideng. All rights reserved.Key words: Risk factor; Barrett's esophagus; Cyclin D1 G870A; Esophageal neoplasm; Susceptibility; Polymorphism Core tip: Here, we investigated the epidemiologic patterns and causes of esophageal cancer. Using population based cancer data from the Surveillance, Epidemiology and End Results Program of the United States; we generated the most up-to-date stage distribution and 5-year relative survival by stage at diagnosis for

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“…The link between esophageal adenocarcinoma is notably stronger for abdominal obesity than general obesity [43]. A potential mechanical mechanism linking abdominal obesity with EAC is via gastroesophageal reflux disease (GERD) due to enhanced intra-abdominal pressure and the lower esophageal sphincter predisposing to Barrett's esophagus and finally leading to EAC [44][45][46][47].…”

Section: Discussionmentioning

confidence: 99%

Abdominal Obesity and Gastroesophageal Cancer Risk: Systematic Review and Meta-Analysis of Prospective Studies

Hidayat¹,

Du²,

Shi³

2016

Preprint

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Correspondence: To systematically and quantitatively review the relation of abdominal obesity, as measured by waist circumference (WC) and waist to hip ratio (WHR), to total gastroesophageal cancer, gastric cancer (GC), and esophageal cancer. PubMed and Web of Science databases were searched for studies assessing the association between abdominal obesity and gastroesophageal cancer (GC and/or esophageal cancer) up to August 2016. A random-effect model was used to calculate the summary relative risks (RRs) and 95% confidence intervals (CIs). Seven prospective cohort studies -one publication included two separate cohorts -from six publications were included in the final analysis. A total of 2130 gastroesophageal cancer cases diagnosed amongst 913182 participants. Higher WC and WHR were significantly associated with increased risk of total gastroesophageal cancer (WC: RR 1.68, 95% CI: 1.38, 2.04; WHR: RR 1.49, 95% CI: 1.19, 1.88), GC (WC: RR 1.48, 95% CI: 1.24, 1.78; WHR: 1.33, 95% CI: 1.04, 1.70), and esophageal cancer (WC: RR 2.06, 95% CI: 1.30, 3.24; WHR: RR 1.99, 95% CI: 1.05, 3.75).Findings from our subgroup analyses showed non-significant positive associations between gastric non-cardia adenocarcinoma (GNCA) and both measures of abdominal adiposity, while gastric cardia adenocarcinoma (GCA) was positively associated with WC but not with WHR. On analysis restricted to studies that adjusted for body mass index (BMI), WC was positively associated with GC and esophageal cancer, whereas WHR was positively associated with risk of GC only. Although limited, the findings from our meta-analysis suggest the potential role of abdominal obesity in the etiology of gastric and esophageal cancers.

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Association Between Markers of Obesity and Progression From Barrett's Esophagus to Esophageal Adenocarcinoma

Cited by 122 publications

References 75 publications

The role of obesity in oesophageal cancer development

The role of obesity in oesophageal cancer development

Epidemiology of esophageal cancer

Abdominal Obesity and Gastroesophageal Cancer Risk: Systematic Review and Meta-Analysis of Prospective Studies

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