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  • POLYMORPHISMS  (15)
  • 1
    Keywords: RECEPTOR ; APOPTOSIS ; CANCER ; GROWTH ; GROWTH-FACTOR ; proliferation ; CELL ; CELL-PROLIFERATION ; Germany ; PATHWAY ; RISK ; SITE ; GENE ; GENES ; PROTEIN ; PROTEINS ; transcription ; DIFFERENTIATION ; SERA ; BINDING ; ASSOCIATION ; LINKAGE ; polymorphism ; POLYMORPHISMS ; BREAST-CANCER ; NO ; SNP ; colorectal cancer ; COLORECTAL-CANCER ; PROSTATE-CANCER ; REGION ; REGIONS ; LINKAGE DISEQUILIBRIUM ; case-control studies ; BINDS ; BINDING PROTEIN ; insulin ; CELL-GROWTH ; signaling ; SERUM ; SINGLE ; ONCOLOGY ; BINDING-PROTEIN ; case control study ; case-control study ; RE ; SNPs ; cell proliferation ; PROMOTER POLYMORPHISM ; GROWTH-FACTOR-I ; LEVEL ; case control studies ; methods ; HAPLOTYPE ; HAPLOTYPES ; single-nucleotide ; IGFBP3 ; SERUM-LEVELS ; HAPLOTYPE RECONSTRUCTION ; CIRCULATING LEVELS ; ENGLAND ; IGFBP-3 ; MULTIETHNIC COHORT ; colorectal ; case control ; UPSTREAM ; REPEAT ; IGF1 ; CASCADE ; GENETIC-VARIATION ; IGF ; INSULIN-LIKE ; cell growth ; BONE-MINERAL DENSITY ; INSULIN-LIKE-GROWTH-FACTOR-1
    Abstract: Background: The insulin-like growth factor1 (IGF1) pathway plays a significant role in both the normal and malignant cell growth. IGF1 binds to the IGF1 receptor and starts a signaling cascade that regulates cell proliferation, differentiation, and apoptosis. The bioavailability of IGF1 is regulated by the binding protein IGFBP3. A CA repeat polymorphism, in the IGF1 gene, which is located 969 bp upstream from the transcription start site and the rs2854744 and rs2854746 single nucleotide polyrnorphisms (SNPs) in the IGFBP3 gene have been associated with the serum levels of the respective proteins and colorectal cancer (CRC), but the results are inconsistent. We wanted to study if these polymorphisms or any haplotypes of the IGF1 and the IGFBP3 genes are associated with CRC. Methods: High linkage disequilibrium was seen in these gene regions. Therefore, the CA repeat along with two SNPs in the IGF1 gene, and rs2854744 (A-202C), rs2854746 (Ala32Gly) and two additional SNPs in the IGFBP3 gene were selected to cover the whole gene regions. A case-control study was carried out using 661 German CRC cases and 607 matched controls. Results: We did not find any association between the CA repeat length or any of the SNPs in the IGF1 and the IGFBP3 genes and the risk of CRC. Nor did the haplotypes of these genes affect the risk of CRC. Conclusion: Our study suggests no major role of the assessed genetic variation within the IGF1 and the IGFBP3 genes in CRC risk. (c) 2007 International Society for Preventive Oncology. Published by Elsevier Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 18031946
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  • 2
    Keywords: APOPTOSIS ; CANCER ; proliferation ; CELL ; Germany ; EXPOSURE ; RISK ; RISKS ; GENE ; PROTEIN ; DRUG ; DIFFERENTIATION ; NF-KAPPA-B ; DNA ; GENETIC POLYMORPHISMS ; cell cycle ; CELL-CYCLE ; CYCLE ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; VARIANTS ; PROGRESSION ; DNA-REPAIR ; REPAIR ; genetics ; colorectal cancer ; COLORECTAL-CANCER ; p53 ; TUMOR-SUPPRESSOR GENE ; cancer risk ; GENOTYPES ; gene-environment interaction ; genetic polymorphism ; MULTIVARIATE ; CARRIERS ; case-control studies ; aspirin ; NONSTEROIDAL ANTIINFLAMMATORY DRUGS ; heredity ; DNA repair ; ARREST ; case control study ; case-control study ; REGRESSION ; RE ; VARIANT ; ALLELE ; genomics ; interaction ; case control studies ; INTERVAL ; analysis ; methods ; GENOTYPE ; HAPLOTYPE ; HAPLOTYPES ; USA ; LINKAGE PHASE ; DRUGS ; odds ratio ; CANCER-RISK ; genomic ; microbiology ; colorectal ; LOGISTIC-REGRESSION ; FUNCTIONAL-ANALYSIS ; ANTIINFLAMMATORY DRUGS ; COLON ADENOCARCINOMA CELLS ; nonsteroidal anti-inflammatory drugs ; P53 POLYMORPHISMS ; SULINDAC SULFIDE ; TP53 gene
