Coffee consumption and risk of colorectal cancer: a meta-analysis of case–control studies

A meta-analysis of case–control studies on coffee consumption and colorectal cancer risk was conducted. Twenty-four eligible studies published before May 2010 were identified, including a total of 14,846 cases of colorectal, colon or rectal cancer. Compared to non/occasional drinkers, the odds ratios (OR) for drinkers were 0.83 (95% CI 0.73–0.95) for colorectal, 0.93 (95% CI 0.81–1.07) for colon and 0.98 (95% CI 0.85–1.13) for rectal cancer, with significant heterogeneity among studies; the corresponding ORs for the increment of 1 cup/day were 0.94 (95% CI 0.91–0.98), 0.95 (95% CI 0.92–0.98), and 0.97 (95% CI 0.95–0.99). For the highest coffee drinkers, the ORs were 0.70 (95% CI 0.60–0.81) for colorectal cancer, 0.75 (95% CI 0.64–0.88) for colon cancer and 0.87 (95% CI 0.75–1.00) for rectal cancer, when compared to non/low drinkers. The results of this meta-analysis of case–control studies suggest a moderate favorable effect of coffee consumption on colorectal cancer risk. The reduced risk was consistent across study design (hospital vs. population based), geographic area, and various confounding factors considered. It may reflect a real protection but also partly or largely be due to reverse causation, i.e. decreased coffee consumption among cases following the onset of bowel symptoms.     

GH1 T1663A polymorphism and cancer risk: a meta-analysis of case–control studies

Many studies have demonstrated that the most common polymorphism (T1663A, rs2665802) in the promoter region of growth hormone 1 (GH1) gene might play an important role in cancer development and progression. This meta-analysis aims to investigate a more precise estimation of the relationship between GH1 T1663A polymorphism and cancer risk. We searched CISCOM, CINAHL, Web of Science, PubMed, Google Scholar, EBSCO, Cochrane Library, and CBM databases from inception through October 1st, 2013. Meta-analysis was performed using the STATA 12.0 software. Seven studies were included with a total of 4,018 cancer patients and 5,308 healthy controls. Our meta-analysis results revealed that GH1 T1663A polymorphism was associated with increased cancer risks. Subgroup analysis by cancer type showed significant associations between GH1 T1663A polymorphism and increased colorectal cancer risk, but there was no evidence of any association with breast cancer. Further subgroup analysis based on ethnicity indicated that GH1 T1663A polymorphism might increase cancer risks among Asian populations. However, no statistically significant association was found among Caucasian populations. Meta-regression analyses also suggested that cancer type and ethnicity may be the main sources of heterogeneity. No publication bias was detected in this meta-analysis. The present meta-analysis indicates that GH1 T1663A polymorphism may contribute to the risk of colorectal cancer, especially among Asian populations.     

Occupational exposure to pesticides and risk of hematopoietic cancers: meta-analysis of case–control studies

Objective In this study we conducted a meta-analysis of 13 case–control studies that examined the occurrence of hematopoietic cancers in pesticide related occupations in order to undertake a qualitative and quantitative evaluation of a possible relationship. Methods Pubmed databases were searched for case–control studies published between 1990 and 2005 investigating the relation between hematopoietic cancers and occupational exposure to pesticides. Fixed and random effect meta-analysis models were used depending on the presence of heterogeneity between studies. Results The overall meta-odds ratio obtained after pooling 44 ORs from 13 studies was 1.3 (95% CI: 1.3–1.5). We realized stratified analysis on three different types of hematopoietic cancers (non-Hodgkin lymphoma (NHL), leukemia and multiple myeloma). A significant increased risk of NHL was found (OR = 1.35; 95% CI = 1.2–1.5). Moreover, increased risks of Leukemia (OR = 1.35; 95% CI = 0.9–2) and multiple myeloma (OR = 1.16; 95% CI = 0.99–1.36) were also detected but these results were not statistically significant. Significant heterogeneity existed among the different studies and a publication bias was detected. Therefore, a meta-regression was carried out. Our results showed that a long period of exposure (more than 10 years) provided an increase in the risk of all hematopoietic cancers and for NHL by fractions of 2.18 (95% CI = 1.43–3.35) and 1.65 (95% CI = 1.08–2.51), respectively. Conclusions: The overall meta-odds ratio suggests that there is a significantly positive association between occupational exposure to pesticides and all hematopoietic cancers as well as NHL. A major limitation of our meta-analysis is the lack of sufficient data about exposure information and other risk factors for hematopoietic cancer (genetic predisposition, ethnic origin, immunodepression…). In addition, data concerning specific subtypes of hematopoietic cancers are often confusing. Thus, future epidemiological studies should undertake a major effort to assess the identity and the level of pesticides exposure and should control for the most likely potential confounders.     

