Quantitative assessment of the influence of CYP1B1 polymorphisms and head and neck squamous cell carcinoma risk

The associations between CYP1B1 polymorphisms and head and neck squamous cell carcinoma (HNSCC) risk have been conflicting. We therefore performed a meta-analysis to derive a more precise relationship. Six published case–control studies were collected; odds ratios (ORs) with 95 % confidence interval (CI) were used to assess the association between CYP1B1 Leu432Val, Asn453Ser polymorphisms, and HNSCC risk. The Sensitivity analysis and publication bias also were performed to guarantee the statistical power. Overall, the pooled OR with 95 % CIs indicated that CYP1B1 Leu432Val polymorphism was significantly related with HNSCC risk (for Val vs. Leu: OR = 1.13, 95 % CI = 1.03–1.25, P?=?0.014, P _{heterogeneity}?=?0.141; for Val/Val vs. Leu/Leu: OR = 1.30, 95 % CI = 1.06–1.60, P?=?0.013, P _{heterogeneity}?=?0.253; for Val/Val vs. Leu/Leu + Leu/Val: OR = 1.23, 95 % CI = 1.05–1.46, P?=?0.013, P _{heterogeneity}?=?0.456). The similar results were also been found in succeeding analysis of HWE and stratified analysis of Caucasian population. Furthermore, no significant association between CYP1B1 Asn453Ser polymorphism and HNSCC risk was found in this meta-analysis. In conclusion, our meta-analysis demonstrates that CYP1B1 Leu432Val polymorphism may be a risk factor for developing HNSCC.     

TGFβ1 Leu10Pro polymorphism contributes to the development of prostate cancer: evidence from a meta-analysis

Transforming growth factor-β1 (TGFβ1) plays a significant role in regulating cellular proliferation and apoptosis. A large number of studies related to the association between TGFβ1 Leu10Pro polymorphism and prostate cancer (PC) risk, but get conflicting results. We performed a meta-analysis based on six studies, assessing the strength of the association using odds ratios (OR) with 95 % confidence intervals (CI). Overall, our evidence has indicated that TGFβ1 Leu10Pro polymorphism had significantly increased PC risk in the allele comparison model (OR?=?1.081, 95 % CI?=?1.003–1.165, P _{heterogeneity}?=?0.141, P?=?0.041). In the stratified analysis by ethnicity, the same results were found among Caucasians (for heterozygote model, OR?=?1.741, 95 % CI?=?1.004–3.020, P _{heterogeneity}?=?0.000, P?=?0.049; recessive model, OR?=?1.339, 95 % CI?=?1.045–1.717, P _{heterogeneity}?=?0.020, P?=?0.021; allele comparison model, OR?=?1.091, 95 % CI?=?1.005–1.184, P _{heterogeneity}?=?0.048, P?=?0.037). In conclusion, this meta-analysis suggested that TGFβ1 Leu10Pro polymorphism contributed to the development of PC. A well-designed and larger study is still required to evaluate this polymorphism and PC risk.     

