CpG island hypermethylation in progression of esophageal and gastric cancer.
The upper gastrointestinal (GI) cancers have various carcinogenic pathways and precursor lesions, such as dysplasia for esophageal squamous cell carcinoma, Barrett esophagus for esophageal adenocarcinoma, and intestinal metaplasia for the intestinal-type of gastric cancer. Recently, many epigenetic events in carcinogenic pathways have been revealed, along with genomic and genetic alterations. This information has provided deeper insight into an understanding of the mechanisms of upper GI carcinogenesis. Moreover, detection methods of aberrant methylation have been applied to clinical fields to stratify high-risk groups, detect early cancer, and to predict clinical outcomes. In this review, a variety of information is summarized regarding gene hypermethylation in esophageal and gastric cancer.
Sato
Fumiaki
F
Department of Pathology, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA. fsato@som.umaryland.edu
Meltzer
Stephen J
SJ
D000230:Adenocarcinoma / Q000235:genetics / Q000473:pathology*; D002294:Carcinoma, Squamous Cell / Q000235:genetics / Q000473:pathology*; D002471:Cell Transformation, Neoplastic; D018899:CpG Islands / Q000235:genetics*; D019175:DNA Methylation; D018450:Disease Progression; D004938:Esophageal Neoplasms / Q000235:genetics / Q000473:pathology*; D006801:Humans; D018895:Microsatellite Repeats; D011230:Precancerous Conditions; D013274:Stomach Neoplasms / Q000235:genetics / Q000473:pathology*