    Abstract: Objective Substantial evidence indicates that nonsteroidal anti-inflammatory drugs protect against colorectal cancer by altering cell cycle progression and/or inducing apoptosis, whereas p53 protein is crucial to maintaining cell-cycle arrest and regulating DNA repair, differentiation, and apoptosis. Genetic variants in TP53 gene might therefore influence colorectal cancer risk and modify the effects of nonsteroidal anti-inflammatory drugs. We assessed the association of TP53 Arg72Pro and p53PIN3 polymorphisms with colorectal cancer risk and their possible interaction with nonsteroidal antiinflammatory drug use. Methods We included 467 cases and 563 controls from a population-based case-control study. Multivariate logistic regression analysis was used to estimate the association between genotypes, environmental exposures and colorectal cancer risk, adjusting for potential confounders. Results Odds ratios of colorectal cancer were 0.75 (95% confidence interval, 0.57-0.99) for TP53 72Pro carriers compared with those homozygous for the TP53 72Arg allele and 0.78 (95% confidence interval, 0.58-1.05) for p53PIN3 A2 carriers compared with p53PIN3 A1A1. Risks differed by nonsteroidal anti -inf lam matory drug use. For both investigated TP53 polymorphisms, we found that the colorectal cancer risk associated with regular nonsteroidal anti-inflammatory drug use was statistically significantly modified by the TP53 genotype (P values for interaction=0.049 and 0.034, respectively), whereby a substantial protective effect of nonsteroidal antiinflammatory drug use was observed for homozygous carriers of the 72Arg allele and of the PIN3 Al allele (odds ratio 0.44; 95% confidence interval, 0.30-0.65 and odds ratio, 0.45; 95% confidence interval, 0.31-0.65). The interaction between nonsteroidal anti-inflammatory drugs and TP53 genetic polymorphisms was confirmed by haplotype analysis. Conclusions These data suggest that the TP53 genotype may modify the influence of nonsteroidal anti-inflammatory drug use on the risk of colorectal cancer. A direct proof of functional analysis is warranted to confirm these findings. Pharmacogenetics and Genomics 17:639-645 (C) 2007 Lippincott Williams & Wilkins
    Type of Publication: Journal article published
    PubMed ID: 17622940
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  • 3
    Keywords: CANCER ; carcinoma ; RISK ; PROTEIN ; POLYMORPHISMS ; AGE ; colonoscopy ; METAANALYSIS ; colorectal neoplasms ; Helicobacter pylori ; COLONIC ADENOMAS ; SEROPREVALENCE ; SEROPOSITIVITY ; ATROPHIC GASTRITIS ; ERADICATION ; HYPERGASTRINEMIA
    Abstract: Evidence concerning the role of Helicobacter pylori infection in the development of colorectal cancer remains controversial. The authors assessed the association of H. pylori seroprevalence with risk of colorectal cancer in a large population-based case-control study from Germany in 2003-2007. Serum antibodies to H. pylori in general and the cytotoxin-associated gene A protein (CagA) were measured in 1,712 incident colorectal cancer cases and 1,669 controls. The association between H. pylori seroprevalence and colorectal cancer risk was estimated by logistic regression, with adjustment for potential confounders and stratification by age group, sex, anatomic subsites, and cancer stage. Overall, H. pylori seroprevalence was higher in cases (46.1%) than in controls (40.1%), resulting in an age- and sex-adjusted odds ratio of 1.30 (95% confidence interval (CI): 1.14, 1.50). Adjustment for established colorectal cancer risk factors decreased the odds ratio to 1.26 (95% CI: 1.09, 1.47), with a further reduction to 1.18 (95% CI: 1.01, 1.38) after additional adjustment for previous colorectal endoscopy. Stratified analyses showed risk elevation to be essentially confined to left-sided colorectal cancer, with an odds ratio of 1.22 (95% CI: 1.02, 1.45), suggesting that H. pylori infection may be associated with a small yet relevant risk increase in the left colorectum.
