scholarly journals Association between serum lipids and breast cancer risk in premenopausal women: systematic review and meta-analysis

2021 ◽  
Vol 49 (11) ◽  
pp. 030006052110610
Author(s):  
Jing Wu ◽  
Xun Lei ◽  
Xianjun Pan ◽  
Xiaohua Zeng ◽  
Wei Li
Keyword(s):  
Breast Cancer ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
Publication Bias ◽  
Serum Lipids ◽  
Meta Analysis ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Premenopausal Breast Cancer ◽  
The Impact

Objective Associations between serum lipids and their individual components with premenopausal breast cancer risk are unclear. This meta-analysis summarized the literature on serum lipids and premenopausal breast cancer risk to elucidate their relationship. Methods Eligible studies were identified by searching the PubMed, Embase, China National Knowledge Infrastructure, and Wanfang databases until 31 December 2020. Standardized mean difference (SMD) scores with 95% confidence intervals (95%CIs) were used to assess the impact of serum lipids on premenopausal breast cancer risk. The I2 statistic was calculated to measure the percentage of heterogeneity, and Egger’s test was performed to measure publication bias. Results Thirteen studies were included. The SMD scores of triglycerides (TG) and low-density lipoprotein cholesterol (LDL-C) were 12.90 (95%CI: 7.19–18.61) and 31.43 (95%CI: 8.72–54.15), respectively. The SMD scores of total cholesterol (TC) and high-density lipoprotein cholesterol (HDL-C) were not significantly different between the groups. The included studies were highly heterogeneous. There were no publication biases found in TC, LDL-C, or HDL-C analyses, whereas publication bias was present in the TG analysis. Conclusions TG and LDL-C were higher in premenopausal breast cancer patients than in women without breast cancer. However, no significant differences were found in TC or HDL-C levels.

Use of Statins and Breast Cancer: A Meta-Analysis of Seven Randomized Clinical Trials and Nine Observational Studies

2005 ◽  
Vol 23 (34) ◽  
pp. 8606-8612 ◽  
Author(s):  
Stefanos Bonovas ◽  
Kalitsa Filioussi ◽  
Nikolaos Tsavaris ◽  
Nikolaos M. Sitaras
Keyword(s):  
Breast Cancer ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
Publication Bias ◽  
Observational Studies ◽  
Fixed Effects ◽  
Randomized Clinical Trials ◽  
Meta Analysis ◽  
Sensitivity Analyses ◽  
Fixed Effects Model

Purpose A growing body of evidence suggests that statins may have chemopreventive potential against breast cancer. Laboratory studies demonstrate that statins induce apoptosis and reduce cell invasiveness in various cell lines, including breast carcinoma cells. However, the clinical relevance of these data remains unclear. The nonconclusive nature of the epidemiologic data prompted us to conduct a detailed meta-analysis of the studies published on the subject in peer-reviewed literature. Patients and Methods A comprehensive search for articles published up until 2005 was performed; reviews of each study were conducted; and data were abstracted. Before meta-analysis, the studies were evaluated for publication bias and heterogeneity. Pooled relative risk (RR) estimates and 95% CIs were calculated using the random and the fixed-effects models. Subgroup and sensitivity analyses were also performed. Results Seven large randomized trials and nine observational studies (five case-control and four cohort studies) contributed to the analysis. We found no evidence of publication bias or heterogeneity among the studies. Statin use did not significantly affect breast cancer risk (fixed effects model: RR = 1.03; 95% CI, 0.93 to 1.14; random effects model: RR = 1.02; 95% CI, 0.89 to 1.18). When the analyses were stratified into subgroups, there was no evidence that study design substantially influenced the estimate of effects. Furthermore, the sensitivity analysis confirmed the stability of our results. Conclusion Our meta-analysis findings do not support a protective effect of statins against breast cancer. However, this conclusion is limited by the relatively short follow-up times of the studies analyzed. Further studies are required to investigate the potential decrease in breast cancer risk among long-term statin users.

scholarly journals Breast Cancer Risk in Rheumatoid Arthritis: An Update Meta-Analysis

