[Show abstract][Hide abstract] ABSTRACT: This meta-analysis was conducted to summarize the association between an N-acetyltransferase 1 (NAT1) gene polymorphism and bladder cancer risk.
PubMed® and EMBASE databases were searched to identify studies that examined the effect of the NAT1*10 allele on the risk of bladder cancer.
Eleven case-control studies, which included 3311 bladder cancer cases and 3906 control subjects, met the inclusion criteria. The pooled analyses based on all studies showed that there was no significant difference in the NAT1*10 allele between bladder cancer cases and controls (odds ratios [OR] 0.96; 95% confidence interval [CI] 0.81, 1.10). When stratifying for race, the results were similar among Caucasians (OR 0.96; 95% CI 0.81, 1.12) and Asians (OR 0.87; 95% CI 0.48, 1.56). No statistical association was found between the NAT1*10 allele and bladder cancer risk upon stratification for smoking status and study design.
This meta-analysis suggests that there was no association between the NAT1*10 allele and bladder cancer risk. Further research should focus on other potentially functional genetic polymorphisms.
The Journal of international medical research 02/2013; 41(1):31-7. · 1.10 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Studies investigating the association between glutathione S-transferase P1 (GSTP1) gene polymorphism and bladder cancer (BC) risk have reported conflicting results. In order to clarify the effect of GSTP1 polymorphism on the BC susceptibility, we conducted an updated system review of published epidemiology studies to provide more precise evidence. We performed a systematic search of PubMed, EMBASE, and China National Knowledge Infrastructure (CNKI). 20 studies with 4,428 BC cases and 5,457 controls were identified. The combined analyses based on all studies showed that there was a significant difference in the genotype distribution in GSTP1(A313G) polymorphism between BC cases and controls not only in Asians (GG vs. AA + AG, OR = 1.59, 95 % CI = 1.01-2.51) but also in Caucasians (GG vs. AA + AG, OR = 1.51, 95 % CI = 1.11-2.06). Upon stratification for smoking status, we observed no statistically significant difference in genotype distribution of GSTP1 in ever-smokers. Combination of the high-risk genotypes (GSTM1 null + GSTT1 null + GSTP1 313 A/G or G/G) demonstrated further increase in the BC risk (OR = 6.64, 95 %CI = 3.63-12.16). This meta-analysis suggests that GSTP1 313 G/G polymorphism is a strong predisposing risk factor for BC.
[Show abstract][Hide abstract] ABSTRACT: To examine the clinical characteristics, treatment, and survival of adult patients with renal sarcoma treated at our institution during the past 2 decades.
A retrospective review of the demographic, presentation, treatment, and outcome data for 41 adult patients with renal sarcoma treated at our institution from January 1989 to December 2009 was performed. The clinicopathologic parameters were analyzed to determine their effect on survival.
Of the 41 patients, 18 were women and 23 were men. Their median age was 42 years (range 19-76). The median tumor size was 13 cm (range 4-35); 29 cases (70.7%) were high grade. The predominant histologic subtype was leiomyosarcoma (39.0%). At diagnosis, 6 patients (14.6%) had metastatic disease. Surgical resection was performed in 34 patients (82.9%), with negative margins in 22 (53.7%). After a median follow-up of 24 months (range 3-80), 3 patients (8.1%) had survived disease free, 11 (29.7%) were alive with disease, and 23 (62.2%) had died of disease. The overall 1-, 3-, and 5-year survival rate was 86.3%, 40.7%, and 14.5%, respectively, and the median survival was 28 months. The median survival after recurrence was 10 months (range 4-24) and that after metastasis 8 months (range 0-22). On univariate analyses, nonmetastatic disease (P = .001) and surgical resection (P = .000) were predictive of a favorable outcome. On multivariate analyses, surgical resection was the only independent predictor of survival (hazard ratio 35.629, P = .022).
Adult renal sarcoma accounts for 0.8% of renal cancer cases and has a poor prognosis. Early diagnosis and surgical resection offer patients the best chance of survival.
[Show abstract][Hide abstract] ABSTRACT: Lifelong premature ejaculation (LPE) is characterized by persistently shorter intravaginal ejaculation latency time (IELT) than found acceptable by the patient or his partner. It has been postulated to be a neurobiological dysfunction with genetic vulnerability and is related to disturbances of central serotonin (5-hydroxytryptamine, 5-HT) neurotransmission and 5-HT receptor function.
To investigate the relationship between the C-759T and G-697C polymorphisms of the 5-HT(2C) receptor and LPE.
A prospective study was conducted in 106 Han Chinese men with LPE, characterized by IELT of less than 1 min, and 84 healthy controls with IELT of more than 3 min. All subjects were genotyped for the C-759T and G-697C polymorphisms located in the promoter region of the 5-HT(2C) receptor. The frequencies of genotypes and single nucleotide mutations were compared between the two groups.
Three genotypes were detected both in the men with LPE and in the control group: -759C/-697G, -759T/-697C, and -759C/ -697C. Genotype -759T/-697G was not detected. The frequency of genotype -759T/-697C was higher in patients with LPE than in the control group (30.2 vs. 11.9%, p < 0.05), whereas the frequency of genotype -759C/-697G was lower in patients with LPE than in the control group (66.0 vs. 83.3%, p < 0.05). No difference was found for genotype -759C/ -697C between the two groups. Mutations at -759T and -697C were more frequent in patients than in the control group (-759T: 30.2 vs. 13.3%, p < 0.05; -697C: 30.4 vs. 16.7%, p < 0.05, respectively).
Our findings indicated that polymorphisms in the 5-HT(2C) receptor gene are associated with LPE, and men who carry the -759T or -697C genotype have increased odds of premature ejaculation. Further investigation in this field is necessary.
Urologia Internationalis 05/2010; 85(2):204-8. · 1.15 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Human papillomavirus (HPV) infection is the second leading cause of cancer-associated morbidity and mortality among women worldwide due to its prerequisite role in cervical carcinogenesis. HPV is strictly species and tissue-restricted and cannot be propagated in vitro, which has retarded the development of in-vivo models for HPV infection. Much of our understanding on HPV, its life cycle, its oncogenicity and its synergy with co-factors was first established in vitro or by animal papillomaviruses in vivo. However, key differences between such systems and natural HPV infection have limited their use in addressing certain important mechanisms of HPV-associated carcinogenesis. With the development of sophisticated molecular techniques, the direct study of HPV in vivo has become less problematic. Although some uncertainty remains, the animal model system for HPV-associated cervical disease has been maintained as the most scientifically and economically powerful in-vivo model. So far, animal model systems, based on HPV virus-like particles, pseudoviruses, transgenic mice, HPV-transformed cervical cell lines, have been invaluable in the recognition of the natural history of HPV infection, the synergy between HPV and its co-factors, as well as evaluating the efficacy and safety of new prophylactic and therapeutic modalities for HPV-associated cervical precancers and invasive cancers.
Reviews in Medical Microbiology 03/2009; 20(2):33-40. · 0.52 Impact Factor