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  • 1. Hedelin, Maria
    et al.
    Chang, Ellen T.
    Wiklund, Fredrik
    Bellocco, Rino
    Klint, Asa
    Adolfsson, Jan
    Shahedi, Katarina
    Xu, Jianfeng
    Adami, Hans-Olov
    Gronberg, Henrik
    Bälter Augustsson, Katarina
    Karolinska institutet, Sweden.
    Association of frequent consumption of fatty fish with prostate cancer risk is modified by COX-2 polymorphism2007Ingår i: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 120, nr 2, s. 398-405Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Dietary intake of marine fatty acids from fish may protect against prostate cancer development. We studied this association and whether it is modified by genetic variation in cyclooxygenase (COX)-2, a key enzyme in fatty acid metabolism and inflammation. We assessed dietary intake of fish among 1,499 incident prostate cancer cases and 1,130 population controls in Sweden. Five single nucleotide polymorphisms (SNPs) were identified and genotyped in available blood samples for 1,378 cases and 782 controls. Odds ratios (OR) and 95% confidence intervals (CI) were estimated by multivariate logistic regression. Multiplicative and additive interactions between fish intake and COX-2 SNPs on prostate cancer risk were evaluated. Eating fatty fish (e.g. salmon-type fish) once or more per week, compared to never, was associated with reduced risk of prostate cancer (OR: 0.57, 95% CI: 0.43-0.76). The OR comparing the highest to the lowest quartile of marine fatty acids intake was 0.70 (95% CI: 0.51-0.97). We found a significant interaction (p < 0.001) between salmon-type fish intake and a SNP in the COX-2 gene (rs5275: +6365 T/C), but not with the 4 other SNPs examined. We found strong inverse associations with increasing intake of salmon-type fish among carriers of the variant allele (OR for once per week or more vs. never = 0.28, 95% CI: 0.18-0.45; p(trend) < 0.01), but no association among carriers of the more common allele. Frequent consumption of fatty fish and marine fatty acids appears to reduce the risk of prostate cancer, and this association is modified by genetic variation in the COX-2 gene. 

  • 2. Lindstrom, S
    et al.
    Wiklund, F
    Jonsson, B A
    Adami, H O
    Bälter, Katarina
    Brookes, A J
    Xu, J F
    Zheng, S L
    Isaacs, W B
    Adolfsson, J
    Gronberg, H
    Comprehensive genetic evaluation of common E-cadherin sequence variants and prostate cancer risk: strong confirmation of functional promoter SNP2005Ingår i: Human Genetics, ISSN 0340-6717, E-ISSN 1432-1203, Vol. 118, nr 3-4, s. 339-347Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The E-cadherin gene (CDH1) has been proposed as a prostate cancer (PC) susceptibility gene in several studies. Aberrant protein expression has been related to prognosis and progression in PC. In addition, a functional promoter SNP (rsl6260) has been found to associate with PC risk. We performed a comprehensive genetic analysis of CDH1 by using the method of haplotype tagged SNPs in a large Swedish population-based case-control study consisting of 801 controls and 1,636 cases. In addition, Swedish PC families comprising a total of 157 cases sampled for DNA were analyzed for selected SNPs. Seven SNPs, including the promoter SNP rsl6260, that captured over 96% of CDH1 haplotype variation were selected as haplotype tagging SNPs and analyzed for associated PC risk. We observed significant confirmation of rsl6260 (P=0.003) for cases with a positive family history of PC (FH+) both in an independent case-control population and in PC families. In addition, a common haplotype (HapB, 25%) including the variant allele of rsl6260 was associated (P=0.004) with PC risk among FH+ cases. The promoter SNP rsl6260 as well as HapB were significantly transmitted to affected offspring in PC families. We report strong confirmation of the association between PC risk in FH+ cases and a functional CDH1 promoter SNP in an independent population. In conjunction with the biological importance of CDH1 our findings encourage further evaluation of genetic variation in CDH1 in relation to PC etiology. Due to the difficulties in replication of genetic association studies. this finding is unusual and novel.

  • 3. Lindstrom, Sara
    et al.
    Wiklund, Fredrik
    Adami, Hans-Olov
    Bälter Augustsson, Katarina
    Karolinska institutet, Sweden.
    Adolfsson, Jan
    Gronberg, Henrik
    Germ-line genetic variation in the key androgen-regulating genes androgen receptor, cytochrome P450, and steroid-5-alpha-reductase type 2 is important for prostate cancer development2006Ingår i: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 66, nr 22, s. 11077-11083Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Prostate cancer risk may be influenced by single genetic variants in the hormone-regulating genes androgen receptor (AR), cytochrome P450 (CYP17), and steroid-5-alpha-reductase type 2 (SRD5A2). In this study, we comprehensively investigated polymorphisms in these three loci and their joint effect in a large population-based study. We selected 23 haplotype-tagging single-nucleotide polymorphisms (htSNP) that could uniquely describe > 95% of the haplotypes (6 in AR, 6 in CYP17, and 11 in SRD5A2). These htSNPs were then genotyped in the Cancer Prostate in Sweden population (2,826 case subjects and 1,705 controls). We observed significant association for several SNPs in the AR gene (P = 0.004-0.02) and CYP17 (P = 0.009-0.05) and one SNP in SRD5A2 (P = 0.02). Carriers of the most common AR haplotype had a significant excess risk to develop prostate cancer [odds ratio (OR), 1.25; 95% confidence interval (95% CI), 1.1-1.5; P = 0.002], yielding an estimated population attributable risk of 16% (95% CI, 0.06-0.25). Combining risk alleles from these genes yielded a 12% risk increase for each additional high-risk allele carried (95% CI, 1.1-1.2; P for trend = 9.2 x 10(-5)), with an overall OR of 1.87 (95% CI, 1.0-3.4) for carriers of all five included risk alleles, an OR of 2.13 (P for trend = 8 x 10(-4)) for advanced disease, and an OR of 4.35 (P for trend = 7 x 10(-5)) for disease onset before age 65 years. Genetic variation in key genes in the androgen pathway is important for development of prostate cancer and may account for a considerable proportion of all prostate cancers. Carriers of rive high-risk alleles in the AR, CYP17, and SRD5A2 genes are at similar to 2-fold excess risk to develop prostate cancer.

