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Expression and mutational analysis of Cip/Kip family in early glottic cancer

Published online by Cambridge University Press:  19 February 2015

D-K Kim
Affiliation:
Nano-Bio Regenerative Medical Institute, Hallym University, Chuncheon, South Korea Department of Otorhinolaryngology – Head and Neck Surgery, Chuncheon Sacred Heart Hospital, Hallym University College of Medicine, Chuncheon, Kangwon-do, South Korea
J H Lee
Affiliation:
Nano-Bio Regenerative Medical Institute, Hallym University, Chuncheon, South Korea Department of Otorhinolaryngology – Head and Neck Surgery, Chuncheon Sacred Heart Hospital, Hallym University College of Medicine, Chuncheon, Kangwon-do, South Korea
O J Lee
Affiliation:
Nano-Bio Regenerative Medical Institute, Hallym University, Chuncheon, South Korea
C H Park*
Affiliation:
Nano-Bio Regenerative Medical Institute, Hallym University, Chuncheon, South Korea Department of Otorhinolaryngology – Head and Neck Surgery, Chuncheon Sacred Heart Hospital, Hallym University College of Medicine, Chuncheon, Kangwon-do, South Korea
*
Address for correspondence: Dr Chan Hum Park, Department of Otorhinolaryngology – Head and Neck Surgery, Chuncheon Sacred Heart Hospital, Hallym University College of Medicine, 153, Kyo-Dong, Chuncheon, Kangwon-do 200-704, South Korea Fax: 82-33-241-2909 E-mail: hlpch@paran.com

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.

Conclusion:

Our results suggest that the Cip/Kip family may have a role as a molecular mechanism of carcinogenesis in early glottic cancer.

Type
Main Articles
Copyright
Copyright © JLO (1984) Limited 2015 

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