title: Expression and mutational analysis of Cip/Kip family in early glottic cancer.
abstract: BACKGROUND
  Genetic alteration of cyclin-dependent kinase inhibitors has been associated with carcinogenesis mechanisms in various organs.
  
  
  OBJECTIVE
  This study aimed to evaluate the expression and mutational analysis of Cip/Kip family cyclin-dependent kinase inhibitors (p21CIP1/WAF1, p27KIP1 and p57KIP2) in early glottic cancer.
  
  
  METHODS
  Expressions of Cip/Kip family and p53 were determined by quantitative reverse transcription polymerase chain reaction and densitometry. For the analysis of p21 inactivation, sequence alteration was assessed using single-strand conformational polymorphism polymerase chain reaction. Additionally, the inactivation mechanism of p27 and p57 were investigated using DNA methylation analysis.
  
  
  RESULTS
  Reduced expression of p27 and p57 were detected in all samples, whereas the expression of p21 was incompletely down-regulated in 6 of 11 samples. Additionally, single-strand conformational polymorphism polymerase chain reaction analysis showed the p53 mutation at exon 6. Methylation of p27 and p57 was detected by DNA methylation assay.
  
  
  CONCLUSIONS
  Our results suggest that the Cip/Kip family may have a role as a molecular mechanism of carcinogenesis in early glottic cancer.
authors.affiliation: Nano-Bio Regenerative Medical Institute, Hallym University,Chuncheon,South Korea.
authors.forename: D-K
authors.initials: DK
authors.lastname: Kim
authors.affiliation: Nano-Bio Regenerative Medical Institute, Hallym University,Chuncheon,South Korea.
authors.forename: J H
authors.initials: JH
authors.lastname: Lee
authors.affiliation: Nano-Bio Regenerative Medical Institute, Hallym University,Chuncheon,South Korea.
authors.forename: O J
authors.initials: OJ
authors.lastname: Lee
authors.affiliation: Nano-Bio Regenerative Medical Institute, Hallym University,Chuncheon,South Korea.
authors.forename: C H
authors.initials: CH
authors.lastname: Park
mesh_terms: D002294:Carcinoma, Squamous Cell / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000096:biosynthesis / Q000235:genetics*; D050760:Cyclin-Dependent Kinase Inhibitor p27 / Q000096:biosynthesis / Q000235:genetics*; D050761:Cyclin-Dependent Kinase Inhibitor p57 / Q000096:biosynthesis / Q000235:genetics*; D004252:DNA Mutational Analysis / Q000379:methods; D005931:Glottis / Q000378:metabolism / Q000473:pathology*; D006258:Head and Neck Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007822:Laryngeal Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D018807:Polymorphism, Single-Stranded Conformational; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D000077195:Squamous Cell Carcinoma of Head and Neck
chemical_list: C493956:CDKN1A protein, human; C436291:CDKN1B protein, human; C493964:CDKN1C protein, human; D050759:Cyclin-Dependent Kinase Inhibitor p21; D050761:Cyclin-Dependent Kinase Inhibitor p57; D050760:Cyclin-Dependent Kinase Inhibitor p27
keywords: Carcinogenesis