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Purpose: Angiotensin I-converting enzyme (ACE) is crucial in the renin–angiotensin–aldosterone system. ACE insertion/deletion (I/D) polymorphism is a common genetic variation of this gene and is associated with several disease phenotypes. However, the results of published studies on the influence of this polymorphism on renal transplantation are inconsistent. Therefore, a meta-analysis was performed to evaluate the association between ACE I/D polymorphism and prognosis of kidney transplantation. Methods: A meta-analysis was performed based on 21 case–control studies from 12 publications (1497 cases and 2029 controls) and 10 studies with quantitative values from 5 publications (814 patients). Pooled odds ratios (ORs) and weighted mean differences (WMDs) with their corresponding 95% confidence intervals (CIs) were used to estimate associations. Results: ACE I/D polymorphism was found to be associated with acute rejection (AR) in genotypes DD+ID versus II (OR = 1.62, 95% CI = 1.14–2.29) and with serum creatinine concentration after renal transplantation in genotypes DD versus ID (WMD = 13.12, 95% CI = 8.09–18.16). Stratified analysis revealed that recipients transplanted within a year had higher serum creatinine concentrations in the DD versus ID model. No significant association was found between hypertension and ACE I/D polymorphism. Conclusion: ACE I/D polymorphism is associated with AR and allograft function after kidney transplantation. [ABSTRACT FROM AUTHOR]

Objective. Previous studies have investigated the relationships between osteopontin gene polymorphism rs1126616 and OPN levels and urolithiasis, but the results were controversial. Our study aimed to clarify such relationships. Methods. A meta-analysis was performed by searching the databases Pubmed, Embase, and Web of Science for relevant studies. Crude odds ratios (ORs) or standardised mean differences with 95% confidence intervals (CIs) were calculated to evaluate the strength of association. Publication bias was estimated using Begg’s funnel plots and Egger’s regression test. Results. Overall, a significantly increased risk of urolithiasis was associated with OPN gene polymorphism rs1126616 for all the genetic models except recessive model. When stratified by ethnicity, the results were significant only in Turkish populations. For OPN level association, a low OPN level was detected in the urine of urolithiasis patients in large sample size subgroup. Results also indicated that urolithiasis patients have lower OPN level in serum than normal controls. Conclusion. This meta-analysis revealed that the T allele of OPN gene polymorphism increased susceptibility to urolithiasis. Moreover, significantly lower OPN levels were detected in urine and serum of urolithiasis patients than normal controls, thereby indicating that OPN has important functions in the progression of urolithiasis. [ABSTRACT FROM AUTHOR]

Background. The calcium-sensing receptor gene (CaSR) is a candidate to explain urolithiasis. A number of case-control studies were conducted to investigate associations between CaSR polymorphisms with risks of hypercalciuria and urolithiasis in humans. But the results were still inconsistent. Methods. A meta-analysis was performed to address this issue. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were calculated to estimate the strength of associations between CaSR polymorphisms and the risk of urolithiasis. The pooled standardized mean difference (SMD) with 95% CI was used for the meta-analysis of CaSR polymorphisms and urine calcium concentration. Results. For urolithiasis association, the SS genotype of A986S polymorphism was a risk factor for urolithiasis in Asians and PHPT patients, but a protective factor in Caucasians. The GG genotype of R990 polymorphism was associated with an increased risk of urolithiasis, especially in Caucasians and healthy population. Regarding urine calcium concentration association, individuals with the G allele had a higher level of urine calcium than the noncarriers. Conclusions. This meta-analysis revealed that the G allele of CaSR R990G polymorphism increases susceptibility to urolithiasis and hypercalciuria. The A986S and Q1011E polymorphisms were associated with urolithiasis and hypercalciuria in specific populations. [ABSTRACT FROM AUTHOR]