Cytochrome P450 1B1 polymorphisms and risk of renal cell carcinoma in men

The cytochrome P450 1B1 (CYP1B1) enzyme activates xenobiotics to reactive forms as well as convert estradiol to 4-hydroxy-estradiol that has been shown to play a role in the carcinogenesis process of the kidney in male but not female animals. Prior reports show polymorphic variants of CYP1B1 to alter catalytic activity, and thus, we hypothesize that polymorphisms of the CYP1B1 gene are involved in the malignant transformation of the renal cell in men. The genetic distributions of five CYP1B1 polymorphisms were analyzed by polymerase chain reaction–restriction fragment length polymorphism in 480 normal healthy subjects and 403 sporadic renal cell carcinoma cases. All subjects were Caucasian men. The sites evaluated were codons 48 (C?→?G, Arg?→?Gly, rs10012), 119 (G?→?T, Ala?→?Ser, rs1056827), 432 (C?→?G, Leu?→?Val, rs1056836), 449 (C?→?T, Asp, rs1056837), and 453 (A?→?G, Asn?→?Ser, rs1800440). A trend was demonstrated for the 432 Val/Val (χ2, P?=?0.06) and 449 T/T (χ2, P?=?0.1) genotypes to play a protective role against renal cancer. Odds ratio (95 % confidence interval) for Val/Val compared to Leu/Leu at codon 432 was 0.65 (0.44–0.95) and T/T compared to C/C at codon 449 was 0.67 (0.45–0.99). Codons 432 and 449 were observed to be linked (D?=?0.24), and haplotype involving 432 Val and 449 T was significantly reduced in cancer cases (P?=?0.04). No association was found, however, when analyzing polymorphic sites with clinical stage of cancer. These results demonstrate polymorphisms of CYP1B1 to be associated with renal carcinogenesis and are of importance in understanding their role in the pathogenesis of renal cell carcinoma.     

Catechol-O-methyltransferase Val158Met polymorphism and breast cancer risk in Asian population

The association between the polymorphism of catechol-O-methyltransferase (COMT) Val158Met and breast cancer risk is still inconclusive. We performed a meta-analysis to derive a more precise estimation of the relationship. A total of 18 studies including 5,175 cases and 6,463 controls were involved in this meta-analysis. When all studies were pooled into the meta-analysis, no significantly elevated breast cancer risk was associated with all genetic models (for additive model: OR?=?1.273, 95 % CI?=?0.947–1.711, P _{heterogeneity}?=?0.000; P?=?0.110; for dominant model: OR?=?1.080, 95 % CI?=?0.945–1.234, P _{heterogeneity}?=?0.001; P?=?0.259; for recessive model: OR?=?1.242, 95 % CI?=?0.941–1.641, P _{heterogeneity}?=?0.000; P?=?0.126; for allele comparison model: OR?=?1.096, 95 % CI?=?0.976–1.230, P _{heterogeneity}?=?0.000; P?=?0.121). In the subgroup analysis by controls source, the same results were found in all genetic models. In summary, this meta-analysis suggests that the COMT Val158Met polymorphism is not a risk factor for breast cancer development. However, large sample and representative population-based studies with homogeneous breast cancer patients and well-matched controls are warranted to confirm this finding.     

Quantitative synthesis of the association between the cytochrome P450 1A1 Ile462Val polymorphism and prostate cancer risk

The association between the cytochrome P450 1A1 (CYP1A1) Ile462Val polymorphism and prostate cancer risk remains inconclusive owing to the conflicting findings from previous studies. To get a more precise estimate of the possible association, we performed the present meta-analysis. We searched the PUBMED, EMBASE, and Wanfang databases for the studies which met the inclusion criteria. The pooled odds ratio (OR) with corresponding 95 % confidence interval (95 % CI) was used to estimate the association between CYP1A1 Ile462Val polymorphism and prostate cancer risk. A total of 13 studies with 2,350 cases and 2,992 controls were included in the meta-analysis. The results indicated that there was an obvious association between CYP1A1 Ile462Val polymorphism and increased risk of prostate cancer (for Val versus Ile: OR?=?1.27, 95 % CI 1.13–1.43, P?<?0.001; for ValVal versus IleIle: OR?=?1.51, 95 % CI 1.14–2.01, P?=?0.004; for ValVal?+?ValIle versus IleIle: OR?=?1.31, 95 % CI 1.14–1.51, P?<?0.001; for ValVal versus IleIle + ValIle: OR?=?1.38, 95 % CI 1.05–1.81, P?=?0.020). Subgroup analyses by ethnicity suggested that CYP1A1 Ile462Val polymorphism was associated with prostate cancer risk in Asians but not in Caucasians. This meta-analysis suggests that there is an association between CYP1A1 Ile462Val polymorphism and increased risk of prostate cancer. More studies with large sample are needed to further assess the association in Caucasians.     