Areca nut chewing and esophageal squamous-cell carcinoma risk in Asians: A meta-analysis of case–control studies

Purpose

This meta-anlaysis quantitatively assessed an overall independent association between areca nut chewing and esophageal squamous-cell carcinoma in Asians.

Methods

Studies (case–control and/or cohort) were identified by searching the PubMed, Medline, and Embase databases through 30 September, 2012, using the keywords o/esophageal squamous-cell carcinoma, o/esophageal cancer, chewing areca nut, betel quid without tobacco, Asia, and the reference lists of retrieved articles. Random-effects model was used to compute adjusted summary OR_RE for the main effect of areca nut chewing and additive (biological) interaction between areca nut chewing and tobacco smoking along with their corresponding 95 % confidence intervals (CI). To quantify the impact of between-study heterogeneity on adjusted main-effect summary OR_RE, Higgins’ H and I ² statistics along with their 95 % uncertainty intervals were used. Funnel plot and Egger’s test were used to evaluate publication bias.

Results

Meta-analysis of 12 case–control studies (2,836 cases; 9,553 controls) showed that areca nut chewing was significantly and independently associated with an increased risk of esophageal squamous-cell carcinoma (adjusted main-effect summary OR_RE = 3.05; 95 % CI 2.41, 3.87). Furthermore, pooled analysis of additive interaction between areca nut chewing and tobacco smoking reported by six of the included studies revealed manifold increased risk of esophageal squamous-cell carcinoma among those who indulged in both the practices compared with those who practiced none (adjusted additive interaction-effect summary OR_RE = 6.79; 95 % CI 4.71, 9.79). There was no significant publication bias (p = 0.289).

Conclusions

Areca nut chewing was significantly and independently associated with an increased risk of esophageal squamous-cell carcinoma in Asians. Additionally, individuals who indulged in both areca nut chewing and tobacco smoking had manifold increased risk of esophageal squamous-cell carcinoma. The efforts aimed at curtailing the addiction to areca nut chewing may contribute to lower the incidence of esophageal squamous-cell carcinoma and related mortality in Asians.     

Consumption of different types of meat and the risk of renal cancer: meta-analysis of case–control studies

Background Kidney cancers account for almost 2% of all cancers worldwide, with 150,000 new cases and 78,000 deaths from the disease occurring annually. An increase in the incidence of kidney neoplasm in western countries was noticed in the past few years. Between 1988 and 1992, the incidence of renal cancer per 100,000 person-year among males in USA, Norway, and France was 34.1, 9.00, and 16.10, respectively. Among females in the same countries, it was 5.70, 5.00, and 7.30, respectively. Although several individual case–control studies examined the association of meat intake and renal cancer risk, the results were inconsistent because of the insufficient statistical power of the individual studies. Therefore, the following meta-analysis was designed to help in clarifying the association. Methods Electronic search of MEDLINE, OVID, and PUBMED databases which have articles published between (1966 and 2006) was conducted to select studies for this meta-analysis. Statistical analysis Fixed and random-effects meta-analytical techniques were used to estimate the overall association between meat consumption and kidney cancer. Results Thirteen case–control studies were found. This meta-analysis supported a positive relationship between meat consumption and risk of renal cancer. Summary results indicated that there was from 20% to 22% higher risk of renal cancer among those in the highest relative to the lowest category of poultry and processed meat consumption. Consumption of all meat and red meat was associated with 27% and 30% higher risk, respectively. The increased risks were statistically significant. Conclusions Increased consumption of all meat, red meat, poultry, and processed meat is associated with an increase risk of kidney cancer. Reduction of meat consumption is an important approach to decreasing the incidence of kidney cancer in the general population. An erratum to this article is available at .     

