The Protective Effect of Dietary Phytosterols on Cancer Risk: A Systematic Meta-Analysis

Backgrounds/Aims. Many studies have explored the association between dietary phytosterols and cancer risk, but the results have been inconsistent. We aimed to provide a synopsis of the current understanding of phytosterol intake for cancer risk through a systematic evaluation of the results from previous studies. Methods. We performed a literature search of PUBMED, EMBASE, CNKI, and Wanfang, and studies published before May 2019 focusing on dietary total phytosterols, β-sitosterol, campesterol, stigmasterol, β-sitostanol, and campestanol, as well as their relationships with cancer risk, were included in this meta-analysis. Summaries of the relative risks from 11 case-control and case-cohort studies were eventually estimated by randomized or fixed effects models. Results. The summary relative risk for the highest versus the lowest intake was 0.63 (95% confidence interval [CI] = 0.49–0.81) for total phytosterols, 0.74 (95% CI = 0.54–1.02) for β-sitosterol, 0.72 (95% CI = 0.51–1.00) for campesterol, 0.83 (95% CI = 0.60–1.16) for stigmasterol, 1.12 (95% CI = 0.96–1.32) for β-sitostanol, and 0.77 (95% CI = 0.65–0.90) for campestanol. In a dose-response analysis, the results suggested a linear association for campesterol and a nonlinear association for total phytosterol intake. Conclusion. Our findings support the hypothesis that high phytosterol intake is inversely related to risk of cancer. Further studies with prospective designs that control for vital confounders and investigate the important anticancer effects of dietary phytosterols are warranted.

Download Full-text

Sex Differences in the Association between Night Shift Work and the Risk of Cancers: A Meta-Analysis of 57 Articles

Disease Markers ◽

10.1155/2018/7925219 ◽

2018 ◽

Vol 2018 ◽

pp. 1-20 ◽

Cited By ~ 5

Author(s):

Wen Liu ◽

Zhonghan Zhou ◽

Dahai Dong ◽

Lijiang Sun ◽

Guiming Zhang

Keyword(s):

Sex Differences ◽

Cancer Risk ◽

Shift Work ◽

Meta Analysis ◽

Night Shift ◽

Case Control ◽

Sensitivity Analyses ◽

Response Analysis ◽

Night Shift Work ◽

Risk Of Cancer

Objectives. To identify the association between night shift work and the risk of various cancers with a comprehensive perspective and to explore sex differences in this association. Methods. We searched PubMed, Embase, and Web of Science for studies on the effect of night shift work on cancer, including case-control, cohort, and nested case-control studies. We computed risk estimates with 95% confidence intervals (CIs) in a random or fixed effects model and quantified heterogeneity using the I2 statistic. Subgroup, metaregression, and sensitivity analyses were performed to explore potential sources of heterogeneity. Contour-enhanced funnel plots and the trim and fill method were used together to analyze bias. Linear dose–response analysis was used to quantitatively estimate the accumulative effect of night shift work on the risk of cancer. Results. Fifty-eight studies were eligible for our meta-analysis, including 5,143,838 participants. In the random effects model, the pooled odds ratio (OR) of cancers was 1.15 (95% CI = 1.08–1.22, P<0.001; I2=76.2%). Night shift work increased the cancer risk in both men (OR = 1.14, 95% CI = 1.05–1.25, P=0.003) and women (OR = 1.12, 95% CI = 1.04–1.20, P=0.002). Subgroup analyses showed that night shift work positively increased the risk of breast (OR = 1.22, 95% CI = 1.08–1.38), prostate (OR = 1.26, 95% CI = 1.05–1.52), and digestive system (OR = 1.15, 95% CI = 1.01–1.32) cancers. For every 5 years of night shift work, the cancer risk increased by 3.2% (OR = 1.032, 95% CI = 1.013–1.051). Conclusion. This is the first meta-analysis identifying the positive association between night shift work and the risk of cancer and verifying that there is no sex difference in the effect of night shift work on cancer risk. Cancer risk increases with cumulative years of night shift work.