NAD(P)H: quinone oxidoreductase 1 (NQO1) C609T polymorphism and lung cancer risk: a meta-analysis

No clear consensus has been reached on the NAD(P)H: quinone oxidoreductase 1 (NQO1) gene C609T polymorphism and lung cancer risk. We performed a meta-analysis to summarize the possible association. We conducted a computer retrieval of PubMed and Embase databases prior to May 2013. References of retrieved articles were also screened. The fixed-effects model and the random-effects model were applied for dichotomous outcomes to combine the results of the individual studies. According to the inclusion criteria, 25 articles (32 studies) were finally included. There was no statistical association between C609T polymorphism and lung cancer risk in overall, East Asians, African Americans, or Hispanics. In Caucasians, a significant association was found in allele comparison model (T vs. C) (P?=?0.04, OR?=?1.09, 95% CI 1.00–1.19, P _{heterogeneity}?=?0.24, fixed-effects model). In the subgroup of squamous cell carcinoma, a borderline significance could be found in the dominant genetic model (TT?+?CT vs. CC) (P?=?0.05, OR?=?1.20, 95% CI 1.00–1.43, P _{heterogeneity}?=?0.65, fixed-effects model). Significant association could also be found in allele comparison (T vs. C) (P?=?0.03, OR?=?1.21, 95% CI 1.01–1.44, P _{heterogeneity}?=?0.68, fixed-effects model). In the subgroup of small cell lung cancer risk, significant association were found in allele comparison (T vs. C) (P?=?0.03, OR?=?1.68, 95%CI 1.05–2.68, P _{heterogeneity}?=?0.10, random-effects model) and in the homozygote comparison (TT vs. CC) (P?=?0.02, OR?=?2.79, 95% CI 1.14–6.85, P _{heterogeneity}?=?0.72, fixed-effects model). No association was observed in adenocarcinoma subgroup. Our study suggested that NQO1 C609T polymorphism might associate with lung cancer risk in Caucasians. This polymorphism might also associate with squamous cell carcinoma and small cell lung cancer risk.     

No association between CYP1B1 Val432Leu polymorphism and breast cancer risk: a meta-analysis involving 40,303 subjects

Breast cancer is the most common cancer in women. To date, many publications have evaluated the association between Cytochrome P450 1B1 (CYP1B1) Val432Leu polymorphism and breast cancer risk. However, the results remain inconclusive. In order to derive a more precise estimation of the association, a meta-analysis was performed in this study. By searching Medline, Pubmed, and ISI Web of Knowledge databases, 26 studies including 19,028 cases and 21,275 controls were collected for CYP1B1 Val432Leu polymorphism. Crude ORs with 95% CIs were used to assess the strength of association between CYP1B1 Val432Leu polymorphism and breast cancer risk. The pooled ORs were performed for codominant model, dominant model, and recessive model, respectively. Overall, no significant associations between CYP1B1 Val432Leu polymorphism and breast cancer susceptibility were found for Val/Val versus Leu/Leu (OR = 0.98; 95% CI: 0.90–1.06), Val/Leu versus Leu/Leu (OR = 1.01; 95% CI: 0.93–1.09), Val/Val + Val/Leu versus Leu/Leu (OR = 1.00; 95% CI: 0.93–1.08) and Val/Val versus Val/Leu + Leu/Leu (OR = 0.96; 95% CI: 0.91–1.01). In the stratified analysis by ethnicity, menopausal status and sources of controls, significant associations were still not observed in all genetic models. In conclusion, this meta-analysis provides strong evidence that CYP1B1 Val432Leu polymorphism is not associated with breast cancer risk.     