Methylenetetrahydrofolate reductase polymorphisms and breast cancer risk in Chinese population: a meta-analysis of 22 case–control studies

The association between methylenetetrahydrofolate reductase (MTHFR) gene polymorphisms and breast cancer risk in the Chinese population has been widely reported, but results were inconsistent. In order to derive a more precise estimation of the relationship, a meta-analysis was performed. Eligible articles were identified through search of databases including Medline, PubMed, Web of Science, Embase, Chinese Biomedical Literature Database (CBM, Chinese), China National Knowledge Infrastructure (CNKI, Chinese), and Wangfang Database (Chinese). The association between the MTHFR polymorphism and breast cancer risk was conducted using odds ratios (ORs) and 95 % confidence intervals (95 % CIs). Finally, a total of 22 studies with 6,103 cases and 7,913 controls were included in our meta-analysis: 13 studies with 3,273 cases and 4,419 controls for C677T polymorphism and 9 studies with 2,830 cases and 3,494 controls for A1298C polymorphism. With regard to C677T polymorphism, significant association was found with breast cancer risk under three models (T vs. C: OR?=?1.12, 95 % CI?=?1.02–1.23, P?=?0.015; TT vs. CC: OR?=?1.35, 95 % CI?=?1.10–1.67, P?=?0.005; TT vs. CC/CT: OR?=?1.37, 95 % CI?=?1.11–1.70, P?=?0.004). There was no significant association found between A1298C polymorphism and breast cancer risk under all genetic models (C vs. A: OR?=?0.96, 95 % CI?=?0.89–1.03, P?=?0.268; CC vs. AA: OR?=?0.98, 95 % CI?=?0.77–1.26, P?=?0.899; AC vs. AA: OR?=?0.95, 95 % CI?=?0.88–1.02, P?=?0.174; CC vs. AC/AA: OR?=?1.00, 95 % CI?=?0.78–1.28, P?=?0.996, CC/AC vs. AA: OR?=?0.96, 95 % CI?=?0.89–1.02, P?=?0.196). In summary, during this meta-analysis, we found that MTHFR C677T polymorphism was significantly associated with breast cancer risk in the Chinese population. Meanwhile, MTHFR A1298C polymorphism was not associated with breast cancer risk in the Chinese population.     

Alcohol and endometrial cancer risk: a case–control study and a meta-analysis

To evaluate the association between alcohol consumption and endometrial cancer risk, we analyzed data from a hospital-based case–control study, conducted in Italy between 1992 and 2006, on 454 endometrial cancer cases and 908 controls, and performed a meta-analysis updated to October 2009. Compared to never alcohol drinkers, the odds ratio was 1.03 (95% confidence interval, CI, 0.76–1.41) for ≤7, 1.27 (95% CI 0.86–1.87) for 8–14, and 1.19 (95% CI 0.80–1.77) for ≥15 drinks/week, with no trend in risk. No association emerged for wine, beer, and spirit consumption analyzed separately. The meta-analysis included 20 case–control and seven cohort studies, for a total of 13,120 cases. Compared to non/low drinkers, the pooled relative risks for drinkers were 0.90 (95% CI 0.80–1.01) for case–control studies, 1.01 (95% CI 0.90–1.14) for cohort studies, and 0.95 (95% CI 0.88–1.03) overall, with no heterogeneity between study design (p = 0.156). The overall estimate for heavy versus non/low drinkers was 1.12 (95% CI 0.87–1.45). The results were consistent according to selected study characteristics, including geographic area, definition of alcohol drinkers, and type of controls in case–control studies. Our findings provide evidence that alcohol drinking is not associated with endometrial cancer risk, although a weak positive association for very high drinkers cannot be excluded.     