Download Full-text

Apple intake and cancer risk: a systematic review and meta-analysis of observational studies

Public Health Nutrition ◽

10.1017/s136898001600032x ◽

2016 ◽

Vol 19 (14) ◽

pp. 2603-2617 ◽

Cited By ~ 8

Author(s):

Roberto Fabiani ◽

Liliana Minelli ◽

Patrizia Rosignoli

Keyword(s):

Cancer Risk ◽

Oral Cavity ◽

Publication Bias ◽

Observational Studies ◽

Statistical Tests ◽

Meta Analysis ◽

Random Effect ◽

Random Effect Model ◽

Case Control ◽

Risk Of Cancer

AbstractObjectiveConflicting results on the association between fruit consumption and cancer risk have been reported. Little is known about the cancer preventive effects of different fruit types. The present meta-analysis investigates whether an association exists between apple intake and cancer risk.DesignRelevant observational studies were identified by literature search (PubMed, Web of Science and Embase). A random-effect model was used to estimate the cancer risk in different anatomical sites. Between-study heterogeneity and publication bias were assessed using adequate statistical tests.ResultsTwenty case–control (three on lung, five on colorectal, five on breast, two on oesophageal, three on oral cavity, two on prostate and one each on pancreas, bladder, larynx, ovary, kidney and brain cancer) and twenty-one cohort (seven on lung, two on colorectal, three on breast and one each on oesophageal, pancreas, bladder, kidney, endometrial, head–neck, urothelial and stomach cancer) studies met the inclusion criteria. Comparing the highest v. lowest level of apple consumption, the reduction of lung cancer risk was statistically highly significant in both case–control (OR=0·75; 95% CI 0·63, 0·88; P=0·001, I2=0 %) and cohort studies (relative risk=0·89; 95% CI 0·84, 0·94; P<0·001, I2=53 %). Instead, in the case of colorectal (OR=0·66; 95% CI 0·54, 0·81; P<0·001, I2=55%), breast (OR=0·79; 95% CI 0·73, 0·87; P<0·001, I2=1 %) and overall digestive tract (OR=0·50; 95% CI 0·36, 0·69; P<0·001, I2=90 %) cancers a significant preventive effect of apples was found only in case–control studies while prospective studies indicated no effect. No evidence of publication bias could be detected for colorectal, oral cavity, oesophageal and breast cancer. However, some confounding effects may be present and related to the consumption of other fruit which have not been considered as adjusting factors.ConclusionsThe present meta-analysis indicates that consumption of apples is associated with a reduced risk of cancer in different anatomical sites.

Download Full-text

Association between PD-1 and PD-L1 Polymorphisms and the Risk of Cancer: A Meta-Analysis of Case-Control Studies

Cancers ◽

10.3390/cancers11081150 ◽

2019 ◽

Vol 11 (8) ◽

pp. 1150 ◽

Cited By ~ 11

Author(s):

Mohammad Hashemi ◽

Shima Karami ◽

Sahel Sarabandi ◽

Abdolkarim Moazeni-Roodi ◽

Andrzej Małecki ◽

...

Keyword(s):