CYP3A4*1B polymorphism and cancer risk: A HuGE review and meta-analysis

CYP450 3A4 (CYP3A4), encoded by the CYP3A4 gene, is a major enzyme catalyzing the metabolism of both endogenous and exogenous agents that may play a role in the etiology of carcinogenesis. Several potentially functional polymorphisms of the CYP3A4 gene have been implicated in cancer risk, but individually published studies have shown inconclusive results. The aim of this Human Genome Epidemiology (HuGE) review and meta-analysis was to investigate the association between CYP3A4*1B (rs2740574 A?>?G) polymorphism and cancer risk. Eleven studies were included with a total of 3,810 cancer patients and 3,173 healthy controls. We found that the G allele and GG genotype of CYP3A4*1B polymorphism were associated with increased risk of cancers using the fixed effects model (allele model: odds ratio (OR)?=?1.24, 95 %CI: 1.09–1.42, P?=?0.001; recessive model: OR?=?1.77, 95 %CI: 1.30–2.41, P?<?0.001; homozygous model: OR?=?1.72, 95 %CI: 1.19–2.47, P?=?0.004). Subgroup analyses by cancer type showed that the G allele and G carrier (AG?+?GG) of CYP3A4*1B polymorphism had significant associations with increased risk of prostate cancer, but not with breast cancer, leukemia, or other cancers. With further subgroup analysis based on different ethnicities, the results indicated that the GG genotype of CYP3A4*1B polymorphism might increase the risk of cancer among African populations. However, similar associations were not observed among Caucasian and Asian populations. Results from the current meta-analysis indicate that the G allele and GG genotype of CYP3A4*1B polymorphism might be associated with increased cancer risk, especially for prostate cancer among African populations.     

CYP1B1 基因 Leu432Val 位点多态性与头颈癌易感性的 Meta 分析

目的：运用Meta分析方法研究CYPlBl基因Leu432Val位点多态性与头颈癌易感性的发生风险。方法：检索CNKI和PubMed数据库中有关CYPlBl基因Leu432Val位点多态性与头颈癌易感性关联研究的文献。对符合纳入标准的文献进行资料提取后，以OR值和95％可信区间为效应指标，应用STATA11．0软件进行Meta分析，并对发表偏倚进行检测。结果：纳入5个对照研究，共计1580例头颈癌患者和2076例正常对照人群。Meta分析结果显示，总人群中，CYPlBl基因Leu432Val位点多态性与头颈癌易感性之间有显著关联（ValVS．Leu：OR=1．13，95％CI=1．03—1．25，P=0．014；Val／ValV8．Leu／Leu：OR=1．30。95％CI=1．06—1．60，P=0．013；Val／ValVS．Leu／Leu＋Leu／Val：OR=1．23，95％CI：1．05—1．46，P=0．013）。在针对种族的亚组分析中，发现CYPlBl基因Leu432Val位点多态性可能会增加欧洲人群发生头颈癌的风险。结论：CYPlBl基因Leu432Val位点多态性可能是增加欧洲人群发生头颈癌易感性的危险因素。     

Association between GSTP1 Ile105Val polymorphism and glioma risk: A systematic review and meta-analysis

Glutathione S-transferase P1 (GSTP1) gene Ile105Val polymorphism has been suggested to be involved in the development of glioma. However, the results from the studies regarding the association between GSTP1 Ile105Val polymorphism and glioma risk have been inconsistent. Thus, we performed a meta-analysis to investigate this association. Pooled odds ratios (ORs) with 95 % confidence intervals (95 %CIs) were calculated using random or fixed effects model. Nine studies with 2,078 cases and 3,970 controls were finally included into this meta-analysis. The results suggested there was no association between GSTP1 Ile105Val polymorphism and glioma risk under recessive model (OR?=?1.138, 95 %CI?=?0.966–1.341, P _{heterogeneity}?=?0.088, P?=?0.123). Subgroup analyses by ethnicity showed there was also no association between GSTP1 Ile105Val polymorphism and glioma risk in mixed populations under recessive model (OR?=?1.199, 95 %CI?=?0.928–1.549, P _{heterogeneity}?=?0.060, P?=?0.166) and Caucasian populations(OR?=?1.097, 95 %CI?=?0.885–1.360, P _{heterogeneity}?=?0.186, P?=?0.398). In conclusion, the meta-analysis suggests that there is no association between GSTP1 Ile105Val polymorphism and glioma risk. However, more well-designed and larger studies are needed to further assess this association.     

