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  • 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: NITRIC-OXIDE ; COLORECTAL-CANCER ; OLIVE OIL ; ULCERATIVE-COLITIS ; PHENOLIC-COMPOUNDS ; 1,N-6-ETHENODEOXYADENOSINE ; 3,N-4-ETHENOCYTOSINE ; 3,N-4-ETHENODEOXYCYTIDINE ; 1,N-6-Ethenoadenine ; GLYCOSYLASES
    Abstract: Molecular pathways to colorectal cancer involve multiple genetic changes that may be caused by overproduction of reactive oxygen species in cancer-related genes. Our aim was to investigate, whether besides direct oxidative DNA damage, reactive oxygen and nitrogen species induce lipid peroxidation (LPO) that could yield etheno-DNA adducts via trans-4-hydroxy-2-nonenal, a major aldehyde generated by LPO, in colon tissue. We analyzed the etheno-DNA adducts by a highly specific, ultrasensitive method involving immunoaffinity chromatography coupled with 32P-postlabelling [Carcinogenesis 16 (1995) 613] in affected colon epithelium from ulcerative colitis, Crohn's disease and familial adenomatous polyposis (FAP) and compared them with asymptomatic colon tissue. In all these cancer prone colon tissues, the formation of markedly enhanced etheno adduct levels was demonstrated for the first time. Etheno-DNA adducts are promutagenic and cause genomic instability that could drive the inflamed colonic epithelia to malignancy. Etheno-DNA adducts appear promising biomarkers for (i) quantifying increased DNA damage in early stages of colon carcinogenesis and for (ii) verifying the efficacy of new antioxidants (e.g. [Lancet Oncol. 1 (2000) 107]) and chemopreventive agents in lowering oxidative stress and related cancer risk.
    Type of Publication: Journal article published
    PubMed ID: 12430635
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  • 3
    Abstract: BACKGROUND: Despite a large body of literature evaluating the association between recreational physical activity and epithelial ovarian cancer (EOC) risk, the extant evidence is inconclusive, and little is known about the independent association between recreational physical inactivity and EOC risk. We conducted a pooled analysis of nine studies from the Ovarian Cancer Association Consortium to investigate the association between chronic recreational physical inactivity and EOC risk. METHODS: In accordance with the 2008 Physical Activity Guidelines for Americans, women reporting no regular, weekly recreational physical activity were classified as inactive. Multivariable logistic regression was utilized to estimate the ORs and 95% confidence intervals (CI) for the association between inactivity and EOC risk overall and by subgroups based upon histotype, menopausal status, race, and body mass index. RESULTS: The current analysis included data from 8,309 EOC patients and 12,612 controls. We observed a significant positive association between inactivity and EOC risk (OR = 1.34; 95% CI, 1.14-1.57), and similar associations were observed for each histotype. CONCLUSIONS: In this large pooled analysis examining the association between recreational physical inactivity and EOC risk, we observed consistent evidence of an association between chronic inactivity and all EOC histotypes. IMPACT: These data add to the growing body of evidence suggesting that inactivity is an independent risk factor for cancer. If the apparent association between inactivity and EOC risk is substantiated, additional work via targeted interventions should be pursued to characterize the dose of activity required to mitigate the risk of this highly fatal disease. Cancer Epidemiol Biomarkers Prev; 25(7); 1114-24. (c)2016 AACR.
