The Interaction between Dietary Selenium Intake and Genetics in Determining Cancer Risk and Outcome.
Ontology highlight
ABSTRACT:
SUBMITTER: Kadkol S
PROVIDER: S-EPMC7468715 | biostudies-literature | 2020 Aug
REPOSITORIES: biostudies-literature
Publications
The Interaction between Dietary Selenium Intake and Genetics in Determining Cancer Risk and Outcome.
Kadkol Shrinidhi S Diamond Alan M AM
Nutrients 20200812 8
There is considerable interest in the trace element selenium as a possible cancer chemopreventive dietary component, but supplementation trials have not indicated a clear benefit. Selenium is a critical component of selenium-containing proteins, or selenoproteins. Members of this protein family contain selenium in the form of selenocysteine. Selenocysteine is encoded by an in-frame UGA codon recognized as a selenocysteine codon by a regulatory element, the selenocysteine insertion sequence (SECI ...[more]
Similar Datasets
Project description:PurposeThe association between dietary acrylamide intake and estrogen receptor-positive (ER+) breast cancer risk in epidemiological studies is inconsistent. By analyzing gene-acrylamide interactions for ER+ breast cancer risk, we aimed to clarify the role of acrylamide intake in ER+ breast cancer etiology.MethodsThe prospective Netherlands Cohort Study on diet and cancer includes 62,573 women, aged 55-69 years. At baseline, a random subcohort of 2589 women was sampled from the total cohort for a case-cohort analysis approach. Dietary acrylamide intake of subcohort members (n = 1449) and ER+ breast cancer cases (n = 844) was assessed with a food frequency questionnaire. We genotyped single nucleotide polymorphisms (SNPs) in genes in acrylamide metabolism, sex steroid systems, oxidative stress and DNA repair. Multiplicative interaction between acrylamide intake and SNPs was assessed with Cox proportional hazards analysis, based on 20.3 years of follow-up.ResultsUnexpectedly, there was a statistically non-significant inverse association between acrylamide and ER+ breast cancer risk among all women but with no clear dose-response relationship, and no association among never smokers. Among the results for 57 SNPs and 2 gene deletions, rs1056827 in CYP1B1, rs2959008 and rs7173655 in CYP11A1, the GSTT1 gene deletion, and rs1052133 in hOGG1 showed a statistically significant interaction with acrylamide intake for ER+ breast cancer risk.ConclusionsThis study did not provide evidence for a positive association between acrylamide intake and ER+ breast cancer risk. If anything, acrylamide was associated with a decreased ER+ breast cancer risk. The interaction with SNPs in CYP1B1 and CYP11A1 suggests that acrylamide may influence ER+ breast cancer risk through sex hormone pathways.
| S-EPMC6499753 | biostudies-literature
Project description:PurposeSelenium has been suggested to be protective against breast cancer, but the evidence remains inconclusive. Hence, it is important to further examine the potential protective effect. This prospective cohort study investigates pre-diagnostic selenium intake in relation to breast cancer risk. In addition, we analyze serum selenium as a marker of dietary intake.MethodsThis study includes 17,035 women in the Malmö Diet and Cancer cohort. Dietary assessment and serum samples were collected at baseline (1991-1996). During 344,584 person-years of follow-up, 1,427 incident cases were retrieved. Cox regression analysis examined breast cancer risks adjusted for potential confounding factors. In addition, odds ratios (ORs) were estimated for 1186 cases and an equal number of controls in relation to quartiles (Q) of selenium intake and groups consisting of a combination of intake and serum selenium levels.ResultsNo overall association between selenium intake, or a combination of intake and serum levels, and breast cancer risk was found. The adjusted relative risk for breast cancer in selenium intake Q4 versus Q1 was 0.96 (0.83-1.12) (Ptrend = 0.65). Similarly, adjusted the OR for breast cancer in selenium intake for Q4 versus Q1 was 0.97 (0.76-1.23). The kappa value, 0.096 (p = 0.001), showed poor agreement between serum selenium and selenium intake.ConclusionOur findings suggest that there is no overall association between selenium intake, or a combination of intake and serum levels, and breast cancer risk. Finally, our results showed a poor correlation between estimated selenium intake and serum selenium.