Regulator of telomere elongation helicase 1 (RTEL1) rs6010620 polymorphism contribute to increased risk of glioma

Regulator of telomere elongation helicase 1 (RTEL1) is critical for genome stability and tumor avoidance. Many studies have reported the associations of RTEL1 rs6010620 with glioma risk, but individually published results were inconclusive. This meta-analysis was performed to quantitatively summarize the evidence for such a relationship. The PubMed, Embase, and Web of Science were systematically searched to identify relevant studies. The odds ratio (OR) and 95 % confidence interval (95 % CI) were computed to estimate the strength of the association using a fixed or random effects model. Ten studies were eligible for meta-analysis including data on glioma with 6,490 cases and 9,288 controls. Overall, there was a significant association between RTEL1 rs6010620 polymorphism and glioma risk in all four genetic models (GG vs. AA: OR?=?1.87, 95 % CI?=?1.60–2.18, P _{heterogeneity} ?=?0.552; GA vs. AA: OR?=?1.30, 95 % CI?=?1.16–1.46, P _{heterogeneity} ?=?0.495; dominant model—GG?+?GA vs. AA: OR?=?1.46, 95 % CI?=?1.31–1.63, P _{heterogeneity} ?=?0.528; recessive model—GG vs. GA?+?AA: OR?=?1.36, 95 % CI?=?1.27–1.46, P _{heterogeneity} ?=?0.093). Subgroup analyses by ethnicity showed that RTEL1 rs6010620 polymorphism resulted in a higher risk of glioma among both Asians and Caucasians. In the stratified analysis by ethnicity and source of controls, significantly increased risk was observed for Asians and Europeans in all genetic models, population-based studies in all genetic models, and hospital-based studies in three genetic models (heterozygote comparison, homozygote comparison, and dominant model). Our meta-analysis suggested that RTEL1 rs6010620 polymorphism is likely to be associated with increased glioma risk, which lends further biological plausibility to these findings.     

Genetic polymorphism of DNA methyltransferase 3B 149 C>T and risk of colorectal cancer: a meta-analysis

Numerous studies have investigated the risk of colorectal cancer (CRC) associated with the polymorphism of DNA methyltransferase 3B (DNMT3B) 149 C>T, but results have been inconsistent. We performed this meta-analysis to drive a more precise estimation of the association between this polymorphism and risk of CRC. A comprehensive search was conducted to identify all case–control studies of the ?149C>T polymorphism of DNMT3B and CRC risk. A total of seven eligible studies, including 2,666 cases and 4,022 controls, relating the DNMT3B polymorphism of ?149C>T to the risk of CRC were identified. It suggested no significant associations between ?149C>T polymorphism of DNMT3B gene and the risk of developing CRC in the recessive, dominant, and co-dominant models (for CC versus TT: OR?=?0.90, 95 % CI?=?0.90–1.25, P _{heterogeneity}?=?0.37; for recessive model: OR?=?0.54, 95 % CI?=?0.28–1.04, P _{heterogeneity}?=?0.00001; for dominant model: OR?=?1.07, 95% CI?=?0.93–1.23, P _{heterogeneity}?=?0.83; and for C allele versus T allele: OR?=?0.70, 95 % CI?=?0.43–1.13, P _{heterogeneity}?=?0.00001). In the subgroup analysis, there is no significant associations were also found in European populations (for CC versus TT: OR?=?1.09, 95 % CI?=?0.92–1.30, P _{heterogeneity}?=?0.88; for recessive model: OR?=?1.00, 95 % CI?=?0.88–1.13, P _{heterogeneity}?=?0.14; for dominant model: OR?=?1.50, 95 % CI?=?0.89–2.54, P _{heterogeneity}?=?0.00001; and for C allele versus T allele: OR?=?0.70, 95 % CI?=?0.38–1.28, P _{heterogeneity}?=?0.00001). In conclusion, no significant association was found between the ?149C>T polymorphisms in DNMT3B and CRC susceptibility.     