    Type of Publication: Journal article published
    PubMed ID: 22294430
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  • 4
    Keywords: COHORT ; HETEROCYCLIC AMINES ; POLYMORPHISMS ; smoking ; COLON-CANCER ; CONSUMPTION ; EXCISION-REPAIR ; GENETIC SUSCEPTIBILITY ; GENOME-WIDE ASSOCIATION ; POULTRY INTAKE
    Abstract: Background: Red meat intake has been associated with risk of colorectal cancer, potentially mediated through heterocyclic amines. The metabolic efficiency of N-acetyltransferase 2 (NAT2) required for the metabolic activation of such amines is influenced by genetic variation. The interaction between red meat intake, NAT2 genotype, and colorectal cancer has been inconsistently reported. Methods: We used pooled individual-level data from the Colon Cancer Family Registry and the Genetics and Epidemiology of Colorectal Cancer Consortium. Red meat intake was collected by each study. We inferred NAT2 phenotype based on polymorphism at rs1495741, highly predictive of enzyme activity. Interaction was assessed using multiplicative interaction terms in multivariate-adjusted models. Results: From 11 studies, 8,290 colorectal cancer cases and 9,115 controls were included. The highest quartile of red meat intake was associated with increased risk of colorectal cancer compared with the lowest quartile [ OR, 1.41; 95% confidence interval (CI), 1.29-1.55]. However, a significant association was observed only for studies with retrospective diet data, not for studies with diet prospectively assessed before cancer diagnosis. Combining all studies, high red meat intake was similarly associated with colorectal cancer in those with a rapid/intermediate NAT2 genotype (OR, 1.38; 95% CI, 1.20-1.59) as with a slow genotype (OR, 1.43; 95% CI, 1.28-1.61; P interaction = 0.9). Conclusion: We found that high red meat intake was associated with increased risk of colorectal cancer only from retrospective case-control studies and not modified by NAT2 enzyme activity. Impact: Our results suggest no interaction between NAT2 genotype and red meat intake in mediating risk of colorectal cancer.
    Type of Publication: Journal article published
    PubMed ID: 25342387
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  • 5
    Keywords: POLYMORPHISMS ; COLON-CANCER ; NONSTEROIDAL ANTIINFLAMMATORY DRUGS ; chemoprevention ; METAANALYSIS ; CYCLOOXYGENASE-2 ; GENOME-WIDE ASSOCIATION ; PROSTAGLANDIN E-2 BIOSYNTHESIS ; PIK3CA MUTATION ; INTERLEUKIN-16
    Abstract: MPORTANCE Use of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with lower risk of colorectal cancer. OBJECTIVE To identify common genetic markers that may confer differential benefit from aspirin or NSAID chemoprevention, we tested gene x environment interactions between regular use of aspirin and/or NSAIDs and single-nucleotide polymorphisms (SNPs) in relation to risk of colorectal cancer. DESIGN, SETTING, AND PARTICIPANTS Case-control study using data from 5 case-control and 5 cohort studies initiated between 1976 and 2003 across the United States, Canada, Australia, and Germany and including colorectal cancer cases (n=8634) and matched controls (n=8553) ascertained between 1976 and 2011. Participants were all of European