The role of calcium and vitamin D dietary intake on risk of colorectal cancer: systematic review and meta-analysis of case–control studies

Cancer Causes & Control - The aim of this study is to analyze the current evidence about the relationships between calcium/vitamin D and CRC based on case–control studies according to...     

Dietary folates and cancer risk in a network of case–control studies

BackgroundFolate deficiency leads to DNA damage and inadequate repair, caused by a decreased synthesis of thymidylate and purines. We analyzed the relationship between dietary folate intake and the risk of several cancers.Patients and methodsThe study is based on a network of case–control studies conducted in Italy and Switzerland in 1991–2009. The odds ratios (ORs) for dietary folate intake were estimated by multiple logistic regression models, adjusted for major identified confounding factors.ResultsFor a few cancer sites, we found a significant inverse relation, with ORs for an increment of 100 μg/day of dietary folate of 0.65 for oropharyngeal (1467 cases), 0.58 for esophageal (505 cases), 0.83 for colorectal (2390 cases), 0.72 for pancreatic (326 cases), 0.67 for laryngeal (851 cases) and 0.87 for breast (3034 cases) cancers. The risk estimates were below unity, although not significantly, for cancers of the endometrium (OR = 0.87, 454 cases), ovary (OR = 0.86, 1031 cases), prostate (OR = 0.91, 1468 cases) and kidney (OR = 0.88, 767 cases), and was 1.00 for stomach cancer (230 cases). No material heterogeneity was found in strata of sex, age, smoking and alcohol drinking.ConclusionsOur data support a real inverse association of dietary folate intake with the risk of several common cancers.     

Citrus fruit and cancer risk in a network of case–control studies

Background

Citrus fruit has shown a favorable effect against various cancers. To better understand their role in cancer risk, we analyzed data from a series of case–control studies conducted in Italy and Switzerland.

Patients and methods

The studies included 955 patients with oral and pharyngeal cancer, 395 with esophageal, 999 with stomach, 3,634 with large bowel, 527 with laryngeal, 2,900 with breast, 454 with endometrial, 1,031 with ovarian, 1,294 with prostate, and 767 with renal cell cancer. All cancers were incident and histologically confirmed. Controls were admitted to the same network of hospitals for acute, nonneoplastic conditions. Odds ratios (OR) were estimated by multiple logistic regression models, including terms for major identified confounding factors for each cancer site, and energy intake.

Results

The ORs for the highest versus lowest category of citrus fruit consumption were 0.47 (95% confidence interval, CI, 0.36–0.61) for oral and pharyngeal, 0.42 (95% CI, 0.25–0.70) for esophageal, 0.69 (95% CI, 0.52–0.92) for stomach, 0.82 (95% CI, 0.72–0.93) for colorectal, and 0.55 (95% CI, 0.37–0.83) for laryngeal cancer. No consistent association was found with breast, endometrial, ovarian, prostate, and renal cell cancer.

Conclusions

Our findings indicate that citrus fruit has a protective role against cancers of the digestive and upper respiratory tract.     