Purpose: UGT2B17 is a vital member of the UGT2 family and functions as a detoxification enzyme which catalyzes the glucuronidation of lipophilic compounds. Accumulating evidences implicates that it may contribute to the susceptibility of tumor risk. Identification of a UGT2B17 deletion polymorphism has attracted studies to evaluate the association between the UGT2B17 deletion polymorphism and tumor risk in diverse populations. However, the available results are conflicting. Methods: A meta-analysis based on 14 studies from 10 publications including 5,732 cases and 5,112 controls was performed. Published literature from PubMed, EMBASE and Web of Science was pooled and the crude odds ratios (ORs) with 95% confidence intervals (CIs) were calculated to estimate the strength of the associations. Results: Conclusively, our results indicate that individuals with a UGT2B17 deletion polymorphism were associated with tumor risks (OR = 1.29, 95% CI = 1.03–1.63, P<0.001) in a recessive model. However, after excluding two studies for their heterogeneity, the result then demonstrated that the UGT2B17 deletion polymorphism was not associated with tumor risks (OR = 1.118, 95%CI = 0.938–1.332, P>0.1). A subgroup analysis based on tumor type, sex or race did not show significant results. Conclusion: These results suggest that the UGT2B17 deletion polymorphism is not associated with tumor risks. [ABSTRACT FROM AUTHOR]

Members of the miR-34 family have been shown to be transcriptional targets of the tumour suppressor gene P53. Aberration expression of miR-34 impairs p53-mediated cell cycle arrest and apoptosis. A single nucleotide polymorphism T > C (rs4938723) located within the CpG island in the promoter region of pri-miR-34b/c may affect its expression and has been suggested to influence cancer risk. In this study, we genotyped rs4938723 using the TaqMan method to explore the relationship between this polymorphism and the risk of renal cell cancer (RCC) in a case-control study of 710 RCC patients and 760 control subjects. We found that individuals carrying the CC genotype had a significantly increased RCC risk compared with those with TT or TT/TC genotypes [odds ratio (OR) = 1.53, 95% confidence interval (CI) = 1.06–2.21 for CC vs. TT and OR = 1.48, 95% CI = 1.05–2.10 for CC vs. TT/TC). Furthermore, the increased risk was more evident in the subgroups of older subjects (OR = 1.80, 95% CI = 1.08–3.01), males (OR = 1.64, 95% CI = 1.08–2.51), smokers (OR = 2.07, 95% CI = 1.16–3.69) and drinkers (OR = 1.94, 95% CI = 1.01–3.73), although no interaction between rs4938723 and these characteristics was observed. Twenty-seven normal tissues adjacent to tumour were used to evaluate the association between the expression level of miR-34b/c and the polymorphism, which revealed higher expression levels of miR-34b/c in normal renal tissues with TT+TC genotypes than in those with CC genotypes (P < 0.01). Furthermore, a luciferase gene assay in 293-T cells showed that the luciferase activities with rs4938723 T allele are higher than that with C allele (P < 0.05). These results suggest that the miR-34b/c rs4938723 C allele may increase susceptibility to RCC by decreasing the activity of pri-miR-34b/c promoter. [ABSTRACT FROM AUTHOR]

Insulin-like growth factor-I (IGF-I) and IGF binding protein-3 (IGFBP-3) are members of the insulin-like growth factor (IGF) family that play important roles in carcinogenesis. We hypothesized that the functional polymorphisms in IGF-I and IGFBP-3 may be associated with the risk of prostate cancer (PCa) in the Chinese population. This hospital-based case-control study included 664 PCa patients and 702 cancer-free controls. Nine SNPs in IGF-I and IGFBP-3 were genotyped using the TaqMan assay. The genetic associations between the pathogenesis and progression of PCa were assessed by logistic regression. We found that the genotype and allele frequency distribution of rs6218, rs35767 and rs5742612 were significantly different when comparing PCa cases to controls (P  = 0.005, 0.005 and 0.020, respectively). In the combined analysis, individuals with 2–6 risk alleles had an elevated risk of PCa compared to those with 0–1 risk alleles. We also found that the association between the combined risk alleles and the risk of PCa appeared stronger in the following subgroups: individuals older than 71 years of age (OR  = 1.41, 95%CI  = 1.05–1.91, P  = 0.020), nonsmokers (OR  = 1.68, 95%CI  = 1.21–2.32, P  = 0.002), nondrinkers (OR  = 1.32, 95%CI  = 1.02–1.61, P  = 0.002), and those with a negative family history of PCa (OR  = 1.28, 95%CI  = 1.02–1.71, P  = 0.022). Our results indicate that the three SNPs (rs6218, rs35767 and rs5742612) and the joint genotypes with 2–6 risk alleles, may contribute to the susceptibility to PCa, but not the progression, in the Chinese population. [ABSTRACT FROM AUTHOR]

