ABSTRACT
<p><b>OBJECTIVE</b>To study the relationship between genetic polymorphism of NAT2 and susceptibility to bladder cancer.</p><p><b>METHODS</b>NAT2 genotypes were determined by PCR-RFLP method in 69 patients with bladder transitional cell carcinoma and 88 healthy controls.</p><p><b>RESULTS</b>The frequency of NAT2 slow genotypes was 26.1% (18/69) in patients compared with 14.8% (13/88) in controls (P < 0.05). Bladder cancer risk in patients with NAT2 slow genotypes was 2 fold as high as that in patients with NAT2 rapid genotypes. When NAT2 rapid genotypes/non-smoker were used as reference, bladder cancer risk increased to 5.8-fold (P < 0.05). Among the smokers with PY higher than 10, the patients showed a higher frequency of NAT2 slow genotype than controls (P < 0.05). It was also shown that the patients with slow NAT2 genotypes were more likely to have high grade tumor (P < 0.05) and advanced stage tumor (P < 0.01).</p><p><b>CONCLUSION</b>The results suggest that NAT2 genetic polymorphism is associated with bladder cancer susceptibility. People with NAT2 slow genotype have higher bladder cancer risk.</p>
Subject(s)
Female , Humans , Male , Middle Aged , Arylamine N-Acetyltransferase , Genetics , Carcinoma, Transitional Cell , Genetics , Pathology , Gene Frequency , Genetic Predisposition to Disease , Genotype , Neoplasm Staging , Polymerase Chain Reaction , Polymorphism, Restriction Fragment Length , Smoking , Urinary Bladder Neoplasms , Genetics , PathologyABSTRACT
<p><b>OBJECTIVE</b>To investigate the expression of androgen receptor (AR) isoforms in normal human prostate.</p><p><b>METHODS</b>Fourteen normal prostatic specimens from donors, aged 25 on average (21-28 yr), were analyzed by high resolution isoelectric focusing (IEF). The expression of AR isoforms was demonstrated in all 14 normal human prostatic tissues.</p><p><b>RESULTS</b>Four types of AR isoforms were detected with isoelectric point value at 6.5, 6.0, 5.8 and 5.3 in 14 prostatic specimens. Binding of 3H-dihydrotestosterone (DHT) to these four AR isoforms was inhibited by the addition of 100-fold excess of DHT and testosterone. No effect of progesterone, estradiol and diethylstilbestrol on tritiated hormone binding was observed.</p><p><b>CONCLUSIONS</b>There are four AR isoforms in normal human prostate. The expression of AR isoforms is different from one another.</p>