Family history of cancer and the risk of cancer: a network of case–control studies

BackgroundThe risk of many cancers is higher in subjects with a family history (FH) of cancer at a concordant site. However, few studies investigated FH of cancer at discordant sites.Patients and methodsThis study is based on a network of Italian and Swiss case–control studies on 13 cancer sites conducted between 1991 and 2009, and including more than 12 000 cases and 11 000 controls. We collected information on history of any cancer in first degree relatives, and age at diagnosis. Odds ratios (ORs) for FH were calculated by multiple logistic regression models, adjusted for major confounding factors.ResultsAll sites showed an excess risk in relation to FH of cancer at the same site. Increased risks were also found for oral and pharyngeal cancer and FH of laryngeal cancer (OR = 3.3), esophageal cancer and FH of oral and pharyngeal cancer (OR = 4.1), breast cancer and FH of colorectal cancer (OR = 1.5) and of hemolymphopoietic cancers (OR = 1.7), ovarian cancer and FH of breast cancer (OR = 2.3), and prostate cancer and FH of bladder cancer (OR = 3.4). For most cancer sites, the association with FH was stronger when the proband was affected at age <60 years.ConclusionsOur results point to several potential cancer syndromes that appear among close relatives and may indicate the presence of genetic factors influencing multiple cancer sites.     

Circulating leptin levels and risk of colorectal cancer and adenoma: a case–control study and meta-analysis

Purpose

Equivocal results regarding the role of leptin in colorectal cancer (CRC) and adenoma (CRA) have been reported. A case–control study investigating the association of leptin with CRC risk and clinicopathological characteristics along with meta-analysis of published data on both CRC and CRA were conducted.

Methods

Pubmed and Embase were searched for the meta-analysis, comprising 28 case–control studies amounting 3,614 CRC and 1,215 CRA cases, along with 5,220 controls. Meticulous contact with the authors of individual studies was undertaken for the provision of additional data. Pooling of standardized mean differences (SMD), relative risks (RR) and 95 % CI (random effects models), subgroup, sensitivity, and meta-regression analyses were conducted.

Results

The meta-analysis suggested positive association of serum leptin with CRA (RR, 95 % CI 1.35, 1.03 to +1.76), but not CRC either at the pooled analysis on SMDs or RRs (SMD, 95 % CI 0.18, ?0.04 to +0.40; RR, 95 % CI 1.04, 0.65 to +1.65). Significant heterogeneity between studies on CRC as well as between studies on CRA providing SMD was noted. Subgroup, meta-regression and sensitivity analyses highlighted potential methodology-, design-, size- and quality-related effect modifiers.

Conclusions

Meta-analysis of current evidence suggests positive association of serum leptin with CRA but not with CRC risk. Given the case–control nature of available studies, the limited number of studies on serum leptin and CRA, and the heterogeneity of CRC studies, carefully designed, prospective studies preferably reporting RRs adjusted for a variety of confounders may be warranted.     

Diabetes and risk of pancreatic cancer: a pooled analysis of three large case–control studies

Racial differences in diabetes-associated pancreatic cancer (PC) and the interaction of diabetes with other risk factors are not well established. We determined the association between diabetes and risk of PC in 2,192 cases and 5,113 controls in three large case–control studies conducted at the National Cancer Institute, the University of California San Francisco, and the M.D. Anderson Cancer Center. In multivariable analyses, diabetes was associated with a 1.8-fold risk of PC [95% confidence interval (CI) = 1.5–2.1]. Risk estimates decreased with increasing years with diabetes (≤2 years OR = 2.9, 95% CI = 2.1–3.9; 3–5 years OR = 1.9, 95% CI = 1.3–2.6; 6–10 years OR = 1.6, 95% CI = 1.2–2.3; 11–15 years OR = 1.3, 95% CI = 0.9–2.0; > 15 years OR = 1.4, 95% CI = 1.0–2.0 (p for trend < 0.0001). Among diabetics, risk was higher in insulin ever users compared with nonusers (OR = 2.2, 95% CI = 1.6–3.7) and was restricted to insulin use of ≤3 years (OR = 2.4). Insulin use of >10 years was associated with a reduced risk of pancreatic cancer (OR = 0.5, 95% CI = 0.3–0.9; p for trend < 0.0001). Hispanic men and Asians had a higher risk of diabetes-associated PC than did whites and blacks, but the differences were not statistically significant. No significant interaction between diabetes and cigarette smoking, alcohol consumption and body mass index was observed. Although reverse causation may explain the association between diabetes diagnosed in close temporal proximity to PC, our results show that long-term diabetes, even though risk diminishes over time, remains a risk factor for PC independent of obesity and smoking.     