| S-EPMC8236480 | biostudies-literature
Project description:Selenium has been suggested to be protective regarding breast cancer risk but no overall effect has been established. Genetics may modify the effect. This study compares the effect of selenium exposure on breast cancer risk between women with different alleles in single-nucleotide polymorphisms (SNPs). The Malmö Cancer and Diet Study, a cohort including 17,035 women and >25 years of follow-up on breast cancer diagnosis, was used. Five promising SNPs regarding interaction with selenium exposure were selected from the literature: rs1050450, rs4880, rs3877899, rs7579, and rs71304. Selenium exposure was assessed in three ways: genetically elevated (n = 16,429), dietary intake (n = 15,891) and serum levels (n = 2037) at baseline. Cox regression and logistic regression analyses evaluated breast cancer risk from selenium exposure, stratified for the SNPs and adjusted for risk factors. A total of 1946 women were diagnosed with breast cancer. Women with T/T alleles in rs1050450 had lower breast cancer risk compared with C/C, HR 0.81 (0.68-0.96). Interaction by rs1050450 limited a protective effect of higher selenium intake to T/T carriers, HR 0.68 (0.43-1.08) for intermediate intake and HR 0.63 (0.40-1.00) for high intake. No interactions or risk differences were seen for other SNPs or for serum selenium or genetically elevated selenium. The results indicate that genetic variation in rs1050450 might affect breast cancer risk and that selenium exposure could be a possible modifiable risk factor for breast cancer among women with that variation.
| S-EPMC8875528 | biostudies-literature
Project description:BackgroundMechanistic hypotheses suggest a potential effect of dietary fiber on breast carcinogenesis through the modulation of insulin-like growth factor bioactivity, estrogen metabolism and inflammation. An association between dietary fiber intake and breast cancer risk has been suggested in epidemiological studies but remains inconclusive. In particular, data is lacking regarding the different types of dietary fibers.ObjectiveThe objective was to investigate the prospective relationship between dietary fiber intake and breast cancer risk, taking into account different types of dietary fiber (overall, insoluble, soluble and from different food sources: cereals, vegetables, fruits and legumes).Design4684 women from the SU.VI.MAX cohort were included in this analysis as they completed at least three 24h-dietary records within the first two years of follow-up. Among them, 167 incident invasive breast cancers were diagnosed during a median follow-up of 12.6 years (between 1994 and 2007). The associations between quartiles of dietary fiber intake and breast cancer risk were characterized using multivariate Cox proportional hazards models.ResultsTotal fiber intake was not associated with breast cancer risk (HR(Quartile4vs.Quartile1)?=?1.29 (95%CI 0.66-2.50), P-trend?=?0.5), nor was fiber intake from cereals (P-trend?=?0.1), fruits (P-trend?=?0.9) and legumes (P-trend?=?0.3). In contrast, vegetable fiber intake was related to a decreased risk of breast cancer (HR(Q4vs.Q1)?=?0.50 (0.29-0.88), P-trend?=?0.03). Overall vegetable intake (in g/day) was not associated with breast cancer risk (P-trend?=?0.2).ConclusionThis prospective study suggests that vegetable fiber intake may contribute to reduce breast cancer risk, in line with experimental mechanistic data.
| S-EPMC3828192 | biostudies-literature
Project description:Some epidemiological studies observed a positive association between dietary acrylamide intake and ovarian cancer risk but the causality needs to be substantiated. By analyzing gene-acrylamide interactions for ovarian cancer risk for the first time, we aimed to contribute to this. The prospective Netherlands Cohort Study on diet and cancer includes 62,573 women, aged 55-69 years. At baseline in 1986, a random subcohort of 2589 women was sampled from the total cohort for a case cohort analysis approach. Dietary acrylamide intake of subcohort members and ovarian cancer cases (n = 252, based on 20.3 years of follow-up) was assessed with a food frequency questionnaire. We selected single nucleotide polymorphisms (SNPs) in genes in acrylamide metabolism and in genes involved in the possible mechanisms of acrylamide-induced carcinogenesis (effects on sex steroid systems, oxidative stress and DNA damage). Genotyping was done on DNA from toenails through Agena's MassARRAY iPLEX platform. Multiplicative interaction between acrylamide intake and SNPs was assessed with Cox proportional hazards analysis. Among the results for 57 SNPs and 2 gene deletions, there were no statistically significant interactions between acrylamide and gene variants after adjustment for multiple testing. However, there were several nominally statistically significant interactions between acrylamide intake and SNPs in the HSD3B1/B2 gene cluster: (rs4659175 (p interaction = 0.04), rs10923823 (p interaction = 0.06) and its proxy rs7546652 (p interaction = 0.05), rs1047303 (p interaction = 0.005), and rs6428830 (p interaction = 0.05). Although in need of confirmation, results of this study suggest that acrylamide may cause ovarian cancer through effects on sex hormones.
