Abstract
Barrett’s esophagus (BE) is a metaplastic condition that is believed to develop in the esophagus due to chronic acid reflux and can progress to esophageal adenocarcinoma (EAC). Obesity, a well-known risk factor for BE and EAC, may increase the risk for BE/EAC indirectly by increasing the frequency of gastro-esophageal reflux and directly through obesity-mediated inflammation and the secretion of cancer-promoting molecules by adipocytes. Epigenetic alterations, which are commonly seen in BE and EAC, have been associated with chronic inflammation in the esophagus and also with obesity in other tissues. There is emerging evidence that elevated BMI is associated with the altered DNA methylation observed in BE, dysplastic BE, and EAC tissues. There is also some suggestion that genes involved in cancer-related pathways and pathways implicated in obesity-related cancers and adipose-mediated inflammation (insulin, IGF-1) demonstrate altered methylation in obese individuals. Thus, obesity appears to influence the formation and progression of BE to EAC via epigenetic mechanisms.
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Abbreviations
- BE:
-
Barrett’s esophagus
- EAC:
-
Esophageal adenocarcinoma
- LGD:
-
Low-grade dysplasia
- HGD:
-
High-grade dysplasia
- SQ:
-
Squamous esophagus
- FFPE:
-
Formalin-fixed paraffin-embedded
- HM450:
-
HumanMethylation450
- UTR:
-
Untranslated region
- DML:
-
Differentially methylated loci/locus
- DMR:
-
Differentially methylated region
- BMI:
-
Body mass index
- NCI-PID:
-
National Cancer Institute Pathway Interaction Database
- KEGG:
-
Kyoto Encyclopedia of Genes and Genomes
- GO:
-
Gene ontology
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Kaz, A.M., Grady, W.M. (2016). Epigenetics in Obesity and Esophageal Cancer. In: Berger, N. (eds) Epigenetics, Energy Balance, and Cancer. Energy Balance and Cancer, vol 11. Springer, Cham. https://doi.org/10.1007/978-3-319-41610-6_8
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