Association between CCND1 and XPC polymorphisms and bladder cancer risk: a meta-analysis based on 15 case–control studies

Perturbations in cell cycle and DNA repair genes might affect susceptibility to cancer. The aim of this meta-analysis is to generate large-scale evidence to determine the degree to which common Cyclin D1 (CCND1) G870A (dbSNP: rs603965) and xeroderma pigmentosum group C (XPC) Ala499Val (dbSNP: rs2228000) polymorphisms are associated with susceptibility to bladder cancer. The electronic databases PubMed, Embase, Web of Science, and CNKI were searched for relevant studies (with an upper date limit of July 25, 2013). The principal outcome measure for evaluating the strength of association was crude odds ratios (ORs) along with their corresponding confidence intervals (95 %CIs). We found and reviewed nine case–control studies on CCND1 G870A with a total of 6,823 subjects and seven studies on XPC Ala499Val with a total of 7,674 subjects. Our meta-analysis provides evidence that the variant genotype of CCND1 G870A showed a significant association in the occurrence of invasive bladder tumors in former and current smokers. The XPC Ala499Val polymorphism correlated with significant differences between patients and unaffected subjects, but when the groups were stratified by ethnicity, the magnitude of the overall effect was similar only among Caucasian populations. Results from our meta-analysis support the view that the G870A polymorphism may modulate the risk of bladder cancer in conjunction with tobacco smoking and that the Ala499Val polymorphism may contribute to the susceptibility to bladder cancer in Caucasian populations. Our findings, however, warrant larger well-designed studies to investigate the significance of these two polymorphisms as markers of susceptibility to bladder cancer.     

Plasma vitamins E and A and risk of bladder cancer: a case–control analysis

Objective  Current results on the association between serum micronutrients and bladder cancer risk have been inconsistent. We assessed plasma vitamin E (α-tocopherol, and γ-tocopherol), vitamin A (retinol), and bladder cancer risk using data collected from a case-control study. Methods  Epidemiologic data were collected via in-person interview. Plasma concentrations of α-tocopherol, γ-tocopherol, and retinol were determined by a high-performance liquid chromatography assay. Multivariate logistic regression analyses were used to estimate bladder cancer risk in association with plasma vitamins E and A. Results  386 bladder cancer patients and 389 age-, gender-, and ethnicity-matched controls were included in the study. The mean plasma α-tocopherol and retinol were significantly lower in cases than in controls (α-tocopherol: 23.93 μg/ml vs. 27.48 μg/ml, P < 0.001; retinol: 1.41 μg/ml vs. 1.53 μg/ml, P < 0.001). There was a significant reduction in bladder cancer risk associated with increasing plasma α-tocopherol level (Adjusted OR: 0.91; 95% CI: 0.85–0.97). In quartile analysis, using subjects with the lowest α-tocopherol level as the reference group, the adjusted ORs and 95% CIs for the second, third, and fourth quartiles were 0.75 (0.50–1.14), 0.69 (0.46–1.05), and 0.50 (0.32–0.78), respectively (P for trend = 0.003). Increased retinol level was also associated with reduced risk with OR of 0.57 (95% CI: 0.40–0.81). The ORs and 95% CIs for the second, third, and fourth quartiles were 0.92 (0.61–1.39), 0.66 (0.43–1.01), and 0.62 (0.40–0.95), respectively, with significant dose-response trend (P for trend = 0.01). Finally, there were significant correlations between plasma levels and dietary intakes for the three micronutrients. Conclusion  Our results suggest potential protective effect of α-tocopherol and retinol on bladder cancer risk. Future large prospective studies are needed to confirm the findings. Supported by NCI grants CA 74880 and CA 91846 All participants included have signed an informed consent to participate in this study. The authors declare no conflict of interest.     

