Author/Authors :
Samzadeh Mohammad نويسنده , Montazeri-Khadem Vahideh نويسنده Department of Psychology, Islamic Azad University, Zarand Branch, Kerman, Iran Montazeri-Khadem Vahideh , Hasanzad Mandana نويسنده Tehran Medical Branch, Islamic Azad University, Tehran , Jamaldini Seyed Hamid نويسنده Genetics Research Center, University of Social Welfare and Rehabilitation Sciences, Tehran , Afshari Mahdi نويسنده Research Center for Modeling of Health, Kerman University of Medical Sciences, Kerman , Ziaei Seyed Amir Mohsen نويسنده Urology and Nephrology Research Center (UNRC), Shahid
Labbafinejad Medical Center, Shahid Beheshti University of Medical
Sciences, Tehran, Iran , Imani Mahdieh نويسنده Medical Genomics Research Center, Tehran Medical Sciences
Branch, Islamic Azad University, Tehran, Iran , Sattari Mahshid نويسنده Medical Genomics Research Center, Tehran Medical Sciences
Branch, Islamic Azad University, Tehran, Iran , Hashemian Leila نويسنده Medical Genomics Research Center, Tehran Medical Sciences
Branch, Islamic Azad University, Tehran, Iran , Kalantar Moaetamed Seyed Rouhollah نويسنده Medical Genomics Research Center, Tehran Medical Sciences
Branch, Islamic Azad University, Tehran, Iran
Abstract :
Background NAT2 enzyme involved in bioconversion of aromatic
amines, heterocyclic arylamines and certain drugs into electrophilic
ions that can be important initiators in tumorigenesis process.
Objectives The aim of this study was to assess the possible association
between NAT2 polymorphisms (857 G > A, 481 T > C, and 590
G > A) and risk of prostate cancer (PC). Methods Totally, 207
benign prostate hyperplasia (BPH) and 147 PC Iranian patients were
evaluated. NAT2 genotypes were detected by restriction fragment length
polymorphism (RFLP). Multiple logistic regression models were used to
estimate the odds ratios for the association between presence of each
genotype and developing PC. Results For NAT2 G857A, the frequency of AA
and AG genotypes was lower among PC patients compared to those without
it (1.01% vs. 0 and 55.88% vs. 54.55%, respectively; P = 0.7). For NAT2
T481c, the odds ratios for the association of TT and CT genotypes with
PC were 0.65 and 0.55, respectively, which were not statistically
significant (P = 0.5 and P = 0.09, respectively). For NAT2 G590a, both
AA (11.11% vs. 12.87%) and AG (45.83% vs. 52.48%) genotypes were
significantly more common among PC patients compared to BPC patients (P
= 0.008). However, none of the relevant odds ratios were statistically
significant (OR = 2.2, P = 0.2 and OR = 1.72, P = 0.1, respectively).
Among PC patients, CT genotype of T481C caused more than 4-fold
significant increase in the risk of developing advanced stages of PC.
Conclusions Our study represented credible evidence that carrying G857A,
G590A and T481C polymorphisms of NAT2 may not affect developing PC, its
grading or invasion, but heterozygote genotype of T481C polymorphism
(Rapid acetylator) can be associated with more advanced stages of cancer
earlier in life. Further longitudinal studies with larger sample sizes
are needed to more precisely assess the genetic risk factors of PC.
