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Cyclin D1 Polymorphism and the Susceptibility to NPC Using DHPLC

Cyclin D1
Polymorphism and the Susceptibility to NPC Using DHPLC

DENG Lin,  ZHAO Xiao-Rong, 
PAN Kai Feng1, 
WANG Yi1,  DENG
Xi-Yun,  Lü You-Yong1,  CAO Ya*
( Laboratory of Molecular Biology, 
Cancer Research Institute, 
Xiang-ya School of Medicine, 
Central South University, 
Changsha
410078, 
China;
1Beijing Institute for Cancer Research,  Peking University School of Oncology,  Beijing 100034,  China )

Abstract    Cyclin D1
is a key cell cycle regulator and a candidate proto-oncogene,  whose deregulation has been implicated
in pathogenesis of several types of cancers,  including NPC. 
A common A/G polymorphism (A870G) in exon 4 of the cyclin D1 gene,  CCND1,  is associated with the presence of 2 distinct mRNA
transcripts for this G1/S regulatory protein,  and CCND1 genotype has been
related to some phenotypes of several tumors.  To investigate the influence of cyclin D1 genotypes on the
genetic susceptibility in humans from Southern China to sporadic nasopharyngeal
carcinoma,  cyclin D1 genotyping
was performed by denaturing high perform ance liquid chromatography (DHPLC) and
DNA sequencing analysis of the PCR products from 84 NPC cases and 91 normal
controls.  Gene frequency
distribution was tested by Hardy-Weinberg equilibrium and comparison of cyclin
D1 gene frequencies between the patient and control groups was performed by χ2
test.  Results showed that in NPC
patients,  the AA genotype of CCND1
was significantly lower (20.24%) than in normal controls (38.46%),  and the GG and AG genotypes (GG + AG)
were significantly higher in NPC group than in the control group (χ2=6.946,  Pcorrected=0.016,  OR=2.463,  95% CI=1.249―4.859). 
These suggest that the A/G polymorphism of CCND1 was associated
with the susceptibility to NPC, 
and the GG and AGgenotypes in NPC patients were significantly higher
than those in normal controls.
Key words    cyclin D1;  polymorphism; 
nasopharyngeal carcinoma; DHPLC; 
genotype

*Corresponding author: Tel,
86-731-4805448; Fax, 86-731-4470589; e-mail,  [email protected]