Positive association between lymphotoxin-alpha variation rs909253 and cancer risk: a meta-analysis based on 36 case–control studies

Lymphotoxin-alpha (LTA) polymorphism rs909253 has been reported to be a risk factor for cancers, but some results are inconsistent. To establish a more conclusive association, we performed a meta-analysis of this variant with cancers. A systematic search was performed for informative case–control studies of rs909253 with cancers among literature databases, including PubMed, Web of Science, Embase, China National Knowledge Infrastructure (CNKI), and Wanfang Chinese Periodical Database. After a comprehensive filtration procedure, 36 publications involved with 35,677 participants were selected for the current meta-analysis. Stratified factors, such as cancer type, populations, and source of control, were used for a better interpretation of this variant. Minimal heterogeneity was shown in the current meta-analysis (I ²?=?0.0 %, P?=?0.48). Our results show a significant association of rs909253 and cancer risk (odds ratio (OR)?=?1.12, P _(z)?<?0.001). In the subgroup analysis, significant association of rs909253 was found in adenocarcinoma (OR?=?1.16, P _(z)?<?0.001) and hematological malignancy (OR?=?1.10, P _(z)?<?0.001). Our meta-analyses established a significant association of rs909253 with cancer risk among multiple populations including North Americans, Asians, and Europeans.     

Transforming growth factor-β1 polymorphisms and breast cancer risk: a meta-analysis based on 27 case–control studies

The association between transforming growth factor-β1 (TGF-β1) gene polymorphisms and breast cancer risk has been widely reported, but results were somewhat controversial and underpowered. To derive a more precise estimation of the relationship between TGF-β1 polymorphisms and breast cancer risk, we conducted a meta-analysis of all available case–control studies relating the T869C and/or C-509T polymorphisms of the TGF-β1 gene to the risk of developing breast cancer. Eligible articles were identified by search of databases including MEDLINE, PubMed, Web of Science, EMBASE, and Chinese Biomedical Literature database (CBM) for the period up to March 2010. Finally, a total of 17 articles involving 27 case–control studies were identified, 25 with 20,022 cases and 24,423 controls for T869C polymorphism and eight with 10,633 cases and 13,648 controls for C-509T polymorphism. The pooled ORs were performed for the allele contrasts, additive genetic model, dominant genetic model and recessive genetic model, respectively. Subgroup analysis was also performed by ethnicity for T869C polymorphism. With respect to T869C polymorphism, no association was found in overall analysis (C vs. T: OR = 1.033, 95% CI = 0.996–1.072). In the subgroup analysis by ethnicity, significantly increased risk was found in Caucasian population (C vs. T: OR = 1.051, 95% CI = 1.018–1.085; CC vs. TT + TC: OR = 1.083, 95% CI = 1.019–1.151), but not in Asian population (C vs. T: OR = 1.054, 95% CI = 0.983–1.130). With respect to C-509T polymorphism, no significant association with breast cancer risk was demonstrated in overall analysis (T vs. C: OR = 0.986, 95% CI = 0.936–1.039). It can be concluded that potentially functional TGF-Β1 T869C polymorphism may play a low penetrance role in breast cancer susceptibility in an ethnicity-specific manner.     

Vascular endothelial growth factor +936C/T polymorphism and breast cancer risk: a meta-analysis of 13 case–control studies