Cell Death ◽

Cancer Risk ◽

Programmed Cell Death ◽

Cancer Susceptibility ◽

Meta Analysis ◽

Case Control ◽

Case Control Studies ◽

Programmed Cell Death 1 ◽

Risk Of Cancer ◽

The Impact

A number of case-control studies regarding the association of the polymorphisms in the programmed cell death 1 (PD-1) and programmed cell death ligand 1 (PD-L1) genes with the risk of cancer have yielded inconsistent findings. Therefore, we have conducted a comprehensive, updated meta-analysis study to identify the impact of PD-1 and PD-L1 polymorphisms on overall cancer susceptibility. The findings revealed that PD-1 rs2227981 and rs11568821 polymorphisms significantly decreased the overall cancer risk (Odds Ratio (OR) = 0.82, 95% CI = 0.68–0.99, p = 0.04, TT vs. CT+CC; OR = 0.79, 95% CI = 0.67–0.94, p = 0.006, AG vs. GG, and OR = 0.82, 95% CI = 0.70–0.96, p = 0.020, AG+AA vs. GG, respectively), while PD-1 rs7421861 polymorphism significantly increased the risk of developing cancer (OR = 1.16, 95% CI = 1.02–1.33, p = 0.03, CT vs. TT). The PD-L1 rs4143815 variant significantly decreased the risk of cancer in homozygous (OR = 0.62, 95% CI = 0.41–0.94, p = 0.02), dominant (OR = 0.70, 95% CI = 0.50–0.97, p = 0.03), recessive (OR = 0.76, 95% CI = 0.60–0.96, p = 0.02), and allele (OR = 0.78, 95% CI = 0.63–0.96, p = 0.02) genetic models. No significant association between rs2227982, rs36084323, rs10204525, and rs2890658 polymorphisms and overall cancer risk has been found. In conclusions, the results of this meta-analysis have revealed an association between PD-1 rs2227981, rs11568821, rs7421861, as well as PD-L1 rs4143815 polymorphisms and overall cancer susceptibility.

Download Full-text

Association between apurinic/apyrimidinic endonuclease 1 rs1760944 T>G polymorphism and susceptibility of cancer: a meta-analysis involving 21764 subjects

Bioscience Reports ◽

10.1042/bsr20190866 ◽

2019 ◽

Vol 39 (12) ◽

Cited By ~ 1

Author(s):

Guowen Ding ◽

Yu Chen ◽

Huiwen Pan ◽

Hao Qiu ◽

Weifeng Tang ◽

...

Keyword(s):

Cancer Risk ◽

Publication Bias ◽

Protective Factor ◽

Cancer Susceptibility ◽

Meta Analysis ◽

Pooled Analysis ◽

Case Control ◽

Current Evidence ◽

Case Control Studies ◽

Risk Of Cancer

Abstract Background: Previous case–control studies have suggested that apurinic/apyrimidinic endonuclease 1 (APE1) rs1760944 T>G polymorphism may be associated with cancer risk. Here, we carried out an updated meta-analysis to focus on the correlation between APE1 rs1760944 T>G locus and the risk of cancer. Methods: We used the crude odds ratios (ORs) with their 95% confidence intervals (CIs) to evaluate the possible relationship between the APE1 rs1760944 T>G polymorphism and cancer risk. Heterogeneity, publication bias and sensitivity analysis were also harnessed to check the potential bias of the present study. Results: Twenty-three independent studies involving 10166 cancer cases and 11598 controls were eligible for this pooled analysis. We found that APE1 rs1760944 T>G polymorphism decreased the risk of cancer in four genetic models (G vs. T: OR, 0.87; 95% CI, 0.83–0.92; P<0.001; GG vs. TT: OR, 0.77; 95% CI, 0.69–0.86; P<0.001; GG/TG vs. TT: OR, 0.83; 95% CI, 0.77–0.89, P<0.001 and GG vs. TT/TG: OR, 0.85; 95% CI, 0.80–0.92, P<0.001). Results of subgroup analyses also demonstrated that this single-nucleotide polymorphism (SNP) modified the risk among lung cancer, breast cancer, osteosarcoma, and Asians. Evidence of publication bias was found in the present study. When we treated the publication bias with ‘trim-and-fill’ method, the adjusted ORs and CIs were not significantly changed. Conclusion: In conclusion, current evidence highlights that the APE1 rs1760944 T>G polymorphism is a protective factor for cancer susceptibility. In the future, case–control studies with detailed risk factors are needed to confirm or refute our findings.

Download Full-text

Sugar-sweetened beverages and risk of hypertension and CVD: a dose–response meta-analysis

British Journal Of Nutrition ◽

10.1017/s0007114514004383 ◽

2015 ◽

Vol 113 (5) ◽

pp. 709-717 ◽

Cited By ~ 111

Author(s):

Bo Xi ◽

Yubei Huang ◽

Kathleen Heather Reilly ◽

Shuangshuang Li ◽

Ruolong Zheng ◽

...

