Title of article :
Analysis of hOGG1 genotype as a prognostic marker for muscle invasive bladder cancer: A novel approach using peptide nucleic acid-mediated, real-time PCR clamping
Author/Authors :
Kim، نويسنده , , Eun-Jung and Yan، نويسنده , , Chunri and Ha، نويسنده , , Yun-Sok and Jeong، نويسنده , , Pildu and Yi Kim، نويسنده , , Isaac and Moon، نويسنده , , Sung-Kwon and Choi، نويسنده , , Yung Hyun and Kim، نويسنده , , Wun-Jae، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2012
Pages :
7
From page :
673
To page :
679
Abstract :
AbstractObjective mage repair mechanisms are a source of genetic mutation and are believed to play an important role in human cancer. Human 8-oxoguanine DNA glycosylase 1 (hOGG1) is involved in the recognition and repair of DNA damage. The value of the hOGG1 genotype as a prognostic indicator for bladder cancer (BC) was assessed using a novel technological approach. als and methods sociation between genetic polymorphisms of hOGG1 codon 326 and clinicopathologic characteristics of 337 patients with BC was analyzed using peptide nucleic acid (PNA)-mediated real-time PCR clamping. s grade and size were significantly associated with the hOGG1 codon 326 genotype in non-muscle-invasive bladder cancer (NMIBC). The Cys326Cys polymorphism was significantly associated with progression and cancer specific survival in patients with muscle-invasive bladder cancer (MIBC). Multivariate Cox regression analysis indicated that the hOGG1 Cys326Cys polymorphism is associated with a protective effect on progression and a more dominant survival benefit than the Ser326Ser polymorphism in MIBC (hazard ratio 0.284 and 0.305, respectively). sions is of genotypes and clinical data for 337 BC patients indicates that the hOGG1 genotype may be a useful prognostic genetic marker for MIBC.
Keywords :
urinary bladder neoplasms , hOGG1 , DNA damage repair mechanisms , PNA , Biological tumor markers , Prognosis
Journal title :
Urologic Oncology
Serial Year :
2012
Journal title :
Urologic Oncology
Record number :
1893747
Link To Document :
بازگشت