The association between vascular endothelial growth factor (VEGF) +936C/T polymorphism and breast cancer risk has been widely reported, but results were inconsistent. In order to derive a more precise estimation of the relationship, a meta-analysis was performed. Eligible articles were identified through search of databases including PubMed, Embase, and Chinese Biomedical Literature Database (CBM). The association between the VEGF +936C/T polymorphism and breast cancer risk was conducted by odds ratios (ORs) and 95 % confidence intervals (95 % CIs). Finally, a total of 13 studies with 6,879 cases and 7,219 controls were included in our meta-analysis. Overall, a significant association was found between VEGF +936C/T polymorphisms and the risk of breast cancer in overall populations under five models (T vs. C: OR?=?0.83, 95 % CI?=?0.73–0.94, P?=?0.002; TT vs. CC: OR?=?0.74, 95 % CI?=?0.61–0.91, P?=?0.004, Fig. 1a; TC vs. CC: OR?=?0.83, 95 % CI?=?0.71–0.96, P?=?0.014; TT vs. CC/CT: OR?=?0.77, 95 % CI?=?0.62–0.94, P?=?0.010; TT/TC vs. CC: OR?=?0.82, 95 % CI?=?0.72–0.95, P?=?0.006). In the subgroup analysis by ethnicity, there were also significant associations found between VEGF +936C/T polymorphism and breast cancer risk in Asians and Caucasians. In conclusion, the results of our meta-analysis suggest that the VEGF +936C/T polymorphism is significantly associated with breast cancer development and the VEGF 936T allele carriers may be associated with decreased breast cancer risk.     

Incomplete pregnancy and risk of ovarian cancer: results from two Australian case–control studies and systematic review

Although full-term pregnancies reduce the risk of ovarian cancer, it has not been conclusively established whether incomplete pregnancies also influence risk. We investigated the relationship between a history of incomplete pregnancy and incident epithelial ovarian cancer among over 4,500 women who participated in two large Australian population-based case–control studies in 1990–1993 and 2002–2005. They provided responses to detailed questions about their reproductive histories and other personal factors. Summary odds ratios (OR) and confidence intervals (CI) derived for each study using the same covariates were aggregated. We found no significant associations between the number of incomplete pregnancies and ovarian cancer, for parous (OR = 0.98, 95% CI: 0.89, 1.08) or nulliparous (OR = 1.06, 95% CI: 0.75, 1.48) women, nor for the number of spontaneous or induced abortions and ovarian cancer for parous women (OR = 0.95, 95% CI 0.82, 1.09; OR = 1.08, 95% CI: 0.86, 1.36) or nulliparous women (OR = 1.2, 95% CI: 0.6, 2.4; OR = 0.8, 95% CI: 0.47, 1.38), respectively. A systematic review of 37 previous studies of the topic confirmed our findings that a history of incomplete pregnancy does not influence a woman’s risk of epithelial ovarian cancer.     

GSTM1 null genotype is associated with increased risk of gastric cancer in both ever-smokers and non-smokers: a meta-analysis of case–control studies

Previous studies have suggested that the glutathione S-transferases M1 (GSTM1) null genotype is associated with the risk of gastric cancer. However, the interaction between GSTM1 null genotype and smoking for the risk of gastric cancer is still elusive. Therefore, we performed a meta-analysis to ascertain this issue. Databases of PubMed, EMBASE, and China National Knowledge Infrastructure were searched to retrieve relevant studies. Smokers were categorized as “ever-smokers” and “non-smokers.” Odds ratios (ORs) and 95 % confidence intervals (95 % CIs) were calculated to estimate the association strength. Subgroup analyses according to ethnicity, source of control, and sample size were also conducted. A total of 15 eligible studies, including 4,687 gastric cancer cases and 7,002 controls, were identified. We found that the GSTM1 null genotype was associated with increased risk of gastric cancer among ever-smokers (OR?=?1.460, 95 % CI 1.064–2.003, heterogeneity: P?=?0.019). The null genotype also significantly increased the risk of gastric cancer among non-smokers (OR?=?1.777, 95 % CI 1.301–2.426, heterogeneity: P?<?0.01). Stratified analysis according to ethnicity showed that the GSTM1 null genotype was associated with increased risk of gastric cancer among Asians both in ever-smokers (OR?=?1.841, 95 % CI 1.184–2.861) and non-smokers (OR?=?1.773, 95 % CI 1.382–2.275). In conclusion, the GSMT1 null genotype significantly increased the risk of gastric cancer both in ever-smokers and non-smokers.