Keyword(s):

Dose Response ◽

Prospective Studies ◽

Fixed Effects ◽

Meta Analysis ◽

Response Analysis ◽

Sugar Sweetened Beverages ◽

Prospective Cohort Studies ◽

Sweetened Beverages ◽

Relative Risks ◽

Incident Cases

A number of prospective cohort studies have investigated the associations between consumption of sugar-sweetened beverages (SSB) and the risk of hypertension, CHD and stroke, but revealed mixed results. In the present study, we aimed to perform a dose–response meta-analysis of these prospective studies to clarify these associations. A systematic literature search was conducted using the PubMed and Embase databases up to 5 May 2014. Random- or fixed-effects models were used to calculate the pooled relative risks (RR) with 95 % CI for the highest compared with the lowest category of SSB consumption, and to conduct a dose–response analysis. A total of six prospective studies (240 726 participants and 80 411 incident cases of hypertension) from four publications on hypertension were identified. A total of four prospective studies (194 664 participants and 7396 incident cases of CHD) from four publications on CHD were identified. A total of four prospective studies (259 176 participants and 10 011 incident cases of stroke) from four publications on stroke were identified. The summary RR for incident hypertension was 1·08 (95 % CI 1·04, 1·12) for every additional one serving/d increase in SSB consumption. The summary RR for incident CHD was 1·17 (95 % CI 1·10, 1·24) for every serving/d increase in SSB consumption. There was no significant association between SSB consumption and total stroke (summary RR 1·06, 95 % CI 0·97, 1·15) for every serving/d increase in SSB consumption. The present meta-analysis suggested that a higher consumption of SSB was associated with a higher risk of hypertension and CHD, but not with a higher risk of stroke.

Download Full-text

Meta-analysis of sweetened carbonated beverage consumption and cancer risk.

Journal of Clinical Oncology ◽

10.1200/jco.2013.31.15_suppl.e12548 ◽

2013 ◽

Vol 31 (15_suppl) ◽

pp. e12548-e12548

Author(s):

Alice Koechlin ◽

Philippe Autier ◽

Peter Boyle

Keyword(s):

Cancer Risk ◽

Meta Analysis ◽

Soft Drinks ◽

Cancer Site ◽

Beverage Consumption ◽

Carbonated Beverage ◽

Primary Hypothesis ◽

Summary Relative Risk ◽

Meta Analyses ◽

Risk Of Cancer

e12548 Background: There is speculation of possible links between sweetened carbonated beverage consumption and the risk of developing cancer. The aim of this study was to examine the association between sweetened, carbonated beverage consumption and cancer risk. Methods: PRISMA guidelines of meta-analyses were followed as closely as possible. Over 50 independent estimates of risk were available, 11 for colas specifically. A random effects meta-analysis was performed with tests for publication bias (Begg, Egger, Macaskill) performed as well as Higgins and Thompson’s I2 measure of the percentage of heterogeneity between studies which could not be explained by chance. Results: Overall the different sites of cancer, the summary relative risk (SRR) when all 56 independent estimates were considered together was SRR=1.04 (95% CI (0.96, 1.13)). On this overall scale, there appears to be no association between consumption of soft-drinks and the risk of cancer. When individual cancer sites were considered, there was no significant increase, or decrease in the meta-analysis estimate of risk of cancer of the pancreas, bladder, kidney, oesophageal squamous cell or adenocarcinoma, colon, gastric cardia, gastric non-cardia, prostate, breast, larynx and ovary nor from the oral cavity, pharynx, glioma, leukaemia or non-Hodgkin’s lymphoma where only one study was available. There was no evidence in a sensitivity analysis from those studies which reported results separately for coke, pepsi or other colas of an associated risk of pancreas cancer (SRR=1.00, 95% CI (0.61; 1.65)) based on three studies. The results for all other forms of cancers were greatly hampered by poor methodology and small numbers of studies (mainly one report on each cancer site studied). Conclusions: Overall, the findings are reassuring regarding the association between soft drinks, including colas and cancer risk, although the quality of many of the studies is quite poor by acceptable, modern standards and no study has been conducted with use of carbonated beverages as a primary hypothesis.