    Type of Publication: Journal article published
    PubMed ID: 27197285
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  • 4
    Keywords: IN-VITRO ; BLOOD ; evaluation ; DNA adducts ; EXPOSURE ; WORKERS ; P450 ; TIME ; DNA ; AIR ; GENETIC POLYMORPHISMS ; BIOMARKERS ; FREQUENCY ; polymorphism ; POLYMORPHISMS ; SUSCEPTIBILITY ; FREQUENCIES ; ACID ; GLUTATHIONE ; DNA-REPAIR ; REPAIR ; MARKERS ; COMET ASSAY ; DAMAGE ; genotoxicity ; DNA-DAMAGE ; PARAMETERS ; ADDUCTS ; T-LYMPHOCYTES ; DNA repair ; glutathione-S-transferase ; GLUTATHIONE S-TRANSFERASE ; DNA repair capacity ; EXPOSED LAMINATION WORKERS ; O-6-GUANINE DNA-ADDUCTS ; SINGLE-STRAND BREAKS ; SISTER-CHROMATID EXCHANGES ; styrene exposure,DNA damage,genotoxicity,individual susceptibility,DNA repair capacity ; WHITE BLOOD-CELLS
    Abstract: We evaluated our data on the occupational exposure to styrene in lamination workers. The battery of parameters included markers of external and internal exposure and biomarkers of biological effects and susceptibility. DNA repair capacities have been determined in both exposed and control groups. Styrene workplace concentration significantly correlated with styrene concentration in blood, exhaled air and urinary mandelic acid. Haemoglobin and O-6-Styrene oxide (SO)-guanine DNA adducts were significantly higher in exposed subjects as compared to controls and correlated with exposure parameters. In styrene-exposed workers I-SO-adenine DNA adducts were detected (2.6 per 10(9) dNp), while in controls these adducts were below the detection limit. I-SO-adenine adduct levels were affected by both acute and cumulative exposure (P = 0.001, F = 86.0 and P = 0.017, F = 59.0, respectively) and associated with cytochrome P450 2E1 (CYP2E1) polymorphisms (R-2 = 0.442). Mutant frequencies (MF) at the hypoxanthine-guanine phosphoribosyltransferase (HPRT) locus appeared to accumulate with exposure over time and were associated with glutathione S-transferase P1 (GSTP1) polymorphism. DNA repair capacity increased with the exposure, except for the group exposed to the highest styrene concentration. In this particular group, increased DNA repair capacity to remove oxidative DNA damage was found. (C) 2003 International Society for Preventive Oncology. Published by Elsevier Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 12893075
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  • 5
    Keywords: CANCER ; CELLS ; BLOOD ; carcinoma ; CELL ; Germany ; human ; IN-VIVO ; MODEL ; VIVO ; DISEASE ; DISEASES ; HEPATOCELLULAR-CARCINOMA ; liver ; RISK ; TISSUE ; PATIENT ; NITRIC-OXIDE ; DNA ; MECHANISM ; MARKER ; primary ; RISK-FACTORS ; CARCINOGENESIS ; BASE ; TISSUES ; INTERVENTION ; mechanisms ; PROGRESSION ; MALIGNANCIES ; ASSAY ; STRESS ; risk factors ; EFFICACY ; MARKERS ; PATHOGENESIS ; RISK FACTOR ; PRODUCT ; DNA-DAMAGE ; HUMAN LIVER ; ADDUCTS ; ALCOHOL ; COLON CARCINOGENESIS ; LIPID-PEROXIDATION ; OXIDATIVE STRESS ; inflammation ; CHRONIC HEPATITIS ; CIRRHOSIS ; ETHENO-ADDUCTS ; exocyclic DNA adducts ; FATTY-ACID ; fibrosis ; free radicals ; IMMUNOHISTOCHEMICAL DETECTION ; lipid peroxidation ; MALIGNANCY ; MUTATIONAL HOTSPOT ; ONCOLOGY ; PERSISTENT ; PRIMARY HEMOCHROMATOSIS ; WILSONS-DISEASE
    Abstract: During chronic inflammatory processes an excess of free radicals and DNA-reactive aldehydes from lipid peroxidation (LPO) are produced, which deregulate cellular homeostasis and can drive normal cells to malignancy. Etheno (epsilon)-modified DNA bases are generated by reactions of DNA with a major LPO product, trans-4-hydroxy-2-nonenal. We investigated steady state levels of epsilon-DNA adducts in organs, blood or urine from patients with cancer prone diseases, especially when related to persistent inflammatory processes. We have developed sensitive and specific methods for adduct detection in vivo. Hepatic etheno-adduct levels