Background: One-carbon metabolism is the basement of nucleotide synthesis and the methylation of DNA linked to cancer risk. Variations in one-carbon metabolism genes are reported to affect the risk of many cancers, including renal cancer, but little knowledge about this mechanism is known in Chinese population. Methods: Each subject donated 5 mL venous blood after signing the agreement. The study was approved by the Institutional Review Board of the Nanjing Medical University, Nanjing, China. 18 SNPs in six one-carbon metabolism-related genes (CBS, MTHFR, MTR, MTRR, SHMT1, and TYMS) were genotyped in 859 clear cell renal cell carcinoma (ccRCC) patients and 1005 cancer-free controls by the Snapshot. Results: Strong associations with ccRCC risk were observed for rs706209 (P = 0.006) in CBS and rs9332 (P = 0.027) in MTRR. Compared with those carrying none variant allele, individuals carrying one or more variant alleles in these two genes had a statistically significantly decreased risk of ccRCC [P = 0.001, adjusted odds ratio (OR) = 0.73, 95% confidence interval (CI) = 0.06–0.90]. In addition, patients carrying one or more variant alleles were more likely to develop localized stage disease (P = 0.002, adjusted OR = 1.37, 95%CI = 1.11–1.69) and well-differentiated ccRCC (P<0.001, adjusted OR = 1.42, 95%CI = 0.87–1.68). In the subgroup analysis, individuals carrying none variant allele in older group (P = 0.007, adjusted OR = 0.67, 95%CI = 0.49–0.91), male group (P = 0.007, adjusted OR = 0.71, 95%CI = 0.55–0.92), never smoking group (P = 0.002, adjusted OR = 0.68, 95%CI = 0.53–0.88) and never drinking group (P<0.001, adjusted OR = 0.68, 95%CI = 0.53–0.88) had an increased ccRCC risk. Conclusions: Our results suggest that the polymorphisms of the one-carbon metabolism-related genes are associated with ccRCC risk in Chinese population. Future population-based prospective studies are required to confirm the results. [ABSTRACT FROM AUTHOR]

Background: A functional -94 insertion/deletion polymorphism (rs28362491) in the promoter of the NFKB1 gene was reported to influence NFKB1 expression and confer susceptibility to different types of cancer. This study aims to determine whether the polymorphism is associated with risk of bladder cancer. Materials and methods: TaqMan assay was used to determine genotype among 609 cases and 640 controls in a Chinese population. Logistic regression was used to assess the association between the polymorphism and bladder cancer risk, and quantitative real-time polymerase chain reaction was used to determine NFKB1 mRNA expression. Results: Compared with the ins/ins/ins/del genotypes, the del/del genotype was associated with a significantly increased risk of bladder cancer [adjusted odd ratio (OR)  = 1.92, 95% confidence interval (CI)  = 1.42–2.59]. The increased risk was more prominent among subjects over 65 years old (OR  = 2.37, 95% CI  = 1.52–3.70), male subjects (OR  = 1.97, 95% CI = 1.40–2.79) and subjects with self-reported family history of cancer (OR  = 3.59, 95% CI  = 1.19–10.9). Furthermore, the polymorphism was associated with a higher risk of developing non-muscle invasive bladder cancer (OR  = 2.07, 95% CI  = 1.51–2.85), grade 1 bladder cancer (OR  = 2.40, 95% CI  = 1.68–3.43), single tumor bladder cancer (OR  = 2.04, 95% CI  = 1.48–2.82) and smaller tumor size bladder cancer (OR  = 2.10, 95% CI  = 1.51–2.92). The expression of NFKB1 mRNA in bladder cancer tissues with homozygous insertion genotype was higher than that with deletion allele. Conclusions: In conclusion, the -94 ins/del ATTG polymorphism in NFKB1 promoter may contribute to the etiology of bladder cancer in the Chinese population. [ABSTRACT FROM AUTHOR]

