title: Young patients with oral squamous cell carcinoma: study of the involvement of GSTP1 and deregulation of the Fanconi anemia genes.
abstract: OBJECTIVE
  To investigate whether oral squamous cell carcinomas (OSCCs) from young (</=40 years) and older (>/=60 years) patients have differential expression levels of GSTP1, FANCA, FANCC, FANCD2, and FANCG.
  
  
  METHODS
  Quantitative real-time reverse transcriptase-polymerase chain reaction and immunohistochemical analysis were used to assess gene and protein expression, respectively.
  
  
  METHODS
  This study was performed in a research institute within a hospital setting.
  
  
  METHODS
  Our study group consisted of 104 patients (42 young and 62 older). We collected RNA from 32 OSCC samples (10 young and 22 older patients) for gene expression analysis. Seventy-seven OSCC samples (37 from young and 40 from older patients) were used for protein expression analysis. Five patients were studied in both analyses.
  
  
  RESULTS
  Lower expression of GSTP1 (P = .04) and FANCA (P = .01) was observed in the tumors of young compared with older patients. We also detected lower expression of GSTP1 in the tumors of young patients compared with their nondysplastic mucosa (P = .01). FANCA was underexpressed in nondysplastic mucosa of young compared with older patients (P = .01). GSTP1 protein showed negative or low expression in 41% (n = 15 of 37) of young vs 5% (n = 2 of 40) of older patient tumors (P = .001). FANCG protein expression was absent or low in 81% (n = 30 of 37) of young compared with 36% (n = 15 of 40) of older patient tumors (P<.001).
  
  
  CONCLUSIONS
  Differences in expression levels of GSTP1, FANCA, and FANCG in OSCC of young and older patients suggest that different mechanisms may be involved in tumor development through defective carcinogen metabolism and/or DNA repair capabilities. GSTP1 plays a key role in detoxification; therefore, underexpression of this gene in tumors of young patients may cause deficient detoxification that could lead to an increased susceptibility to the development of oral carcinoma.
authors.affiliation: Faculte de Medecine Dentaire, Universite Laval, Quebec City, Quebec.
authors.forename: Steve
authors.initials: S
authors.lastname: Tremblay
authors.forename: Patricia
authors.initials: P
authors.lastname: Pintor Dos Reis
authors.forename: Grace
authors.initials: G
authors.lastname: Bradley
authors.forename: Natalie Naranjo
authors.initials: NN
authors.lastname: Galloni
authors.forename: Bayardo
authors.initials: B
authors.lastname: Perez-Ordonez
authors.forename: Jeremy
authors.initials: J
authors.lastname: Freeman
authors.forename: Dale
authors.initials: D
authors.lastname: Brown
authors.forename: Ralph
authors.initials: R
authors.lastname: Gilbert
authors.forename: Patrick
authors.initials: P
authors.lastname: Gullane
authors.forename: Jonathan
authors.initials: J
authors.lastname: Irish
authors.forename: Suzanne
authors.initials: S
authors.lastname: Kamel-Reid
mesh_terms: D000328:Adult; D002294:Carcinoma, Squamous Cell / Q000235:genetics*; D051856:Fanconi Anemia Complementation Group Proteins / Q000235:genetics*; D005260:Female; D015870:Gene Expression; D051549:Glutathione S-Transferase pi / Q000235:genetics*; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009062:Mouth Neoplasms / Q000235:genetics*; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D051856:Fanconi Anemia Complementation Group Proteins; D051549:Glutathione S-Transferase pi