were significantly elevated in patients with Wilson's disease and primary hemochromatosis. Excess storage of copper/ironcausing oxidative stress and LPO-derived DNA-damage, are implicated in disease pathogenesis as confirmed by studies in LEC-rats, a model for Wilson's disease. When patients with alcohol related hepatitis, fatty liver, fibrosis and cirrhosis were compared with asymptomatic livers, excess hepatic DNA-damage was seen in all patients, except those with hepatitis. Etheno-deoxyadenosine excreted in urine was measured in HBV-infected patients diagnosed with chronic hepatitis, cirrhosis and hepatocellular carcinoma: as compared to controls, patients had 20-90-fold increased urinary levels. In conclusion: epsilon-DNA adducts may serve as potential markers for assessing progression of inflammatory cancer-prone diseases. Also the efficacy of human chemopreventive interventions could be verified by using our non-invasive urine assay. Mechanisms and host-factors that influence the steady-state levels of epsilon-DNA adducts in cancer prone tissues are under investigation. (C) 2004 International Society for Preventive Oncology. Published by Elsevier Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 15582261
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  • 6
    Keywords: CANCER ; tumor ; Germany ; MODEL ; THERAPY ; INFORMATION ; LUNG-CANCER ; DISEASE ; EPIDEMIOLOGY ; HISTORY ; incidence ; MORTALITY ; POPULATION ; RISK ; TUMORS ; PATIENT ; FAMILY ; prognosis ; RISK-FACTORS ; SUSCEPTIBILITY ; BREAST ; DECREASE ; NUMBER ; AGE ; etiology ; risk factors ; RISK FACTOR ; RECURRENCE ; case-control studies ; CHILDREN ; PREDICTORS ; SARCOMA ; HEART-DISEASE ; AGENT ; ONCOLOGY ; PERSISTENT ; case-control study ; CHILDHOOD ; DISTRESS ; Ewing's sarcoma ; osteosarcoma
    Abstract: This case-control study investigates etiologically important factors for juvenile osteosarcomas and possible reasons for the relative scarcity of their incidence in the population. Information on a variety of risk factors, psychosocial factors, and factors possibly occurring in early childhood was obtained by interviewing 88 patients (ages 8-25 years) with osteosarcoma, Ewing's sarcomas and other bone tumors, and three age- and sex-matched control groups (hospital, neighbour and family controls), and their mothers. For both sexes, children's diseases in their history, which increased the risk were measles (RR = 1.56, not significant) and mumps (RR = 1.81, 95% Cl = 1.05-3.13), whereas clinically apparent chickenpox was associated with a significant decrease for bone tumors (RR = 0.46, 95% Cl = 0.26-0.8). Dermal and respiratory allergies (without hay fever) were also inversely associated with bone tumors. Breast feeding for longer than 2 months was associated with low risk for bone tumors for boys, whereas for girls, paternal age was a risk factor; remaining stable in a multivariate model (RR = 2.36, 95% CI = 0.90-6.21). A change in the presence of an emotionally significant person or changes of residence were risk factors both in univariate and multivariate analyses. The strongest and most persistent risk factor was difficulties in school, indicative of emotional disturbances (RR 2.58, 95% Q = 1.39-4.78). Considering such host factors as possibly . important modifiers of risk in addition to exogenous carcinogenic agents, these factors were consistent and statistically significant for both sexes and despite the small numbers recruited for this study, thus predicting susceptibility. The factors may become relevant for preventive psychotherapy applied to susceptible persons for improvement of prognosis after surgical therapy in preventing recurrences. (C) 2004 International Society for Preventive Oncology. Published by Elsevier Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 15225895
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