Objective: Activated nuclear factor-κB is associated with the pathogenesis of numerous malignancies, including renal cell carcinoma (RCC). This study aimed to clarify the influence of a common insertion/deletion polymorphism (-94 ins/del ATTG, rs28362491) in the NFKB1 promoter on RCC susceptibility. Methods: We genotyped the NFKB1 -94 ins/del ATTG promoter polymorphism by the TaqMan method and assessed the association with RCC risk, clinicopathological parameters in a case-control study of 1,027 cases and 1,094 controls. Results: The genotype frequencies were significantly different between RCC cases and controls (p = 0.046). Compared with individuals carrying the ins/del + del/del genotypes, those with the ins/ins genotype had an increased RCC risk [p = 0.036, adjusted odds ratio (OR) = 1.23, 95% confidence interval (CI) = 1.02-1.48], particularly in the subgroup of younger age (p = 0.005, adjusted OR = 1.42, 95% CI = 1.11-1.83) and never smokers (p = 0.013, adjusted OR = 1.34, 95% CI = 1.07-1.69). Furthermore, the polymorphism was significantly associated with the risk of developing localized stage RCC (p = 0.020, OR = 1.26, 95% CI = 1.04-1.53). Conclusions: The functional NFKB1 promoter polymorphism is associated with an increased risk of RCC. © 2012 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Much evidence show that over-expression of epidermal growth factor receptor (EGFR) plays an important role in regulating carcinogenesis. Genetic variations in 3′ untranslated region (3′UTR) of gene have been reported to affect gene expression by interfering with microRNAs (miRNAs), which are thought to function as either tumour suppressors or oncogenes by binding to their target mRNA. In this study, we investigated the association between the EGFR 3′UTR 774T>C polymorphism and bladder cancer risk. We used the TaqMan technology to genotype this genetic variant in a hospital-based case–control study of 908 bladder cancer patients and 1239 controls in a Chinese population. We found that the 774CC genotype was associated with a statistically significantly increased risk of bladder cancer [adjusted odds ratio = 1.29, 95% confidence interval = 1.05–1.58], compared with the 774TT/TC genotype, and this increased risk was more pronounced among subgroups of age > 65 years, non-smokers and patients’ tumour invasive stage. Furthermore, luciferase assays in T24 cell showed that EGFR 3′UTR 774 T to C substitution could increase the expression of EGFR, which was consistent with the association study finding. Additionally, we also provide evidence that 774T>C polymorphism increasing EGFR expression was not regulated by hsa-miR-214 binding. These findings suggested that EGFR 3′UTR 774T>C polymorphism may contribute to susceptibility to bladder cancer. [ABSTRACT FROM PUBLISHER]

The DNA repair gene Ku70 plays a key role in the DNA double-strand breaks (DSBs) repair system. Defects in DSBs repair capacity can lead to genomic instability. We hypothesized that the Ku70 A-31G polymorphism (rs132770) was associated with the risk of renal cell carcinoma (RCC). In a hospital-based case-control study of 620 RCC patients and 623 cancer-free controls frequency matched by age and sex, we genotyped the functional polymorphism Ku70 A-31G (rs132770). Thirty-eight normal renal tissue samples with different genotypes were tested to estimate the Ku70 mRNA expression by real-time quantitative reverse transcription. Compared with the GG genotype, the GA and GA/AA genotypes had a significantly decreased risk of RCC [adjusted odds ratio (OR)=0.62, 95% confidence interval (CI)=0.44-0.87 for GA, and OR=0.62, 95% CI=0.45-0.86 for GA/AA]. The in vivo experiments with normal renal tissues revealed that a statistically significantly higher Ku70 mRNA expression was identified in samples with GA/AA genotypes compared with those with GG genotypes ( p=0.001). These results suggested that the Ku70 A-31G polymorphism is involved in the etiology of RCC and, thus, may be a marker for genetic susceptibility to RCC in the Chinese populations. [ABSTRACT FROM AUTHOR]

A recent genome-wide association study of renal cell carcinoma (RCC) in European population has identified genetic variants in the regions of 2p21 (rs7579899), 11q13.3 (rs7105934) and 12q24.31 (rs4765623) conferred susceptibility to RCC. In our study, we assessed whether these polymorphisms are also associated with RCC risk in a Chinese population. We genotyped these polymorphisms using TaqMan method and assessed their associations with RCC risk in a case–control study of 710 patients with histologically confirmed RCC and 760 cancer-free controls. Normal renal tissues adjacent to tumors were used to evaluate the functional consequences of these polymorphisms. We found that rs7105934 was significantly associated with reduced RCC risk [adjusted odds ratio (OR) = 0.67, 95% confidence intervals (CIs) = 0.47–0.95, GA+AA versus GG], particularly among subgroups of normal-weight individuals (OR = 0.51, 95%CI = 0.29–0.88), never-smokers (OR = 0.53, 95%CI = 0.33–0.85) and non-drinkers (OR = 0.57, 95%CI = 0.370.87). Furthermore, the rs7105934 GA genotype was associated with lower levels of CCND1 mRNA compared with GG genotype, although this association was only marginally significant (P = 0.055). No significant association between rs7579899 or rs7105934 and RCC risk was observed. Our results suggest that rs7105934 on 11q13.3 may confer susceptibility to RCC in our population. Large population-based prospective and functional studies are required to validate the associations between these loci and RCC risk. [ABSTRACT FROM PUBLISHER]

