title: Aberrant methylation of the CHFR gene in digestive tract cancer.
abstract: BACKGROUND
  Recently, aberrant methylation of the CHFR gene associated with gene silencing has been reported in several cancers. The methylation status of the CHFR gene was examined in primary esophageal and gastric carcinomas.
  
  
  METHODS
  The methylation status of the CHFR promoter region and mRNA expression in cancer cell lines were examined first. The methylation status of the CHFR gene in 38 esophageal and 53 gastric cancers was subsequently examined and the correlation between CHFR methylation and the clinicopathological findings was investigated.
  
  
  RESULTS
  Aberrant methylation of the CHFR gene was detected in 9 out of 38 (24%) primary esophageal and 16 out of 53 (30%) primary gastric cancers. After methylation analysis of all the samples, the clinicopathological data were correlated with these results. There was a significant difference according to gender (p = 0.0404), indicating that female esophageal cancers were more frequently methylated than male. On the other hand, abnormal methylation was found in esophageal and gastric cancer patients at all clinical stages.
  
  
  CONCLUSIONS
  Aberrant methylation of the CHFR gene was frequently shown in esophageal and gastric cancers. In addition, abnormal methylation was found in these cancer patients at all clinical stages, suggesting that this cancer could be methylated at an early stage.
authors.affiliation: Gastroenterological Surgery, Nagoya University Graduate School of Medicine, Nagoya 466-8560, Japan.
authors.forename: Yuki
authors.initials: Y
authors.lastname: Morioka
authors.forename: Kenji
authors.initials: K
authors.lastname: Hibi
authors.forename: Mitsuru
authors.initials: M
authors.lastname: Sakai
authors.forename: Masahiko
authors.initials: M
authors.lastname: Koike
authors.forename: Michitaka
authors.initials: M
authors.lastname: Fujiwara
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Kodera
authors.forename: Katsuki
authors.initials: K
authors.lastname: Ito
authors.forename: Akimasa
authors.initials: A
authors.lastname: Nakao
mesh_terms: D000368:Aged; D018797:Cell Cycle Proteins / Q000096:biosynthesis / Q000235:genetics*; D045744:Cell Line, Tumor; D015179:Colorectal Neoplasms / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D019175:DNA Methylation; D004938:Esophageal Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D005260:Female; D015870:Gene Expression; D006801:Humans; D008297:Male; D009363:Neoplasm Proteins / Q000096:biosynthesis / Q000235:genetics*; D000075223:Poly-ADP-Ribose Binding Proteins; D011401:Promoter Regions, Genetic; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013274:Stomach Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D044767:Ubiquitin-Protein Ligases
chemical_list: D018797:Cell Cycle Proteins; D009363:Neoplasm Proteins; D000075223:Poly-ADP-Ribose Binding Proteins; C412002:CHFR protein, human; D044767:Ubiquitin-Protein Ligases