| 1. |
- Garte, S, et al.
(författare)
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Metabolic gene polymorphism frequencies in control populations
- 2001
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Ingår i: Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology. - 1055-9965. ; 10:12, s. 1239-1248
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Tidskriftsartikel (refereegranskat)
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| 2. |
- Benhamou, S, et al.
(författare)
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Meta- and pooled analyses of the effects of glutathione S-transferase M1 polymorphisms and smoking on lung cancer risk
- 2002
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Ingår i: Carcinogenesis. - : Oxford University Press (OUP). - 0143-3334 .- 1460-2180. ; 23:8, s. 1343-1350
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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.
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| 3. |
- Smits, KM, et al.
(författare)
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Association of metabolic gene polymorphisms with tobacco consumption in healthy controls
- 2004
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Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 110:2, s. 266-270
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Tidskriftsartikel (refereegranskat)abstract
- Polymorphisms in genes that encode for metabolic enzymes have been associated with variations in enzyme activity between individuals. Such variations could be associated with differences in individual exposure to carcinogens that are metabolized by these genes. In this study, we examine the association between polymorphisms in several metabolic genes and the consumption of tobacco in a large sample of healthy individuals. The database of the International Collaborative Study on Genetic Susceptibility to Environmental Carcinogens was used. All the individuals who were controls from the case-control studies included in the data set with information on smoking habits and on genetic polymorphisms were selected (n = 20,938). Sufficient information was available on the following genes that are involved in the metabolism of tobacco smoke constituents: CYPIAI, GSTMI, GSTTI, NAT2 and GSTPI. None of the tested genes was clearly associated with smoking behavior. Information on smoking dose, available for a subset of subjects, showed no effect of metabolic gene polymorphisms on the amount of smoking. No association between polymorphisms in the genes studied and tobacco consumption was observed; therefore, no effect of these genes on smoking behavior should be expected.
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| 4. |
- Taioli, E, et al.
(författare)
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Polymorphisms in CYP1A1, GSTM1, GSTT1 and lung cancer below the age of 45 years
- 2003
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Ingår i: International Journal of Epidemiology. - : Oxford University Press (OUP). - 1464-3685 .- 0300-5771. ; 32:1, s. 60-63
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Tidskriftsartikel (refereegranskat)abstract
- Background A genetic component of early-onset lung cancer has been suggested. The role of metabolic gene polymorphisms has never been studied in young lung cancer cases. Phase 1 and Phase 2 gene polymorphisms are involved in tobacco carcinogens' metabolism and therefore in lung cancer risk. Methods The effect of metabolic gene polymorphisms on lung cancer at young ages was studied by pooling data from the Genetic Susceptibility to Environmental Carcinogens (GSEC) database. All primary lung cancer cases of both sexes who were Caucasian and less than or equal to45 years of age at diagnosis, and the corresponding controls were selected. We obtained 261 cases and 1452 controls. Results There was a marginally significant association between lung cancer and GST1 null genotype (OR = 1.2; 95% Cl: 1.0-1.6), and a significant association between lung cancer and the homozygous CYP1A1 Msp1 variant allele (CYP1A1*2A and *2B) genotype (OR = 4.7 95% Cl: 1.2-19.0). When data were stratified by smoking status, the association between CYP1A1 genotype and lung cancer was confined to never smokers. Conclusions These results suggest that metabolic genetic factors play a role in lung cancer developing at young ages.
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| 5. |
- Kalliokoski, KK, et al.
(författare)
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Myocardial perfusion after marathon running
- 2004
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Ingår i: Scandinavian Journal of Medicine and Science in Sport. - : Wiley. - 0905-7188 .- 1600-0838. ; 14:4, s. 208-214
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Tidskriftsartikel (refereegranskat)abstract
- We investigated the effects of acute prolonged exercise (marathon running) on cardiac function and myocardial perfusion. Cardiac dimensions and function were measured in seven endurance-trained men using echocardiography before and repeatedly after marathon (42.2 km) running (at 10 min, 150 min, and 20 h). Myocardial perfusion and perfusion resistance were measured using positron emission tomography and 15O-H2O before and 85-115 min after running. Echocardiographic indices showed only mild and clinically non-significant changes in cardiac function after running. Rate-pressure-corrected basal myocardial perfusion (0.89+/-0.13 vs. 1.20+/-0.32 mL min(-1) g(-1), P=0.04) was increased after running. Also, adenosine-stimulated perfusion tended to be higher (3.67+/-0.81 vs. 4.47+/-0.52 mL min(-1) g(-1), P=0.12) and perfusion resistance during adenosine stimulation was significantly lower after running (26+/-6 vs. 18+/-3 mmHg min g mL(-1), P=0.03). Plasma free fatty acid (FFA) concentration was significantly increased after running. These results show that marathon running does not cause marked changes in cardiac function in healthy men. Basal perfusion was increased after exercise, probably reflecting changes in fuel preferences to increased use of FFAs. Strenuous exercise also seems to enhance coronary reactivity, which could thereby serve as a protective mechanism to vascular events after exercise.
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| 6. |
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| 7. |
- Stenvik, J, et al.
(författare)
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Variable region diversity of the Atlantic cod (Gadus morhua L.) immunoglobulin heavy chain
- 2000
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Ingår i: IMMUNOGENETICS. - : SPRINGER-VERLAG. - 0093-7711. ; 51:8-9, s. 670-680
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Tidskriftsartikel (refereegranskat)abstract
- This study was undertaken to determine whether a lack of VH domain diversity could explain, in part, the failure of Atlantic cod to respond to immunization with the production of specific antibodies. The variability of cod VH regions was studied in 113 cD
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