Download Full-text

Exposure to Secondhand Smoke and Risk of Cancer in Never Smokers: A Meta-Analysis of Epidemiologic Studies

International Journal of Environmental Research and Public Health ◽

10.3390/ijerph15091981 ◽

2018 ◽

Vol 15 (9) ◽

pp. 1981 ◽

Cited By ~ 15

Author(s):

A-Sol Kim ◽

Hae-Jin Ko ◽

Jin-Hyun Kwon ◽

Jong-Myung Lee

Keyword(s):

Breast Cancer ◽

Cancer Risk ◽

Secondhand Smoke ◽

Meta Analysis ◽

Case Control ◽

Case Control Studies ◽

Prospective Cohort Studies ◽

Never Smokers ◽

Risk Of Cancer ◽

Exposure To Secondhand Smoke

This is first meta-analysis to evaluate cancer risk associated with secondhand smoking across all cancers. A literature search was conducted for articles published before June 2014 on Pubmed, SCOPUS, Cochrane library, and CINAHL, and 40 articles on secondhand smoke and the prevalence of cancer among never smokers were selected for final analysis as per the inclusion criteria. Of the 40 articles, 27 were case-control studies and 13 were prospective cohort studies. With respect to overall cancer risk, odds ratio (OR) involving never smokers with significant exposure to secondhand smoke compared to never smokers without such exposure was 1.163 (95%CI 1.058–1.279). Subgroup meta-analyses by study design showed significant positive associations for both case-control studies and prospective cohort studies (OR 1.165, 95%CI 1.029–1.320; and OR 1.160, 95%CI 1.002–1.343, respectively). The association was stronger in the case of females (OR 1.253, 95%CI 1.142–1.374), lung cancer (OR 1.245, 95%CI 1.026–1.511), and breast cancer (OR 1.235, 95%CI 1.102–1.385). Secondhand smoking may increase the overall risk of cancer for never smokers, particularly lung and breast cancer, and especially in women. Strict implementation of smoking cessation programs should be encouraged, not only to reduce active smoking but also to limit exposure to secondhand smoke.

Download Full-text

Analyzing Association of theXRCC3Gene Polymorphism with Ovarian Cancer Risk

BioMed Research International ◽

10.1155/2014/648137 ◽

2014 ◽

Vol 2014 ◽

pp. 1-9 ◽

Cited By ~ 6

Author(s):

Cunzhong Yuan ◽

Xiaoyan Liu ◽

Shi Yan ◽

Cunfang Wang ◽

Beihua Kong

Keyword(s):

Ovarian Cancer ◽

Cancer Risk ◽

Fixed Effects ◽

Genetic Model ◽

Meta Analysis ◽

Case Control ◽

Ovarian Cancer Risk ◽

Case Control Studies ◽

African Populations ◽

Eligible Case

This meta-analysis aims to examine whether theXRCC3polymorphisms are associated with ovarian cancer risk. Eligible case-control studies were identified through search in PubMed. Pooled odds ratios (ORs) were appropriately derived from fixed effects models. We therefore performed a meta-analysis of 5,302 ovarian cancer cases and 8,075 controls from 4 published articles and 8 case-control studies for 3 SNPs ofXRCC3. No statistically significant associations betweenXRCC3rs861539 polymorphisms and ovarian cancer risk were observed in any genetic models. ForXRCC3rs1799794 polymorphisms, we observed a statistically significant correlation with ovarian cancer risk using the homozygote comparison (T2T2 versus T1T1: OR = 0.70, 95% CI = 0.54–0.90,P=0.005), heterozygote comparison (T1T2 versus T1T1: OR = 1.10, 95% CI = 1.00–1.21,P=0.04), and the recessive genetic model (T2T2 versus T1T1+T1T2: OR = 0.67, 95% CI = 0.52–0.87,P=0.002). ForXRCC3rs1799796 polymorphisms, we also observed a statistically significant correlation with ovarian cancer risk using the heterozygote comparison (T1T2 versus T1T1: OR = 0.91, 95% CI = 0.83–0.99,P=0.04). In conclusion, this meta-analysis shows that theXRCC3were associated with ovarian cancer risk overall for Caucasians. Asian and African populations should be further studied.

