A pooled analysis of molecular epidemiological studies on modulation of DNA repair by host factors

2022 ◽  
pp. 503447
Author(s):  
Alena Opattova ◽  
Sabine A.S. Langie ◽  
Mirta Milic ◽  
Andrew Collins ◽  
Asgeir Brevik ◽  
...  
Keyword(s):  
Dna Repair ◽  
Epidemiological Studies ◽  
Pooled Analysis ◽  
Host Factors

The Associations of Plasma/Serum Carotenoids with Alzheimer’s Disease: A Systematic Review and Meta-Analysis

2021 ◽  
pp. 1-12
Author(s):  
Mingyue Qu ◽  
Hanxu Shi ◽  
Kai Wang ◽  
Xinggang Wang ◽  
Nan Yu ◽  
...  
Keyword(s):  
Systematic Review ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Meta Analysis ◽  
Scoring Systems ◽  
Serum Levels ◽  
Epidemiological Studies ◽  
Pooled Analysis ◽  
Protective Effects ◽  
Mean Differences

Background: Multiple lines of evidence indicate protective effects of carotenoids in Alzheimer’s disease (AD). However, previous epidemiological studies reported inconsistent results regarding the associations between carotenoids levels and the risk of AD. Objective: Our study aims to evaluate the associations of six major members of carotenoids with the occurrence of AD by conducting a systematic review and meta-analysis. Methods: Following PRISMA guidelines, a comprehensive literature search of PubMed, Web of Science, Ebsco, and PsycINFO databases was conducted, and the quality of each included studies was evaluated by a validated scoring systems. Standardized mean differences (SMD) with 95%confidence intervals (CI) were determined by using a random effects model. Heterogeneity was evaluated by I2 statistics. Publication bias was detected using funnel plots and Egger’s test. Results: Sixteen studies, with 10,633 participants were included. Pooled analysis showed significantly lower plasma/serum levels of lutein (SMD = –0.86, 95%CI: –1.67 to –0.05, p = 0.04) and zeaxanthin (SMD = –0.59; 95%CI: –1.12 to –0.06, p = 0.03) in patients with AD versus cognitively intact controls, while α-carotene (SMD = 0.21, 95%CI: –0.68 to 0.26, p = 0.39), β-carotene (SMD = 0.04, 95%CI: –0.57 to 0.65, p = 0.9), lycopene (SMD = –0.12, 95%CI: –0.96 to 0.72, p = 0.78), and β-cryptoxanthin (SMD = –0.09, 95%CI: –0.83 to 0.65, p = 0.81) did not achieve significant differences. Conclusion: Of six major members of carotenoids, only lutein and zeaxanthin concentrations in plasma/serum were inversely related to the risk of AD. More high-quality longitudinal studies are needed to verify these findings.

scholarly journals Polymorphisms in DNA repair genes and risk of non-Hodgkin lymphoma in a pooled analysis of three studies

2010 ◽  
Vol 151 (3) ◽  
pp. 239-244 ◽  
Author(s):  
Min Shen ◽  
Idan Menashe ◽  
Lindsay M. Morton ◽  
Yawei Zhang ◽  
Bruce Armstrong ◽  
...  
Keyword(s):  
Dna Repair ◽  
Hodgkin Lymphoma ◽  
Pooled Analysis ◽  
Dna Repair Genes ◽  
Non Hodgkin Lymphoma ◽  
Repair Genes

scholarly journals Germline HOXB13 p.Gly84Glu mutation and cancer susceptibility: a pooled analysis of 25 epidemiological studies with 145,257 participates

Oncotarget ◽  
2015 ◽  
Vol 6 (39) ◽  
pp. 42312-42321 ◽  
Author(s):  
Qiliang Cai ◽  
Xinpeng Wang ◽  
Xiaodong Li ◽  
Rui Gong ◽  
Xuemei Guo ◽  
...  
Keyword(s):  
Cancer Susceptibility ◽  
Epidemiological Studies ◽  
Pooled Analysis

scholarly journals International Lung Cancer Consortium: Pooled Analysis of Sequence Variants in DNA Repair and Cell Cycle Pathways

2008 ◽  
Vol 17 (11) ◽  
pp. 3081-3089 ◽  
Author(s):  
Rayjean J. Hung ◽  
David C. Christiani ◽  
Angela Risch ◽  
Odilia Popanda ◽  
Aage Haugen ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Dna Repair ◽  
Pooled Analysis ◽  
Sequence Variants

Meta-analysis

2018 ◽  
pp. 233-246
Author(s):  
Alan J. Silman ◽  
Gary J. Macfarlane ◽  
Tatiana Macfarlane
Keyword(s):  
Meta Analysis ◽  
Original Data ◽  
Epidemiological Studies ◽  
Pooled Analysis ◽  
Published Data ◽  
Potential Bias ◽  
Quantitative Synthesis ◽  
Analysis Of Results ◽  
Using Data

The previous chapter has discussed how to gather and evaluate existing evidence from epidemiological studies. Here further consideration is given to summarizing the identified evidence in such a way that it can be used for decision-making, including approaches to control for chance and potential bias. Meta-analysis refers to the statistical analysis of results from individual studies for integrating the findings. There are other terms related to meta-analysis such as quantitative review, combined analysis, pooled analysis, or quantitative synthesis. Some of them use different methods, for example, meta-analysis of published data considers each study as a unit of analysis while individual patient data analysis includes the original data from each study on a participant level. This chapter describes how to numerically summarize data through performing a meta-analysis using data from a systematic review of epidemiological studies. It also considers possible bias, reporting guidelines, and statistical software available for meta-analysis.

scholarly journals A trial sequential meta-analysis of TNF-α –308G>A (rs800629) gene polymorphism and susceptibility to colorectal cancer