Association of four polymorphisms in the death receptor 4 gene with cancer risk: an updated meta-analysis

To date, no scientific consensus about the associations of DR4 C626G, A683C, A1322G, and G422A polymorphisms with cancer risk has been reached. Therefore, we conducted a meta-analysis to assess the associations. This meta-analysis involved 16 studies, of which 15 (4,261 cases and 4,598 controls) described C626G genotypes, 8 (2,898 cases and 3,135 controls) described A683C genotypes, 6 (1,564 cases and 1,673 controls) described A1322G genotypes, and 5 (584 cases and 607 controls) described A683C genotypes. We associated all the four polymorphisms with cancer risk. The C626G polymorphism was associated with slightly elevated cancer risk in recession model comparison [odds ratio (OR)?=?1.12, 95 % confidence interval (CI)?=?1.00–1.26, P _{heterogeneity}?=?0.425]. In the subgroup analysis by cancer type, significantly elevated cancer risks were found among groups with lung cancer for heterozygote comparison (OR?=?1.76, 95 % CI?=?1.00–3.09, P _{heterogeneity}?=?0.863). The A1322G polymorphism was associated with significantly elevated cancer risk in the different models (heterozygote comparison: OR?=?1.21, 95 % CI?=?1.00–1.46, P _{heterogeneity}?=?0.347; dominant model: OR?=?1.21, 95 % CI?=?1.01–1.46, P _{heterogeneity}?=?0.189; allele model comparison for G allele vs. A allele: OR?=?1.17, 95 % CI?=?1.02–1.35, P _{heterogeneity}?=?0.173). The A683C and G422A polymorphisms were not associated with cancer risk in all genetic models. The C626G and A1322G polymorphisms are associated with increased cancer risk, but the A683C polymorphism is rarely associated with cancer risk.     

HIF-1α P582S and A588T polymorphisms and digestive system cancer risk—a meta-analysis

Hypoxia-inducible factor-1 (HIF-1) influences cancer progression and metastasis through various mechanisms, and HIF-1α polymorphisms are reportedly associated with many cancers; however, the associations of HIF-1α P582S and A588T polymorphisms with the risk of digestive system cancer remain inconclusive. To understand the role of HIF-1α P582S and A588T genotypes in digestive cancer development, we conducted a comprehensive meta-analysis involving 1,517 cases and 3,740 controls. Overall, the P582S polymorphism was not significantly associated with digestive system cancers in all genotypes. By contrast, the A588T polymorphism was significantly associated with digestive system cancers in the dominant model (TT/AT vs. AA: OR?=?3.17, 95 % CI: 1.21, 8.25; P _{heterogeneity}?<?0.001). In subgroup analysis for cancer types, the two polymorphisms were only associated with increased risk of pancreatic cancer (P582S: SS vs. PP: OR?=?2.51, 95 % CI: 1.31, 4.81; SS vs. PP/PS: OR?=?8.73, 95 % CI: 1.33, 57.1; A588T: TT vs. AA: OR?=?9.30, 95 % CI: 1.12, 77.6; P _{heterogeneity}?=?0.478; TT vs. AA/AT: OR?=?3.14, 95 % CI: 1.99, 4.97; P _{heterogeneity}?=?0.098; TT/AT vs. AA: OR?=?8.65, 95 % CI: 1.05, 71.6; P _{heterogeneity}?=?0.418). According to the source of ethnicity, the P582S and the A588T polymorphisms are both significantly associated with an increased risk of cancer among Caucasians in the homozygote model (SS vs. PP: OR?=?2.41, 95 % CI: 1.24, 4.691; P _{heterogeneity}?=?0.010; TT vs. AA: OR?=?98.6, 95 % CI: 4.37, 2,224; P _{heterogeneity}?=?0.040) and the recessive model (SS vs. PP/PS: OR?=?9.48, 95 % CI: 1.12, 80.3; P _{heterogeneity}?<?0.001; TT vs. AA/AT: OR?=?82.7, 95 % CI: 3.79, 1,802; P _{heterogeneity}?=?0.041). Our findings suggest that the HIF-1α A588T polymorphism is significantly associated with higher cancer risk and the P582S polymorphism is significantly associated with pancreatic cancer risk. Furthermore, the effect of both polymorphisms on digestive system cancer is more pronounced among Caucasians than that among Asians.     