Download Full-text

The Association between PON1 (Q192R and L55M) Gene Polymorphisms and Risk of Cancer: A Meta-Analysis Based on 43 Studies

BioMed Research International ◽

10.1155/2019/5897505 ◽

2019 ◽

Vol 2019 ◽

pp. 1-14 ◽

Cited By ~ 3

Author(s):

Xiaolan Pan ◽

Lei Huang ◽

Meiqin Li ◽

Dan Mo ◽

Yihua Liang ◽

...

Keyword(s):

Breast Cancer ◽

Cancer Risk ◽

Gene Polymorphisms ◽

Meta Analysis ◽

Population Based ◽

Case Control ◽

Cancer Type ◽

Case Control Studies ◽

Increased Risk ◽

Risk Of Cancer

Q192R and L55M polymorphism were considered to be associated with the development of multiple cancers. Nevertheless, the results of these researches were inconclusive and controversial. Therefore, we conducted a meta-analysis of all eligible case-control studies to assess the association between PON1 (Q192R and L55M) gene polymorphisms and risk of cancer. With the STATA 14.0 software, we evaluated the strength of the association by using the odds ratios (ORs) and 95% confidence intervals (CIs). A total of 43 case-control publications 19887 cases and 23842 controls were employed in our study. In all genetic models, a significant association between PON1-L55M polymorphisms and overall cancer risk was observed. Moreover, in the stratified analyses by cancer type, polymorphism of PON1-L55M played a risk factor in the occurrence of breast cancer, hematologic cancer, and prostate cancer. Similarly, an increased risk was observed in the Caucasian and Asian population as well as hospital-based group and population-based group. For PON1-Q192R polymorphisms, in the stratified analyses by cancer type, PON1-Q192R allele was associated with reduced cancer risks in breast cancer. Furthermore, for racial stratification, there was a reduced risk of cancer in recession model in Caucasian population. Similarly, in the stratification analysis of control source, the overall risk of cancer was reduced in the heterozygote comparison and dominant model in the population-based group. In conclusion, PON1-Q192R allele decreased the cancer risk especially breast cancer; there was an association between PON1-L55M allele and increased overall cancer risk. However, we need a larger sample size, well-designed in future and at protein levels to confirm these findings.

Download Full-text

Association between lncRNA H19 rs217727 polymorphism and the risk of cancer: an updated meta-analysis

BMC Medical Genetics ◽

10.1186/s12881-019-0904-x ◽

2019 ◽

Vol 20 (1) ◽

Cited By ~ 1

Author(s):

Xue Wang ◽

Jialing Zhong ◽

Fang Chen ◽

Kang Hu ◽

Suhong Sun ◽

...

Keyword(s):

Cancer Risk ◽

Confidence Interval ◽

Subgroup Analysis ◽

Odds Ratio ◽

Cancer Susceptibility ◽

Smoking Status ◽

Meta Analysis ◽

Case Control ◽

Potential Association ◽

Risk Of Cancer

Abstract Background We have performed this study to evaluate the association between H19 rs217727 polymorphism and the risk of cancer. Methods An odds ratio (OR) with a 95% confidence interval (CI) was applied to determine a potential association. Results A total of 17 case–control publications were selected. This meta-analysis showed that H19 rs217727 has a significant increased association with cancer risk in allelic, homozygous, heterozygote, dominant and recessive models (T vs C: OR = 1.16, 95% CI = 1.06–1.27, I2 = 75.7; TT vs CC: OR = 1.29, 95% CI = 1.06–1.56, I2 = 71.6; CT vs CC: OR = 1.15, 95% CI = 1.01–1.31, I2 = 75.4; CT + TT vs CC: OR = 1.20, 95% CI = 1.05–1.36, I2 = 76.5; TT vs CT + CC: OR = 1.22, 95% CI = 1.02–1.45, I2 = 70.6;). In the subgroup analysis of smoking status, both smokers and nonsmokers showed an increase in cancer risk in allelic, homozygous, dominant and heterozygote models. Conclusion This meta-analysis revealed H19 rs217727 may influence cancer susceptibility.

Download Full-text