descent. EXPOSURES Genome-wide SNP data and information on regular use of aspirin and/or NSAIDs and other risk factors. MAIN OUTCOMES AND MEASURES Colorectal cancer. RESULTS Regular use of aspirin and/or NSAIDs was associated with lower risk of colorectal cancer (prevalence, 28% vs 38%; odds ratio [OR], 0.69 [95% Cl, 0.64-0.74]; P = 6.2 x 10(-28)) compared with nonregular use. In the conventional logistic regression analysis, the SNP rs2965667 at chromosome 12p12.3 near the MGST1 gene showed a genome-wide significant interaction with aspirin and/or NSAID use (P = 4.6 x 10(-9) for interaction). Aspirin and/or NSAID use was associated with a lower risk of colorectal cancer among individuals with rs2965667-TT genotype (prevalence, 28% vs 38%; OR, 0.66 [95% CI, 0.61-0.70]; P =7.7 x 10(-33)) but with a higher risk among those with rare (4%) TA or AA genotypes (prevalence, 35% vs 29%; OR, 1.89 [95% Cl, 1.27-2.81]; P = .002). In case-only interaction analysis, the SNP rs16973225 at chromosome 15q25.2 near the IL16 gene showed a genome-wide significant interaction with use of aspirin and/or NSAIDs (P = 8.2 x 10(-9) for interaction). Regular use was associated with a lower risk of colorectal cancer among individuals with rs16973225-AA genotype (prevalence, 28% vs 38%; OR, 0.66 [95% CI, 0.62-0.71]; P = 1.9 x 10(-30)) but was not associated with risk of colorectal cancer among those with less common (9%) AC or CC genotypes (prevalence, 36% vs 39%; OR, 0.97 [95% Cl, 0.78-1.20]; P = .76). CONCLUSIONS AND RELEVANCE In this genome-wide investigation of gene x environment interactions, use of aspirin and/or NSAIDs was associated with lower risk of colorectal cancer, and this association differed according to genetic variation at 2 SNPs at chromosomes 12 and 15. Validation of these findings in additional populations may facilitate targeted colorectal cancer prevention strategies.
    Type of Publication: Journal article published
    PubMed ID: 25781442
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  • 6
    Keywords: RECEPTOR ; SIMULATIONS ; APOPTOSIS ; CANCER ; EXPRESSION ; proliferation ; tumor ; CELL ; CELL-PROLIFERATION ; Germany ; LUNG-CANCER ; screening ; DEATH ; POPULATION ; RISK ; GENE ; TIME ; LIGAND ; SIMULATION ; BINDING ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; VARIANTS ; BREAST-CANCER ; STAGE ; AGE ; colorectal cancer ; COLORECTAL-CANCER ; cancer risk ; PREVALENCE ; RECEPTORS ; APOPTOSIS-INDUCING LIGAND ; RECTAL-CANCER ; RE ; TUMOR-SUPPRESSOR ; VARIANT ; SUPPRESSOR GENE ; INCREASE ; cell proliferation ; INTERVAL ; tumor suppressor gene ; TESTS ; death receptor ; LINKAGE PHASE ; CANDIDATE ; population-based ; general population ; CANCER-RISK ; RARE ; NECROSIS ; APO2L/TRAIL
    Abstract: The tumor necrosis factor-related apoptosis-inducing ligand receptor modulates apoptotic response by binding to the proapoptotic death receptor 4 (DR4). Perturbed apoptosis due to missense alterations in the candidate tumor suppressor gene DR4 leads to deregulated cell proliferation and cancer predisposition. Recent studies have discussed the association of DR4 variants with cancer risk. We evaluated, for the first time, the role of the Thr(209)Arg (626C 〉 G) and Glu(228)AIa (683A 〉 