2019 ◽  
Vol 39 (1) ◽  
Author(s):  
Raju K. Mandal ◽  
Munawwar Ali Khan ◽  
Arif Hussain ◽  
Naseem Akhter ◽  
Arshad Jawed ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Gene Polymorphism ◽  
Meta Analysis ◽  
Asian Population ◽  
Epidemiological Studies ◽  
Pooled Analysis ◽  
Asian Ethnicity ◽  
Tnf Α ◽  
Factor Α ◽  
The Relationship

Abstract Purpose: Tumor necrosis factor-α (TNF-α), secreted by the activated macrophages, may participate in the onset and progression of colorectal cancer (CRC). The association of TNF-α –308 G>A (rs1800629) single-nucleotide polymorphism (SNP) with CRC risk has been investigated by many studies but the results are inconclusive. A trial sequential meta-analysis was performed for precise estimation of the relationship between TNF-α –308 G>A gene polymorphism with CRC risk. Methods: Medline (PubMed), EMBASE (Excerpta-Medica) and Google Scholar were mined for relevant articles. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to estimate the significance of association. Results: The pooled analysis indicated no risk associated with TNF-α –308 G>A SNP and overall CRC risk in five genetic comparison models, i.e. allelic (A vs. G: P = 0.524; OR = 1.074, 95% CI = 0.863–1.335), homozygous (AA vs. GG: P = 0.489; OR = 1.227, 95% CI = 0.688–2.188), heterozygous (AG vs. GG: P = 0.811; OR = 1.024, 95% CI = 0.843–1.244), dominant (AA+AG vs. GG: P = 0.630; OR = 1.055, 95% CI = 0.849–1.311) and recessive (AA vs. AG+GG: P = 0.549; OR = 1.181, 95% CI = 0.686–2.033). Subgroup analysis revealed that TNF-α –308 G>A SNP is associated with reduced risk of CRC in Asian ethnicity. The study showed no publication bias. Conclusions: No association of TNF-α –308 G>A SNP with overall CRC risk was found. This SNP is likely to be protective against CRC in Asian population when compared with Caucasian population. Larger prospective-epidemiological studies are warranted to elucidate the roles of TNF-α –308 G>A SNP in the etiology of CRC and to endorse the present findings.

Role of asbestos clearance in explaining long-term risk of pleural and peritoneal cancer: a pooled analysis of cohort studies

2019 ◽  
Vol 76 (9) ◽  
pp. 611-616
Author(s):  
Francesco Barone-Adesi ◽  
Daniela Ferrante ◽  
Elisabetta Chellini ◽  
Enzo Merler ◽  
Venere Pavone ◽  
...  
Keyword(s):  
Epidemiological Studies ◽  
Pooled Analysis ◽  
External Exposure ◽  
Multistage Model ◽  
Peritoneal Cancer ◽  
Long Term Trends ◽  
Over Time ◽  
Better Than

ObjectivesModels based on the multistage theory of cancer predict that rates of malignant mesothelioma continuously increase with time since first exposure (TSFE) to asbestos, even after the end of external exposure. However, recent epidemiological studies suggest that mesothelioma rates level off many years after first exposure to asbestos. A gradual clearance of asbestos from the lungs has been suggested as a possible explanation for this phenomenon. We analysed long-term trends of pleural and peritoneal cancer mortality in subjects exposed to asbestos to evaluate whether such trends were consistent with the clearance hypothesis.MethodsWe used data from a pool of 43 Italian asbestos cohorts (51 801 subjects). The role of asbestos clearance was explored using the traditional mesothelioma multistage model, generalised to include a term representing elimination of fibres over time.ResultsRates of pleural cancer increased until 40 years of TSFE, but remained stable thereafter. On the other hand, we observed a monotonic increase of peritoneal cancer with TSFE. The model taking into account asbestos clearance fitted the data better than the traditional one for pleural (p=0.004) but not for peritoneal (p=0.09) cancer.ConclusionsRates of pleural cancer do not increase indefinitely after the exposure to asbestos, but eventually reach a plateau. This trend is well described by a model accounting for a gradual elimination of the asbestos fibres. These results are relevant for the prediction of future rates of mesothelioma and in asbestos litigations.

Effect of Retinoic Acid on Apoptosis and DNA Repair in Human Keratinocytes after UVB Irradiation

2000 ◽  
Vol 4 (1) ◽  
pp. 2-7 ◽  
Author(s):  
Gang Li ◽  
Jason A. Bush ◽  
Vincent C. Ho
Keyword(s):  
Dna Repair ◽  
Retinoic Acid ◽  
Skin Cancer ◽  
Human Keratinocytes ◽  
Epidemiological Studies ◽  
Skin Carcinogenesis ◽  
Apoptosis Assay ◽  
Initiation Stage ◽  
Induced Apoptosis ◽  
Damaged Dna

Background: Skin cancer is extremely common. Epidemiological studies indicated that ultraviolet radiation (UV) is the primary cause for skin cancers, and that retinoic acid (RA) is able to inhibit this UV-induced skin carcinogenesis; however, the molecular mechanism of the anti-UV action of RA is unclear. Objective: The purpose of this study is to investigate if RA enhances the removal of UV-induced DNA damage. Methods: The effect of RA on UV-induced apoptosis and DNA repair was investigated by ELISA apoptosis assay and CAT assay. Results: Both all-trans-RA and 9-cis-RA did not promote UV-induced apoptosis nor the repair of UV-damaged DNA in human keratinocytes. Furthermore, RA did not induce the expression of p53. Conclusion: The inhibition of RA on skin carcinogenesis is not due to enhanced removal of UV-damaged DNA. Therefore, RA does not inhibit skin cancer development at the initiation stage, but possibly at the promotion and progression stages.

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