Quantitative assessment of the association between CYP1A1 A4889G polymorphism and endometrial cancer risk

Cytochrome P450 1A1 (CYP1A1) A4889G polymorphism was supposed to be associated with endometrial cancer risk, but previous studies reported conflicting results. We therefore performed a meta-analysis of all relevant studies to get a comprehensive assessment of the association between CYP1A1 A4889G polymorphism and endometrial cancer risk. The pooled odds ratios (OR) with the corresponding 95 % confidence interval (95 % CI) was calculated to assess the association. Finally, ten studies with a total of 1,682 endometrial cancer cases and 2,510 controls were finally included into the meta-analysis. Meta-analysis of the total ten studies showed that CYP1A1 A4889G polymorphism was not associated with endometrial cancer risk (OR_{G versus A}?=?1.14, 95 % CI 0.83–1.57, P _OR?=?0.417; OR_{GG versus AA}?=?1.23, 95 % CI 0.70–2.18, P _OR?=?0.470; OR_{GG versus AA/AG}?=?1.03, 95 % CI 0.59–1.81, P _OR?=?0.919; OR_{GG/AG versus AA}?=?1.22, 95 % CI 0.82–1.81, P _OR?=?0.336). Subgroup analyses by ethnicity further showed that there was also no obvious association between CYP1A1 A4889G polymorphism and endometrial cancer risk in both Caucasians and Asians. Sensitivity analysis by excluding single study in turns showed that the pooled estimations were not stable. Therefore, evidence for currently available data suggests that CYP1A1 A4889G polymorphism is not associated with endometrial cancer risk. However, more studies with large number of participants are needed to further assess the association precisely.     

Assessment of the association between XRCC1 Arg399Gln polymorphism and glioma susceptibility

The Arg399Gln polymorphism, located in the region of the BRCT-I interaction domain of XRCC1, has been extensively explored in its function and association with glioma risk. However, these studies generated contradictory instead of conclusive results. A meta-analysis was performed to derive a more precise evaluation of the relationship between XRCC1 Arg399Gln polymorphism and glioma risk. We searched the PubMed, EMBASE, and Web of Science and extracted 12 eligible studies with 4,062 glioma cases and 5,302 glioma-free controls for this meta-analysis. The pooled odds ratios (ORs) and 95 % confidence intervals (CIs) were calculated to assess the strength of the association. In the overall analysis, we found that the XRCC1 Arg399Gln polymorphism was statistically associated with the risk of glioma (OR_{GG vs. AG + AA}?=?0.90, 95 % CI?=?0.84–0.97, P _{heterogeneity}?=?0.020; OR_{allele G vs. allele A}?=?0.96, 95 % CI?=?0.91–1.00, P _{heterogeneity}?=?0.110). We also observed significant association between this polymorphism and glioma risk in Asian populations. The results of the meta-analysis suggest a potential decreased susceptibility to glioma in association with the XRCC1 Arg399Gln polymorphism, especially in Asians. Yet, it is necessary to conduct future prospective explorations to gain a better insight into the impact of XRCC1 Arg399Gln polymorphism on glioma risk.     

