title: Role of microsatellite instability in young patients with laryngeal carcinoma.
abstract: OBJECTIVE
  To determine whether early development of carcinoma in young patients could be explained by an alternative pathway such as microsatellite instability or whether it follows the classical tumor suppressor pathway characterized by loss of heterozygosity.
  
  
  METHODS
  Microsatellite instability, loss of heterozygosity, and multiple mismatch repair, p16, p53, and p63 protein expression were analyzed in a series of 18 young patients with laryngeal cancer.
  
  
  RESULTS
  Only 2 of the 18 cases showed low microsatellite instability, whereas 9 of 17 presented loss of heterozygosity in at least one of the markers tested. All cases retained multiple mismatch repair protein expression. The p53, p16, and p63 expression profiles were consistent with the classical tumor suppressor pathway.
  
  
  CONCLUSIONS
  Laryngeal carcinoma in young patients develops through the classical tumor suppressor pathway.
authors: Clinic Foundation for Biomedical Research, Barcelona, Spain.
authors: Laura
authors: L
authors: Conde
authors: Susana
authors: S
authors: Moyano
authors: Isabel
authors: I
authors: Vilaseca
authors: Miguel
authors: M
authors: Moragas
authors: Antonio
authors: A
authors: Cardesa
authors: Alfons
authors: A
authors: Nadal
mesh_terms: D000328:Adult; D053843:DNA Mismatch Repair; D005260:Female; D016147:Genes, Tumor Suppressor; D006801:Humans; D007822:Laryngeal Neoplasms / Q000235:genetics*; D019656:Loss of Heterozygosity; D008297:Male; D053842:Microsatellite Instability; D008875:Middle Aged