Interleukin-10 (IL-10) is a multifunctional cytokine with both immunosuppressive and anti-angiogenic properties and play an important role in the pathogenesis of cancer. IL-10-1082A>G polymorphism is the most extensively studied polymorphism in the IL-10 gene in cancer susceptibility. To date, a number of case–control studies were conducted to investigate the association between IL-10-1082A>G polymorphism and cancer risk in humans. However, the association between the IL-10-1082A>G polymorphism and cancer risk is still ambiguous. In an effort to solve this controversy, we performed a meta-analysis based on 61 case–control studies, including 14 499 cancer cases and 16 967 controls. We used odds ratios (ORs) with 95% confidence intervals (CIs) to assess the strength of the association. In the stratified analyses by specific cancer type, increased risk was found in lung cancer (OR = 3.16, 95% CI = 1.16–8.63 for GA versus AA; OR = 2.07, 95% CI = 1.16–3.70 for GG versus AA; OR = 3.17, 95% CI = 1.31–7.68 for GA/GG versus AA) and non-Hodgkin’s lymphoma (OR = 1.18, 95% CI = 1.02–1.36 for GA versus AA; OR = 1.17, 95% CI = 1.02–1.35 for GA/GG versus AA). The meta-analysis also indicated that the variant genotypes were associated with a moderately increased risk in Asians in all genetic models (OR = 1.80, 95% CI = 1.17–2.76 for GA versus AA; OR = 3.32, 95% CI = 1.62–6.82 for GG versus AA; OR = 1.67, 95% CI = 1.07–2.60 for GA/GG versus AA; OR= 2.93, 95% CI = 1.43–6.03 for GG versus AA/GA). The meta-analysis suggested that the IL-10-1082A>G polymorphism was associated with increased risk of cancer in Asians and lung cancer and non-Hodgkin’s lymphoma. To draw comprehensive and true conclusions, more researches with larger numbers of worldwide participants are needed to examine associations between IL-10-1082A>G polymorphism and cancer risk. [ABSTRACT FROM PUBLISHER]

Purpose: Accumulating evidences implicate the selenium-containing cytosolic glutathione peroxidase, GPx- 1, as a determinant of cancer risk and a mediator of the chemopreventive properties of selenium. Since the identification of a well-characterized functional polymorphism named Pro198Leu (rs1050450 C>T) in GPx- 1, abundant studies have evaluated the association between Pro198Leu polymorphism and tumor risk in diverse population. But, the available results are conflicting. Methods: To derive a more precise estimation, we performed a meta-analysis based on 14,372 cases with different tumor types and 18,081 controls from 31 published case-control studies. Published literature from PubMed was retrieved. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were calculated to estimate the strength of the association. Results: Overall, the results indicated that individuals who carried variant Leu allele (Pro/Leu and Leu/Leu) were associated with an increased cancer risk [odds ratio (OR) = 1.12, 95% confidence interval (CI) = 1.02-1.23] in a dominant genetic model. In further subgroup analyses, the increased risk of cancer was observed in subgroup of Asians and sample size more than 500 subjects. Conclusion: These results suggest that the GPx- 1 Pro198Leo polymorphism contributes to cancer susceptibility through a disturbed antioxidant balance. [ABSTRACT FROM AUTHOR]

Abstract: Caspase-8 (CASP8) plays a key role in apoptosis. We examined by genotyping whether the −652 six-nucleotide insertion-deletion (6N ins/del) polymorphism in the CASP8 promoter region was associated with prostate cancer risk in a hospital-based case-control study of 406 Chinese prostate cancer patients and 408 age-matched cancerfree controls. Additionally, 23 prostate cancer tissues were analyzed for CASP8 mRNA expression. We found a significantly decreased prostate cancer risk for the 6N ins/del genotype [adjusted odds ratio (OR)=0.68; 95% confidence interval (CI)=0.51-0.92] and del/del genotype (OR=0.34; 95%CI=0.19-0.63) compared with the ins/ins genotype. The 6N del allele was associated dose-dependently with decreased prostate cancer risk (P trend = 0.001). RT-PCR showed that individuals with the 6N del allele had lower CASP8 mRNA levels than those with the ins/ins genotype (P = 0.024). These findings suggested that the CASP8-652 6N ins/del polymorphism may affect the susceptibility to prostate cancer and reduce prostate cancer risk among Chinese men. [Copyright &y& Elsevier]