C) polymorphisms on colorectal cancer risk by genotyping 659 incident cases and 607 healthy controls drawn from the German population-based Darmkrebs: Chancen der Verhutung durch Screening (DACHS) study. Whereas DR4 Glu(228)Ala was not associated with colorectal cancer, Thr(209)Arg heterozygotes were at a significantly decreased colorectal cancer risk [odds ratio (OR), 0.73; 95% confidence interval (95% CI), 0.54-0.97]. Stratification according to sex and age exhibited a significant association of Thr(209)Arg with a decreased risk for male heterozygotes (OR, 0.68; 95% CI, 0.46-0.99) and for Arg(209) carriers 〉= 65 years of age (OR, 0.65; 95% CI, 0.46-0.92) as well as an enhanced risk for female Ala(228) carriers in a allele dose-dependent manner (P-trend = 0.01). Subsite analysis revealed a protective effect of Thr(209)Arg for rectal cancer risk (OR, 0.67; 95% CI, 0.48-0.95) and a significant risk increase for Ala 228 carriers with advanced colorectal cancer stages (P-trend = 0.04). Haplotype analysis revealed a 2.4-fold risk for carriers of the rare 626C-683C haplotype (1% prevalence in the general population; OR, 2.37; 95% CI, 0.98-5.76). The score statistic yielded an empirical P of 0.03 of the haplotype-specific test for 626C-683C based on 20,000 simulations, suggesting that DR4 626C-683C may affect colorectal cancer predisposition
    Type of Publication: Journal article published
    PubMed ID: 17035413
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  • 7
    Keywords: CANCER ; EXPRESSION ; LUNG-CANCER ; RISK ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; PROGRESSION ; POPULATIONS ; GASTRIC-CANCER ; FINLAND ; TUMOR-SUPPRESSOR ; 15-HYDROXYPROSTAGLANDIN DEHYDROGENASE ; PROSTAGLANDIN DEHYDROGENASE
    Abstract: A recent study examined associations of tagging single nucleotide polymorphisms (tagSNPs) in 43 fatty acid metabolism-related genes and risk of colorectal cancer (CRC), showing rs8752, rs2612656 and a haplotype [comprising both of the single nucleotide polymorphisms (SNPs)] in the hydroxyprostaglandin dehydrogenase 15-(NAD) (HPGD) gene to be positively associated with CRC risk. In the present study, we attempted to replicate these single marker and haplotype associations, using 1795 CRC cases and 1805 controls from the German Darmkrebs: Chancen der Verhütung durch Screening study (DACHS). In addition to rs8752 and rs2612656, HPGD tagSNPs rs9312555, rs17360144 and rs7349744 were genotyped for haplotype analyses. Except for a marginally significant inverse association of HPGD rs8752 with CRC risk [odds ratio (OR) = 0.85; 95% confidence interval (CI) = 0.74, 0.98; P = 0.03], none of the analyzed tagSNPs showed any association with CRC. Subset analyses for colon and rectal cancers yielded similar, yet non-significant risk estimates at all five loci. Also, none of the haplotypes was found to be associated with CRC, colon or rectal cancers. However, rs8752 was significantly associated with a decreased risk of CRC among individuals with a body mass index 〈 30 (OR = 0.82, 95% CI = 0.70, 0.95, P = 0.01) as well as among smokers (OR = 0.74, 95% CI = 0.61, 0.90, P = 0.003). Yet, our data do not support the previously reported associations of HPGD tagSNPs and risk of CRC.
