title: Loss of fragile histidine triad gene expression is associated with progression of esophageal squamous cell carcinoma, but not with the patient's prognosis and smoking history.
abstract: BACKGROUND
  Recently, fragile histidine triad (FHIT) gene abnormality has been thought to be associated with several malignancies and smoking history. The authors previously discovered that methylation of the 5' CpG island of the FHIT gene was closely associated with transcriptional inactivation in esophageal squamous cell carcinoma (SCC); however, the clinical impact of the FHIT gene in esophageal carcinoma is still unknown.
  
  
  METHODS
  In this article, the authors evaluated the clinical impact of the FHIT gene in 149 esophageal squamous cell carcinoma (SCC) patients retrospectively using immunohistochemical analysis. They also examined the correlation between FHIT protein expression and smoking history.
  
  
  RESULTS
  Among 149 curative resection (R0) cases of esophageal SCC, normal FHIT protein expression was noted in only 33 cases (22.1%), whereas reduced FHIT protein expression was noted in 67 cases and there was no FHIT expression in 50 cases. When a tumor invaded the muscle layer, FHIT protein expression was markedly reduced. The cases with reduction or loss of FHIT protein expression tended to have poor prognoses (P = 0.069). However, Cox multivariate analysis revealed that FHIT protein reduction had no relation to prognosis. FHIT protein expression had no relation to smoking history.
  
  
  CONCLUSIONS
  FHIT protein expression was associated with progression of esophageal SCC, however, it may not be associated with the patient's prognosis and smoking history.
authors.affiliation: Department of Surgery and Surgical Basic Science, Graduate School of Medicine, Kyoto University, Kawaracho 54, Shogoin Sakyo-ku, Kyoto 606-8507, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Shimada
authors.forename: F
authors.initials: F
authors.lastname: Sato
authors.forename: G
authors.initials: G
authors.lastname: Watanabe
authors.forename: S
authors.initials: S
authors.lastname: Yamasaki
authors.forename: M
authors.initials: M
authors.lastname: Kato
authors.forename: M
authors.initials: M
authors.lastname: Maeda
authors.forename: M
authors.initials: M
authors.lastname: Imamura
mesh_terms: D000368:Aged; D002294:Carcinoma, Squamous Cell / Q000235:genetics* / Q000473:pathology; D002873:Chromosome Fragility / Q000235:genetics*; D004273:DNA, Neoplasm / Q000235:genetics; D018450:Disease Progression; D004938:Esophageal Neoplasms / Q000235:genetics* / Q000473:pathology; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006639:Histidine / Q000235:genetics; D006801:Humans; D019656:Loss of Heterozygosity; D008297:Male; D008487:Medical History Taking; D008875:Middle Aged; D011379:Prognosis; D012189:Retrospective Studies; D012907:Smoking / Q000009:adverse effects*; D019680:Trinucleotide Repeat Expansion
chemical_list: D004273:DNA, Neoplasm; D006639:Histidine