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Sökning: L773:0143 3334 > (2000-2004)

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1.
  • Hemminki, K., et al. (författare)
  • Molecular epidemiology of VHL gene mutations in renal cell carcinoma patients relation to dietary and other factors
  • 2002
  • Ingår i: Carcinogenesis. - Oxford, United Kingdom : Oxford University Press. - 0143-3334. - 0143-3334 (Print) 0143-3334 (Linking) ; 23:5, s. 809-815
  • Tidskriftsartikel (refereegranskat)abstract
    • Carcinogenic chemicals act through DNA damage and mitogenic effects. No established mechanism explains the cancer preventive effects, if any, of food items, such as vegetables and fruit. If such data were available, preferably on tumor-initiating genes, the evidence for the protective effects would become stronger. The von Hipple-Lindau (VHL) gene is the tumor suppressor gene predisposing to both sporadic renal cell carcinoma (RCC) and von Hippel-Lindau disease. We have earlier analyzed VHL mutations in RCCs from 102 Swedish patients identified in a case-control study and here examine associations between patient characteristics, including dietary habits and mutations, considering the type of mutation. The results are given as odds ratios (OR), separately for smokers and all patients. In univariate analysis, consumption of vegetables and citrus fruit decreased the frequency of VHL mutations among smokers and citrus fruit among all patients. In multivariate analysis of smokers' characteristics, welding fumes showed a risk of 5.63 for multiple VHL mutations. In smokers, citrus fruit decreased the OR of GC to AT mutations to 0.13 and that of multiple mutations to 0.17; vegetables decreased the OR for single mutations to 0.22. Among all subjects, welding fumes were a risk factor and citrus fruit a protective factor. Additionally, an intake of selenium protected against multiple mutations. The present results provide evidence that the intake of vegetables, selenium and particularly of citrus fruit protects the renal VHL gene from mutational insults that may be endogenous or common in a population. Even though most of the associations are biologically plausible, and vegetables and fruit were an a priori hypothesis, fortuitous results cannot be ruled out in this relatively small study.
2.
  • Alexandrie, A K, et al. (författare)
  • CYP1A1 and GSTM1 polymorphisms affect urinary 1-hydroxypyrene levels after PAH exposure
  • 2000
  • Ingår i: Carcinogenesis. - Oxford University Press. - 0143-3334. ; 21:4, s. 669-676
  • Tidskriftsartikel (refereegranskat)abstract
    • Certain human biotransformation enzymes have been implicated in the formation and scavenging of the ultimate reactive metabolites, the diolepoxides, from polycyclic aromatic hydrocarbons (PAHs). In the present study, performed on aluminum smelter workers, we have analyzed airborne PAH, the pyrene metabolite 1-hydroxypyrene (1-OHP) in urine, and genotypes for biotransformation enzymes involved in PAH metabolism. The aim was to evaluate the correlation between external exposure and biomarkers of exposure and to investigate to what extent genetic polymorphism in metabolic enzymes can explain interindividual variation in urinary 1-OHP levels. DNA was prepared from blood samples from 98 potroom workers and 55 controls and altogether eight polymorphisms in the CYP1A1, mEH, GSTM1, GSTP1 and GSTT1 genes were analyzed. The 1-OHP excretion was found to correlate significantly (P </= 0.005) to the exposure. The interindividual difference in excretion of 1-OHP was vast (>100-fold) and univariate and multivariate regression analyses were used to find the variables that could determine differences in excretion. The variation could, to some degree, be explained by differences in exposure to airborne particulate-associated PAHs, the use of personal respiratory protection devices, smoking habits and genetic polymorphisms in the cytochrome P450 1A1, GSTM1 and GSTT1 enzymes. The part of the variance that could be explained by differences in biotransformation genotypes seemed to be of the same order of magnitude as the variance explained by differences in exposure. In the control group as well as in the occupationally exposed group, the highest 1-OHP levels were observed in individuals carrying the CYP1A1 Ile/Val genotype who were also of the GSTM1 null genotype. The results show that urinary 1-OHP is a sensitive indicator of recent human exposure to PAHs and that it may also to some extent reflect the interindividual variation in susceptibility to PAHs.
3.
  • Barrett, J H, et al. (författare)
  • Investigation of interaction between N-acetyltransferase 2 and heterocyclic amines as potential risk factors for colorectal cancer
  • 2003
  • Ingår i: Carcinogenesis. - 0143-3334. ; 24:2, s. 275-282
  • Tidskriftsartikel (refereegranskat)abstract
    • Fast N-acetyltransferase 2 (NAT2) acetylators may be at increased risk of colorectal cancer through the activation of carcinogenic heterocyclic amines (HA), which are produced by meat cooked at high temperatures and are found in cigarette smoke. A study of 500 incident colorectal cancer cases and population controls, matched for age, sex and general practitioner, was conducted in the UK to investigate this hypothesis. Usual meat intake and lifetime smoking habits were estimated using a detailed questionnaire administered by interview. Subjects also indicated how well cooked they ate their meat. Subjects were classified as fast or slow NAT2 acetylators on the basis of NAT2 genotype. Complete genotype data were available on 433 matched pairs. The risk of colorectal cancer showed a steady increase with meat intake, rising to an odds ratio of 1.51 [95% confidence interval (1.03, 2.23)] for the highest versus the lowest quartile, after adjustment for total energy intake, and this was even more pronounced for red meat [odds ratio 1.97 (1.30, 2.98)]. However, this effect was not influenced by the preference for well-done meat. Smoking was also associated with an increased risk [odds ratio 1.47 (1.10, 1.98) for ever- versus never-smokers]. In both cases and controls similar to40% of subjects were classified as fast acetylators, and the risks associated with (red) meat intake and smoking did not vary with NAT2 status. This study provides no support for the hypothesis that fast NAT2 acetylators are at increased risk of colorectal cancer, even if exposed to high levels of HA from well-cooked meat or smoking.