| S-EPMC5506210 | biostudies-literature
Project description:BackgroundOsteoporosis, characterized by reduced bone mineral density (BMD) increases the risk of all-cause mortality. Assessments of whether dietary selenium intake is related to bone health are scarce, with few relevant studies limited by a small sample size. The aim of the present study was to investigate the association between dietary selenium intake and BMD levels in the National Health and Nutrition Examination Survey (NHANES) database.MethodsWe extracted and aggregated data from 4 cycles of the NHANES [2005-2010, 2013-2014]. Dietary selenium intake was obtained from 24-hour dietary recall interviews. BMD measurement, including the femur, femur neck, trochanter and intertrochanter of the femur, and lumbar spine, was performed using dual-energy X-ray absorptiometry. The multivariable linear regression model for the association between dietary selenium intake and BMD and the generalized additive model (GAM) for the dose-response relationship were used.ResultsA total of 21,939 participants were included. The mean age was 40.68±22.42 years, and 51.28% were male. In the multivariable adjustment model, participants with the highest quintiles of dietary selenium intake (Q5) were associated with increased BMD levels in the total femur (β=0.014, 95% CI: 0.008-0.020, P<0.001), femur neck (β=0.010, 95% CI: 0.004-0.016, P=0.001), trochanter (β=0.011, 95% CI: 0.005-0.017, P<0.001), intertrochanter (β=0.017, 95% CI: 0.010-0.025, P<0.001), and lumbar spine (β=0.013, 95% CI: 0.005-0.020, P<0.001) compared with those in quintile 1 (Q1). The dose-response relationship showed an inverted U-shape relationship between dietary selenium intake and BMD levels (P for nonlinearity <0.05). Participants tended to have increased levels of BMD as the dietary selenium intake increased when dietary selenium was below the turning point, and then a negative relationship was observed when dietary intake was higher than the turning point.ConclusionsOur study indicated that dietary selenium intake exhibited an inverted U-shape trend in relation to BMD levels, which demonstrates the need for selenium status in the body to be considered when discussing the role of dietary selenium intake in BMD. Future studies are needed to confirm these findings and explore the underlying biological mechanism.
| S-EPMC9469114 | biostudies-literature
Project description:BackgroundCardiometabolic diseases are complex traits which are influenced by several single nucleotide polymorphisms (SNPs). Thus, analysing the combined effects of multiple gene variants might provide a better understanding of disease risk than using a single gene variant approach. Furthermore, studies have found that the effect of SNPs on cardiometabolic traits can be influenced by lifestyle factors, highlighting the importance of analysing gene-lifestyle interactions.AimsIn the present study, we investigated the association of 15 gene variants with cardiometabolic traits and examined whether these associations were modified by lifestyle factors such as dietary intake and physical activity.MethodsThe study included 110 Minangkabau women [aged 25-60 years and body mass index (BMI) 25.13 ± 4.2 kg/m2] from Padang, Indonesia. All participants underwent a physical examination followed by anthropometric, biochemical and dietary assessments and genetic tests. A genetic risk score (GRS) was developed based on 15 cardiometabolic disease-related SNPs. The effect of GRS on cardiometabolic traits was analysed using general linear models. GRS-lifestyle interactions on continuous outcomes were tested by including the interaction term (e.g. lifestyle factor*GRS) in the regression model. Models were adjusted for age, BMI and location (rural or urban), wherever appropriate.ResultsThere was a significant association between GRS and BMI, where individuals carrying 6 or more risk alleles had higher BMI compared to those carrying 5 or less risk alleles (P = 0.018). Furthermore, there were significant interactions of GRS with protein intake on waist circumference (WC) and triglyceride concentrations (Pinteraction = 0.002 and 0.003, respectively). Among women who had a lower protein intake (13.51 ± 1.18% of the total daily energy intake), carriers of six or more risk alleles had significantly lower WC and triglyceride concentrations compared with carriers of five or less risk alleles (P = 0.0118 and 0.002, respectively).ConclusionsOur study confirmed the association of GRS with higher BMI and further showed a significant effect of the GRS on WC and triglyceride levels through the influence of a low-protein diet. These findings suggest that following a lower protein diet, particularly in genetically predisposed individuals, might be an effective approach for addressing cardiometabolic diseases among Southeast Asian women.