Association between Cyclin D1 polymorphism and oral cancer susceptibility: a meta-analysis

Data from several case–control studies on the relation between the Cyclin D1 (CCND1) G870A polymorphism and oral cancer susceptibility implicated conflicting conclusions. Thus, a meta-analysis was performed to derive a more precise evaluation of the association. We searched PubMed and Embase for related studies that had been published in English and eight available studies were finally included in the meta-analysis. Odd ratios (ORs) and 95 % confidence intervals (CIs) were calculated for each study. Our meta-analysis suggested that CCND1 G870A polymorphism was not associated with oral cancer risk (OR _{AA vs. GG}?=?1.08, 95 % CI?=?0.90–1.30, P _{heterogeneity}?=?0.175; OR _{AA + GA vs. GG}?=?1.02, 95 % CI?=?0.91–1.14, P _{heterogeneity}?=?0.781; OR _{AA vs. GA + GG}?=?1.16, 95 % CI?=?0.98–1.36, P _{heterogeneity}?=?0.107; OR _{A vs. G}?=?1.05 95 % CI?=?0.96–1.15, P _{heterogeneity}?=?0.211; OR _{GA vs. GG}?=?0.94, 95 % CI?=?0.82–1.08, P _{heterogeneity}?=?0.935). However, in the subgroup analysis by ethnicity, possible significance among Asian groups was indicated in two genetic models (OR _{AA vs. GA + GG}?=?1.27, 95 % CI?=?1.05–1.54, P _{heterogeneity}?=?0.572; OR _{allele A vs. allele G}?=?1.11, 95 % CI?=?1.00–1.24, P _{heterogeneity}?=?0.211). Taken together, the meta-analysis revealed that CCND1 G870A polymorphism might be correlated with the susceptibility of oral cancer in Asians.     

Association of genetic variants of xenobiotic and estrogen metabolism pathway (CYP1A1 and CYP1B1) with gallbladder cancer susceptibility

Gallbladder carcinoma is a highly aggressive cancer with female predominance. Interindividual differences in the effectiveness of the activation/detoxification of environmental carcinogens and endogenous estrogens may play a crucial role in cancer susceptibility. The present study included 410 patients with carcinoma of the gallbladder (GBC) and 230 healthy subjects. This study examined association of CYP1A1-MspI, CYP1A1-Ile462Val, and CYP1B1-Val432Leu with GBC susceptibility. CYP1A1-MspI [CC] and CYP1A1-Ile462Val [iso/val] genotypes were found to be significantly associated with GBC (p?=?0.006 and p?=?0.03, respectively), as compared to healthy controls, while CYP1B1-Val432Leu was not associated with GBC. The CYP1A1 haplotype [C-val] showed a significant association with GBC (p?=?0.006). On stratification based on gender, the CYP1A1-MspI [CC] genotype showed an increased risk of GBC in females (p?=?0.018). In case-only analysis, tobacco users with CYP1A1-MspI [CT] genotypes were at a higher risk of GBC (p?=?0.008). Subdividing the GBC patients on the basis of gallstone status, the CYP1A1 haplotype [C-val] imparted a higher risk in patients without stones when compared to controls (p?=?0.001). The results remained significant even after applying Bonferroni correction. Multivariate analysis revealed an increased risk of CYP1A1 iso/val and val/val genotypes in GBC patients having BMI >25 (p?=?0.021). The CYP1A1 polymorphisms may confer increased risk of GBC, probably due to impaired xenobiotic or hormone metabolism through a gallstone-independent pathway.     

Genetic polymorphisms of cytochrome P450 19 and 1B1, alcohol use,and breast cancer risk in Korean women

A case-control study was performed to assess the potential influence of CYP19 Arg(264)Cys and CYP1B1 Leu(432)Val polymorphisms on breast cancer risk in a series of Korean breast cancer patients and controls. The results suggest that the CYP19 Arg(264)Cys polymorphism modifies breast cancer risk (OR=1.5, 95% CI=1.1-2.2), especially in association with alcohol consumption (P for interaction=0.04), whereas the CYP1B1 Leu(432)Val polymorphism appears to play no role here.