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Guo Tian ◽  
Jia-Ning Liang ◽  
Zhuo-Yun Wang ◽  
Dian Zhou
Keyword(s):  
Breast Cancer ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
Subgroup Analysis ◽  
Meta Analysis ◽  
Random Effect ◽  
Random Effect Model ◽  
Cochrane Library ◽  
Number Of Patients ◽  
The Impact

Background. The incidence of breast cancer in RA patients remains controversial. Thus we performed a meta-analysis to investigate the impact of RA on breast cancer.Methods. Published literature was available from PubMed, Embase, and Cochrane Library. Pooled standardized incidence rate (SIR) was computed by random-effect model analysis.Results. We identified 16 separate studies in the present study, in which the number of patients ranged from 458 to 84,475. We did not find the increased cancer risk in RA patients (SIR=0.86, 95%CI=0.72–1.02). However, subgroup analysis showed that breast cancer risk in RA patients was positively different in Caucasians (SIR=0.82, 95%CI=0.73–0.93) and non-Caucasians (SIR=1.21, 95%CI=1.19–1.23), respectively. In subgroup analysis by style, a reduced incidence was found in hospital-based case subjects (SIR=0.82, 95%CI=0.69–0.97). Similarly, subgroup analysis for adjusted factors indicated that in A3 (age and sex) and A4 (age, sex, and race/ethnicity) the risk was decreased (SIR=0.87, 95%CI=0.76–0.99;SIR=0.63, 95%CI=0.59–0.67).Conclusions. The meta-analysis revealed no increased breast cancer risk in RA patients. However, in the subgroup analysis, the risk of breast cancer is increased in non-Caucasians patients with RA while it decreased in Caucasian population, hospital-based case subjects, and A3 group. Such relationship may provide preference for risk of breast cancer in different population.

Abstract P124: Network Meta-analysis of the Effects of Breast Cancer Hormone Therapy on Changes in Lipid Profiles

Circulation ◽  
2017 ◽  
Vol 135 (suppl_1) ◽  
Author(s):  
Hsin-Hui Huang ◽  
Emma Barinas-Mitchell ◽  
Brenda Diergaarde ◽  
Chung-Chou Chang ◽  
Marnie Bertolet
Keyword(s):  
Breast Cancer ◽  
Hormone Therapy ◽  
Randomized Clinical Trials ◽  
Early Stage ◽  
Meta Analysis ◽  
Random Effect Model ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Adjuvant Hormone Therapy ◽  
The Impact

Introduction: Adjuvant hormone therapy prolongs survival of patients with early-stage hormone receptor-positive breast cancer (BC). For postmenopausal patients, aromatase inhibitors (AIs) have been shown to improve disease free survival compared to tamoxifen, but the impact on overall survival has been inconsistent. A meta-analysis showed higher risk of cardiovascular diseases (CVDs) for patients taking AIs. Deteriorating lipids induced by AIs may contribute to this result. This analysis aims to compare the effects of hormone therapeutic options on changes in lipids from published randomized clinical trials (RCTs). Methods: RCTs evaluating effects of adjuvant hormone therapy on lipids (total cholesterol, high-density lipoprotein cholesterol (HDLc), low density lipoprotein cholesterol (LDLc), and/or triglycerides) in postmenopausal early-stage BC patients published in PubMed and Embase, prior to Jan. 31, 2016 were reviewed. Bayesian network meta-analysis was used to compare effects of placebo, selective estrogen receptor modulators (SERMs- tamoxifen and toremifene) and AIs (letrozole, anastrozole, and exemstane) on lipids across longitudinal time points. Heterogeneity was examined by meta-regressions adjusting for mean age, baseline lipid value, and prior tamoxifen use. An arm-based random effect model tested the consistency of the direct and indirect evidence of the drug effects. Results: We identified 17 articles from 13 RCTs for a total of 1,913 subjects. The Table summarizes the results, with statistically significant results bolded. Toremifene significantly improved all lipids and was the best choice regardless of covariate adjustment, while tamoxifen had weaker but significant LDLc lowering but opposite HDLc/triglyceride effects to toremifene. AIs generally had little effect on lipids. Conclusions: In general, AIs tend to have worse effects on lipids than SERMs, while only toremifene had beneficial effects on all lipid values. Patients on AIs with high risk of CVD should monitor their lipids.