| S-EPMC7552350 | biostudies-literature
Project description:ImportanceCandidate gene analysis approaches have shown that colorectal cancer (CRC) risk attributable to diet may differ according to genotype. A genome-wide approach further allows for the exploration of underlying pathways for associations between diet and CRC risk across the genome.ObjectivesTo identify genetic variants that modify diet-CRC associations and to further explore the underlying pathways in the cause of CRC.Design, setting, and participantsThis nested case-control study used data on White British participants from the prospective cohort UK Biobank. Participants were recruited between March 13, 2006, and October 1, 2010, and data were censored June 25, 2021.ExposuresThe average frequency intake of 11 dietary factors in the year preceding baseline was obtained via a touchscreen questionnaire. After quality control for more than 93 million variants of imputed genetic data, 4 122 345 variants remained.Main outcomes and measuresColorectal cancer cases were identified according to the International Statistical Classification of Diseases and Related Health Problems, Tenth Revision. Genome-wide interaction analysis was performed to test interactions between dietary factors and variants using a conditional logistic regression model. Summary statistics of interactions at the variant level were used to calculate empirical P values for interactions at gene and gene-set levels in gene-based and gene-set enrichment analyses.ResultsA total of 4686 participants with CRC (mean [SD] age, 60.7 [6.6] years; 2707 men [57.8%]) received a new diagnosis during a median of 12.4 years (IQR, 11.6-13.1 years) of follow-up. Once a case was detected, 3 matched controls were identified, for a total of 14 058 controls (mean [SD] age, 60.4 [6.6] years; 8121 men [57.8%]). A total of 324 variants were identified that interacted with diet consumption at the suggestive threshold (P < 1 × 10-5). In gene-based analysis, aggregation of multiple EPDR1 gene variants was found to interact with fish intake regarding CRC risk. Furthermore, gene-set enrichment analysis found that several sets of protein-coding genes, which were overrepresented with particular functions and pathways, interacted with the consumption of milk (ART), cheese (OR), tea (KRT), and alcohol (PRM and TNP).Conclusions and relevanceIn this nested case-control study, the risk of CRC associated with fish intake was modified by multiple single-nucleotide polymorphisms of the EPDR1 gene. The findings further suggested possible functions and pathways that might link the consumption of milk, cheese, tea, and alcohol with CRC development.
| S-EPMC10900970 | biostudies-literature
Project description:Several papers studied dietary protein intake as a potential influence factor for esophageal cancer, but their findings were inconsistent. Thus, this meta-analysis was performed to identify the effect of protein intake on esophageal cancer risk. Potential case-control studies or cohort studies from the databases of Embase, Web of Science and PubMed were searched. The strength of association was quantified by pooling odds ratio (OR) and 95% confidence interval (CI). In total, 11 articles involving 2537 cases and 11432 participants were included in this meta-analysis. As a result, dietary protein intake had non-significant association on esophageal cancer risk overall (pooled OR = 1.11, 95% CI = 0.88-1.40). Meanwhile, we obtained consistent results in the subgroups analyses by study design, protein type, geographic locations and number of cases. Interestingly, dietary protein intake could significantly increase the risk of esophageal squamous cell carcinoma (pooled OR = 1.29, 95% CI = 1.02-1.62), instead of other disease type. To sum up, dietary protein intake had no significant association with esophageal cancer risk in the overall analysis; but, protein intake may be associated with the risk of esophageal squamous cell carcinoma. While some limitations existed in the present paper, more studies with large sample size are warranted to further confirm this result.
| S-EPMC6970082 | biostudies-literature
Project description:The trace element selenium (Se) plays an important role in thyroid hormone metabolism. Low Se intake is associated with atuoimmune hypothyroidism. The interaction of Se and Graves’ disease (GD) is only poorly characterized. We have investigated the importance of dietary Se supply for GD by performing a more in-depth analysis of a large cross-sectional study of 6152 participants from two counties within the Shaanxi Province, China, which are characterized by different habitual Se intakes, and studied the effects of different dietary Se supply (0.02, 0.18, 0.6 or 2.0 ppm Se) on disease development in a mouse model of GD. In the cross-sectional study, prevalence of GD in the two areas of different Se intake was similar, and the Se status of GD patients was not different from healthy control subjects. The dietary Se supply in the animal model was not affecting thyroid hormone levels, malondialdehyde concentrations, total antioxidant capacity or the titer of GD-causing TSH receptor autoantibodies (TRAb). Expression analysis of transcripts in spleen indicated regulatory effects of Se intake on genes implicated in the immune response, erythropoiesis and oxygen status. However, the humoral immune response including the ratio of CD4/CD8 or Th1/Th2 cells, and the concentration of Treg cells were similar between the experimental groups despite their varying Se intakes. Our data from both the epidemiological analysis and animal experiment do not indicate a major role of Se in the development of GD, and highlight that autoimmune hypothyroidism and GD differ in their relation to Se status.
2021-05-30 | GSE115152 | GEO