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  • Benhamou, S, et al. (författare)
  • Meta- and pooled analyses of the effects of glutathione S-transferase M1 polymorphisms and smoking on lung cancer risk
  • 2002
  • Ingår i: Carcinogenesis. - Oxford University Press. - 0143-3334. ; 23:8, s. 1343-1350
  • Tidskriftsartikel (refereegranskat)abstract
    • Susceptibility to lung cancer may in part be attributable to inter-individual variability in metabolic activation or detoxification of tobacco carcinogens. The glutathione S-transferase M1 (GSTM1) genetic polymorphism has been extensively studied in this context; two recent meta-analyses of case-control studies suggested an association between GSTM1 deletion and lung cancer. At least 15 studies have been published after these overviews. We undertook a new meta-analysis to summarize the results of 43 published case-control studies including >18 000 individuals. A slight excess of risk of lung cancer for individuals with the GSTM1 null genotype was found (odds ratio (OR) = 1.17, 95% confidence interval (CI) 1.07-1.27). No evidence of publication bias was found (P = 0.4), however, it is not easy to estimate the extent of such bias and we cannot rule out some degree of publication bias in our results. A pooled analysis of the original data of about 9500 subjects involved in 21 case-control studies from the International Collaborative Study on Genetic Susceptibility to Environmental Carcinogens (GSEC) data set was performed to assess the role of GSTM1 genotype as a modifier of the effect of smoking on lung cancer risk with adequate power. Analyses revealed no evidence of increased risk of lung cancer among carriers of the GSTM1 null genotype (age-, gender- and center-adjusted OR = 1.08, 95% CI 0.98-1.18) and no evidence of interaction between GSTM1 genotype and either smoking status or cumulative tobacco consumption.
6.
  • Bianchini, Franca, et al. (författare)
  • Inverse correlation between alcohol consumption and lymphocyte levels of 8-hydroxydeoxyguanosine in humans
  • 2001
  • Ingår i: Carcinogenesis. - Oxford University Press. - 0143-3334. ; 22:6, s. 885-890
  • Tidskriftsartikel (refereegranskat)abstract
    • In a cross-sectional study of 115 premenopausal non-smoking women, we examined the relationship between lymphocyte levels of 8-hydroxy-2'-deoxyguanosine (8-oxodGuo) and habitual alcohol consumption. The study was conducted in four different regions of Europe, including Potsdam (Germany), Turin (Italy), Malmo (Sweden) and Granada (Spain). Mean 8-oxodGuo levels differed significantly across study centres (P = 0.001), with the highest levels in Granada [2.17 8-oxodGuox10(-6) 2'-deoxyguanosine (95% confidence interval 1.27-4.40)] and lowest levels in Turin [1.19 (0.36-4.29)]. Mean levels of total alcohol intake and of types of alcoholic beverages consumed (wine, fortified wines, beer and cider) also differed across the study centres (P < 0.05), with the highest total alcohol consumption in Turin, and the lowest intake in GRANADA: When combining all the data, but adjusting for study centre, individual 8-oxodGuo level correlated inversely with alcohol intake. This inverse association remained unaltered after further adjustment for Quetelet Index, fruit and vegetable consumption, and plasma carotenoid levels. Furthermore, the inverse association was also observed for each of the study centres separately, and for different beverage types, with the exception of Granada, where the majority of women were non-drinkers and where alcohol intakes were also very low for the consumers. Finally, on a group level, mean levels of 8-oxodGuo and alcohol intake were also inversely associated between the four study centres. The finding of a relationship between alcohol consumption and 8-oxodGuo in lymphocytes was unexpected and not based on a prior hypothesis. This finding consequently requires confirmation from a randomized intervention study.
7.
  • Bianchini, Franca, et al. (författare)
  • Oxidative DNA damage in human lymphocytes : Correlations with plasma levels of α-tocopherol and carotenoids
  • 2000
  • Ingår i: Carcinogenesis. - Oxford University Press. - 0143-3334. ; 21:2, s. 321-324
  • Tidskriftsartikel (refereegranskat)abstract
    • In order to investigate whether oxidative damage is associated with differences in antioxidant intake, we measured the levels of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodGuo) in lymphocytes and α-tocopherol and several carotenoids in plasma of women with different dietary habits. We found that women from Granada (Spain), a region with a typically Mediterranean diet, had significantly higher levels of 8-oxodGuo compared with Malmo (Sweden), a region with a Northern European dietary intake pattern (2.30 ± 0.78 versus 1.59 ± 1.01 8-oxodGuo/10-6 deoxyguanosine). Levels of plasma α-tocopherol and carotenoids were higher in Granada and these values were significantly positively correlated with levels of 8-oxodGuo. Our results do not support the hypothesis that a Mediterranean diet rich in α-tocopherol and carotenoids protects cells against oxidative DNA damage. It is possible, however, that consumption of foods other than fruits and vegetables, including fats, are responsible for the higher levels of 8-oxodGuo in Granada. Further studies are warranted to better elucidate the role of antioxidants in the modulation of oxidative stress in vivo.
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  • Resultat 1-10 av 51
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