DNA damaged by exposure to exogenous and endogenous carcinogens could be removed effectively by the base excision repair pathway, in which the XRCC1, APE1, and ADPRT genes play a key role. Genetic variations in these important genes may alter repair function and contribute to cancer risk. We hypothesized that XRCC1, APE1, and ADPRT polymorphisms are associated with risk of bladder cancer. In a hospital-based case-control study of 234 patients with bladder cancer and 253 cancer-free controls, we genotyped the XRCC1-77T>C, Arg194Trp, Arg280His, Arg399Gln, APE1-656T>G, Asp148Glu, ADPRT−442G>A, and Val762Ala polymorphisms using polymerase chain reaction–restriction fragment length polymorphism method. We found an increased risk of bladder cancer associated with the XRCC1 194Trp/Trp and 280Arg/His genotypes (adjusted odds ratio = 3.90, 95% confidence interval = 1.69–8.98 for 194Trp/Trp and 2.53, 1.67–3.83 for 280Arg/His) compared with the 194Arg/Arg and 280Arg/Arg genotypes, respectively. In contrast, the APE1-656GG genotype was associated with a decreased risk of bladder cancer (0.57, 0.33–0.98) compared with the TT genotype. When we evaluated these eight polymorphisms together, we found that the combined genotypes with 9–13 variant (risk) alleles were associated with an increased risk of bladder cancer (2.25, 1.48–3.40) compared with those with 3–8 variants. These findings suggest that the XRCC1 and APE1 polymorphisms may contribute to susceptibility to bladder cancer. Larger studies are warranted to verify these findings. [ABSTRACT FROM AUTHOR]

Background:Cytochrome P450 1A1 (CYP1A1) is a member of the CYP1 family, which is a key enzyme in the metabolism of many endogenous substrates and exogenous carcinogens. To date, many studies have examined the association between CYP1A1 MspI and Ile462Val polymorphisms and cancer risk in various populations, but their results have been conflicting rather than consistent. Methods:To assess this relationship more precisely, a meta-analysis based on 198 publications was performed. Odds ratios (OR) and corresponding 95% confidence intervals (CIs) were used to assess the association. The statistical heterogeneity across studies was examined with a chi-square-based Q-test. Results:Overall, a significant elevated risk of cancer was associated with CYP1A1 MspI and Ile462Val polymorphisms for all genetic models studied. Further stratified analysis by cancer types revealed that the MspI polymorphism may increase the risk of lung cancer and cervical cancer whereas the Ile462Val polymorphism may contribute to a higher risk of lung cancer, leukemia, esophageal carcinoma, and prostate cancer. In the subgroup analysis by ethnicity, obvious associations were found in the Asian population for the MspI polymorphism while an increased risk of cancer was observed in Asians and Caucasians for the Ile462Val polymorphism. Conclusions:The results of this meta-analysis suggest that CYP1A1 MspI and Ile462Val polymorphisms contribute to increased cancer susceptibility among Asians. Additional comprehensive system analyses are required to validate this association and other related polymorphisms. [ABSTRACT FROM AUTHOR]

Thrombospondin-1 (TSP-1) is a glycoprotein that plays a major role in bladder cancer. We investigated the relationship between the distribution of the TSP-1 -696 C/T polymorphism (rs2664139) and the clinical features of bladder cancer. TaqMan assay was used to determine the genotype among the 609 cases and 670 controls in a Chinese population. Logistic regression was used to assess the association between the polymorphism and bladder cancer risk. Compared with the CT/TT genotypes, the CC genotype was associated with a significantly increased risk of bladder cancer (adjusted odds ratio [OR] 1.43, 95% CI 1.01–2.04), which was more prominent among the male participants (OR 1.82, 95% CI 1.20–2.76). The polymorphism was associated with a higher risk of developing grade 3 (OR 1.84, 95% CI 1.00–3.36), multiple-tumor (OR 1.81, 95% CI 1.08–3.02), and large-tumor (OR 1.94, 95% CI 1.22–3.10) bladder cancers. These observations suggest that the TSP-1 -696 C/T polymorphism may contribute to bladder cancer susceptibility in the Chinese population. [ABSTRACT FROM AUTHOR]