Obesity, metabolic syndrome and esophageal adenocarcinoma: epidemiology, etiology and new targets.

Hdl Handle:
http://hdl.handle.net/10147/198713
Title:
Obesity, metabolic syndrome and esophageal adenocarcinoma: epidemiology, etiology and new targets.
Authors:
Ryan, Aoife M; Duong, Michelle; Healy, Laura; Ryan, Stephen A; Parekh, Niyati; Reynolds, John V; Power, Derek G
Affiliation:
Department of Nutrition, Food Studies & Public Health, New York University, New York, NY 10044, USA. aoife.ryan1@gmail.com
Citation:
Obesity, metabolic syndrome and esophageal adenocarcinoma: epidemiology, etiology and new targets. 2011, 35 (4):309-19 Cancer Epidemiol
Journal:
Cancer epidemiology
Issue Date:
Aug-2011
URI:
http://hdl.handle.net/10147/198713
DOI:
10.1016/j.canep.2011.03.001
PubMed ID:
21470937
Abstract:
Rates of distal and junctional adenocarcinomas are increasing in Western countries.; Systematic review of epidemiological evidence linking obesity to esophageal adenocarcinoma (EA) was performed for studies published from 2005 to 2010. The current understanding of obesity's role in the etiology and potential dysplastic progression of Barrett's esophagus (BE) to EA is reviewed.; Accumulating epidemiological studies provide evidence of obesity's role as a driving force behind the increasing rates of EA. The simplest construct is that obesity promotes reflux, causing chronic inflammation and BE, predisposing to adenocarcinoma. However, as obesity is positively associated with the prevalence of many cancers, other mechanisms are important. A link may exist between fat distribution patterns and the risk of BE and EA. Altered metabolic profiles in the metabolic syndrome (MetS) may be a key factor in cell cycle/genetic abnormalities that mark the progression of BE towards cancer. Research highlighting a unique role of MetS in the length of BE, and its association with systemic inflammation and insulin resistance is discussed, as well as adipokine receptor expression in both BE and esophageal epithelium, and how MetS and the systemic response impacts on key regulators of inflammation and tumorigenesis. CONCLUSIONS/IMPACT: Obesity is positively associated with EA. The systemic inflammatory state consequent on the altered metabolism of obese patients, and the associated impact of adipocytokines and pro-coagulant factors released by adipocytes in central fat, may underlie obesity's relationship to this cancer. Novel therapeutic agents that may antagonize adipo-cytokines and potentially offer a promising role in cancer therapy are discussed.
Item Type:
Article
Language:
en
ISSN:
1877-783X

Full metadata record

DC FieldValue Language
dc.contributor.authorRyan, Aoife Men
dc.contributor.authorDuong, Michelleen
dc.contributor.authorHealy, Lauraen
dc.contributor.authorRyan, Stephen Aen
dc.contributor.authorParekh, Niyatien
dc.contributor.authorReynolds, John Ven
dc.contributor.authorPower, Derek Gen
dc.date.accessioned2011-12-22T15:02:49Z-
dc.date.available2011-12-22T15:02:49Z-
dc.date.issued2011-08-
dc.identifier.citationObesity, metabolic syndrome and esophageal adenocarcinoma: epidemiology, etiology and new targets. 2011, 35 (4):309-19 Cancer Epidemiolen
dc.identifier.issn1877-783X-
dc.identifier.pmid21470937-
dc.identifier.doi10.1016/j.canep.2011.03.001-
dc.identifier.urihttp://hdl.handle.net/10147/198713-
dc.description.abstractRates of distal and junctional adenocarcinomas are increasing in Western countries.-
dc.description.abstractSystematic review of epidemiological evidence linking obesity to esophageal adenocarcinoma (EA) was performed for studies published from 2005 to 2010. The current understanding of obesity's role in the etiology and potential dysplastic progression of Barrett's esophagus (BE) to EA is reviewed.-
dc.description.abstractAccumulating epidemiological studies provide evidence of obesity's role as a driving force behind the increasing rates of EA. The simplest construct is that obesity promotes reflux, causing chronic inflammation and BE, predisposing to adenocarcinoma. However, as obesity is positively associated with the prevalence of many cancers, other mechanisms are important. A link may exist between fat distribution patterns and the risk of BE and EA. Altered metabolic profiles in the metabolic syndrome (MetS) may be a key factor in cell cycle/genetic abnormalities that mark the progression of BE towards cancer. Research highlighting a unique role of MetS in the length of BE, and its association with systemic inflammation and insulin resistance is discussed, as well as adipokine receptor expression in both BE and esophageal epithelium, and how MetS and the systemic response impacts on key regulators of inflammation and tumorigenesis. CONCLUSIONS/IMPACT: Obesity is positively associated with EA. The systemic inflammatory state consequent on the altered metabolism of obese patients, and the associated impact of adipocytokines and pro-coagulant factors released by adipocytes in central fat, may underlie obesity's relationship to this cancer. Novel therapeutic agents that may antagonize adipo-cytokines and potentially offer a promising role in cancer therapy are discussed.-
dc.language.isoenen
dc.titleObesity, metabolic syndrome and esophageal adenocarcinoma: epidemiology, etiology and new targets.en
dc.typeArticleen
dc.contributor.departmentDepartment of Nutrition, Food Studies & Public Health, New York University, New York, NY 10044, USA. aoife.ryan1@gmail.comen
dc.identifier.journalCancer epidemiologyen
dc.description.provinceMunster-

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