    Type of Publication: Journal article published
    PubMed ID: 21047993
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  • 8
    Keywords: CANCER ; POPULATION ; RISK ; POLYMORPHISMS ; WOMEN ; colorectal cancer ; MEN ; COLON-CANCER ; GAMMA ; GENDER ; LOCI ; GENOME-WIDE ASSOCIATION ; TCF7L2 ; Type 2 diabetes mellitus
    Abstract: Background: The link between colorectal cancer (CRC) and type 2 diabetes mellitus (T2D) has been extensively studied. Although it is commonly accepted that T2D is a risk factor for CRC, the underlying mechanisms are still poorly understood. Research Design and Methods: Given that the genetic background contributes to both traits, it is conceivable that genetic variants associated with T2D may also influence the risk of CRC. We selected 26 T2D-related single-nucleotide polymorphisms (SNP) previously identified by genome-wide association studies and assessed their association with CRC and their interaction with known risk factors (gender, T2D, and body mass index) of CRC. Selected SNP were genotyped in 1798 CRC cases and 1810 controls from the population-based Darmkrebs: Chancen der Verhutung durch Screening (DACHS) study (Germany). Results: Patients carrying the TCF7L2_rs7903146_T allele had an increased risk of CRC(P-trend = 0.02), whereas patients harboring the IL13_rs20541_T allele had a reduced risk (P-trend = 0.02). A further analysis revealed gender-specific effects: the TCF7L2_rs7903146_T allele was associated with an increased risk of CRC in women (P-trend = 0.003) but not in men (P-interaction = 0.06); the LTA_rs1041981_A allele was associated with a decreased risk for CRC in women (P-trend = 0.02), with an opposite effect in men (P-trend = 0.05; P-interaction = 0.002); the CDKAL1_rs7754840_C allele was associated with a decreased risk for CRC in men (P-trend = 0.03), with no effect in women (P-interaction = 0.03). The risk associated with the presence of T2D was modified both by IGF2BP2_rs4402960 and PPAR gamma_rs1801282 SNP (P-interaction = 0.04 and 0.04, respectively). None of the findings were significant after correction for multiple comparisons. Conclusions: These findings suggest that T2D-related variants modify CRC risk independently and/or in an interactive manner according to the gender and the presence or absence of T2D.
    Type of Publication: Journal article published
    PubMed ID: 22419714
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  • 9
    Keywords: CANCER ; COHORT ; RISK ; GENE ; RISK-FACTORS ; ASSOCIATION ; POLYMORPHISMS ; SUSCEPTIBILITY ; VARIANTS ; HEALTH ; COLON-CANCER ; ALCOHOL ; CONSUMPTION ; FRUIT ; LIFE-STYLE ; MASS INDEX ; CANCER SUSCEPTIBILITY ; METAANALYSIS ; VEGETABLE CONSUMPTION ; LOCI ; GENOME-WIDE ASSOCIATION ; sex ; SCAN ; RISK LOCI ; CHROMOSOME 8Q24
    Abstract: Genome-wide association studies (GWAS) have identified more than a dozen loci associated with colorectal cancer (CRC) risk. Here, we examined potential effect-modification between single-nucleotide polymorphisms (SNP) at 10 of these loci and probable or established environmental risk factors for CRC in 7,016 CRC cases and 9,723 controls from nine cohort and case-control studies. We used meta-analysis of an efficient empirical-Bayes estimator to detect potential multiplicative interactions between each of the SNPs [rs16892766 at8q23.3 (EIF3H/UTP23), rs6983267 at 8q24 (MYC), rs10795668 at 10p14 (FLJ3802842), rs3802842 at 11q23 (LOC120376), rs4444235 at 14q22.2 (BMP4), rs4779584 at 15q13 (GREM1), rs9929218 at 16q22.1 (CDH1), rs4939827 at 18q21 (SMAD7), rs10411210 at 19q13.1 (RHPN2), and rs961253 at 20p12.3 (BMP2)] and select major CRC risk factors (sex, body mass index, height, smoking status, aspirin/nonsteroidal anti-inflammatory drug use, alcohol use, and dietary intake of calcium, folate, red meat, processed meat, vegetables, fruit, and fiber). The strongest statistical evidence for a gene-environment interaction across studies was for vegetable consumption and rs16892766, located on chromosome 8q23.3, near the EIF3H and UTP23 genes (nominal P-interaction = 1.3 x 10(-4); adjusted P = 0.02). The magnitude of the main effect of the SNP increased with increasing levels of vegetable consumption. No other interactions were statistically significant after adjusting for multiple comparisons. Overall, the association of most CRC susceptibility loci identified in initial GWAS seems to be invariant to the other risk factors considered; however, our results suggest potential modification of the rs16892766 effect by vegetable consumption.
    Type of Publication: Journal article published
    PubMed ID: 22367214
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  • 10
    Keywords: MODIFIERS ; CANCER-RISK ; USA ; polymorphism ; POLYMORPHISMS ; HEALTH ; colorectal cancer ; COLORECTAL-CANCER ; cancer risk ; CANCER ; RISK
    Type of Publication: Meeting abstract published
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