scholarly journals Metabolic Syndrome Is Associated with Increased Breast Cancer Risk: A Systematic Review with Meta-Analysis

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Ruchi Bhandari ◽  
George A. Kelley ◽  
Tara A. Hartley ◽  
Ian R. H. Rockett
Keyword(s):  
Breast Cancer ◽  
Systematic Review ◽  
Metabolic Syndrome ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
Publication Bias ◽  
Meta Analysis ◽  
Positive Association ◽  
Adult Women ◽  
Adult Females

Background. Although individual metabolic risk factors are reported to be associated with breast cancer risk, controversy surrounds risk of breast cancer from metabolic syndrome (MS). We report the first systematic review and meta-analysis of the association between MS and breast cancer risk in all adult females.Methods. Studies were retrieved by searching four electronic reference databases [PubMed, Cumulative Index to Nursing and Allied Health Literature (CINAHL), Web of Science, and ProQuest through June 30, 2012] and cross-referencing retrieved articles. Eligible for inclusion were longitudinal studies reporting associations between MS and breast cancer risk among females aged 18 years and older. Relative risks and 95% confidence intervals were calculated for each study and pooled using random-effects models. Publication bias was assessed quantitatively (Trim and Fill) and qualitatively (funnel plots). Heterogeneity was examined usingQandI2statistics.Results. Representing nine independent cohorts and 97,277 adult females, eight studies met the inclusion criteria. A modest, positive association was observed between MS and breast cancer risk (RR: 1.47, 95% CI, 1.15–1.87;z=3.13;p=0.002;Q=26.28,p=0.001;I2=69.55%). No publication bias was observed.Conclusions. MS is associated with increased breast cancer risk in adult women.

scholarly journals Assessing a causal relationship between circulating lipids and breast cancer risk: Mendelian randomization study

2019 ◽  
Author(s):  
Kelsey E. Johnson ◽  
Katherine M. Siewert ◽  
Derek Klarin ◽  
Scott M. Damrauer ◽  
Kyong-Mi Chang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
Causal Relationship ◽  
Genetic Variants ◽  
Mendelian Randomization ◽  
Plasma Lipid ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Breast Cancers

AbstractObjectiveTo assess a potential causal relationship between genetic variants associated with plasma lipid traits (high-density lipoprotein cholesterol, HDL; low-density lipoprotein cholesterol, LDL; triglycerides, TG) with risk for breast cancer.DesignMendelian randomization (MR) study.Setting and ParticipantsData from genome-wide association studies in up to 215,551 subjects from the Million Veterans Project were used to construct genetic instruments for plasma lipid traits. The effect of these instruments on breast cancer risk was evaluated using genetic data from the BCAC consortium based on 122,977 breast cancer cases and 105,974 controls.ExposuresGenetically modified plasma levels of LDL, HDL, or TG.Main Outcomes and MeasuresOdds ratio (OR) for breast cancer risk per standard-deviation increase in HDL, LDL, or TG.ResultsWe observed that a 1-SD genetically determined increase in HDL levels is associated with an increased risk for all breast cancers (HDL: OR=1.08, 95% CI=1.04-1.13, P=7.4×10−5).Multivariable MR analysis, which adjusted for the effects of LDL, TG, body mass index, and age at menarche, corroborated this observation for HDL (OR=1.06, 95% CI=1.03-1.10, P=4.9×10−4) and also a relationship between LDL and breast cancer risk (OR=1.03, 95% CI=1.01-1.07, P=0.02). We did not observe a difference in these relationships when stratified by breast tumor estrogen receptor status. We repeated this analysis using genetic variants independent of the leading association at core HDL pathway genes and found that these variants were also associated with risk for breast cancers (OR=1.11, 95% CI=1.06–1.16, P=1.5×10−6), including gene-specific associations at ABCA1, APOE-APOC1-APOC4-APOC2 and CETP. In addition, we find evidence that genetic variation at the ABO locus affects both lipid levels and breast cancer.ConclusionsGenetically elevated plasma HDL levels appear to increase breast cancer risk. Future studies are required to understand the mechanism underlying this putative causal relationship, with the goal to develop potential therapeutic strategies aimed at altering the HDL-mediated effect on breast cancer risk.

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