  • 4. Lindstrom, Sara
    et al.
    Zheng, S. Lilly
    Wiklund, Fredrik
    Jonsson, Bjoern-Anders
    Adami, Hans-Olov
    Bälter, Katarina
    Brookes, Anthony J.
    Sun, Jielin
    Chang, Bao-Li
    Liu, Wennuan
    Li, Ge
    Isaacs, William B.
    Adolfsson, Jan
    Gronberg, Henrik
    Xu, Jianfeng
    Systematic replication study of reported genetic associations in prostate cancer: Strong support for genetic variation in the androgen pathway2006Ingår i: The Prostate, ISSN 0270-4137, E-ISSN 1097-0045, Vol. 66, nr 16, s. 1729-1743Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    BACKGROUND. Association studies have become a common and popular method to identify genetic variants predisposing to complex diseases. Despite considerable efforts and initial promising findings, the field of prostate cancer genetics is characterized by inconclusive reports and no prostate cancer gene has yet been established. METHODS. We performed a literature review and identified 79 different polymorphisms reported to influence prostate cancer risk. Of these, 46 were selected and tested for association in a large Swedish population-based case-control prostate cancer population. RESULTS. We observed significant (P < 0.05) confirmation for six polymorphisms located in five different genes. Three of them coded for key enzymes in the androgen biosynthesis and response pathway; the CAG repeat in the androgen receptor (AR) gene (P = 0.03), one SNP in the CYP17 gene (P = 0.04), two SNPs in the SRD5A2 gene (P = 0.02 and 0.02, respectively), a deletion of the GSTT1. gene (P = 0.006), and one SNP in the MSR1 gene, IVS5-59C > A, (P = 0.009). CONCLUSIONS. Notwithstanding the difficulties to replicate findings in genetic association studies, our results strongly support the importance of androgen pathway genes in prostate cancer etiology.

  • 5.
    Moller, Elisabeth
    et al.
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Galeone, Carlotta
    Ist Ric Farmacol Mario Negri, Dept Epidemiol, Milan, Italy.;Univ Milan, Luigi Devoto Dept Occupat Hlth, Milan, Italy..
    Adami, Hans-Olov
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden.;Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA..
    Adolfsson, Jan
    Karolinska Inst, Dept Clin Innovat & Technol CLINTEC, Oncol Ctr, SE-17177 Stockholm, Sweden..
    Andersson, Therese M-L
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Bellocco, Rino
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden.;Univ Milano Bicocca, Dept Stat, Milan, Italy..
    Gronberg, Henrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    Mucci, Lorelei A.
    Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.;Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA.;Harvard Univ, Sch Med, Boston, MA USA..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden..
    The Nordic Nutrition Recommendations and prostate cancer risk in the Cancer of the Prostate in Sweden (CAPS) study2012Ingår i: Public Health Nutrition, ISSN 1368-9800, E-ISSN 1475-2727, Vol. 15, nr 10, s. 1897-1908Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Objective: The Nordic Nutrition Recommendations (NNR) aim at preventing diet-associated diseases such as cancer in the Nordic countries. We evaluated adherence to the NNR in relation to prostate cancer (PC) in Swedish men, including potential interaction with a genetic risk score and with lifestyle factors. Design: Population-based case-control study (Cancer of the Prostate in Sweden (CAPS), 2001-2002). Using data from a semi-quantitative FFQ, we created an NNR adherence score and estimated relative risks of PC by unconditional logistic regression. Individual score components were modelled separately and potential modifying effects were assessed on the multiplicative scale. Setting: Four regions in the central and northern parts of Sweden. Subjects: Incident PC patients (n 1386) and population controls (n 940), frequency-matched on age and region. Results: No overall association with PC was found, possibly due to the generally high adherence to the NNR score and its narrow distribution in the study population. Among individual NNR score components, high compared with low intakes of polyunsaturated fat were associated with an increased relative risk of localized PC. No formal interaction with genetic or lifestyle factors was observed, although in stratified analysis a positive association between the NNR and PC was suggested among men with a high genetic risk score but not among men with a medium or low genetic risk score. Conclusions: Our findings do not support an association between NNR adherence and PC. The suggestive interaction with the genetic risk score deserves further investigations in other study populations.

  • 6.
    Vikstrom, Anna C.
    et al.
    Stockholm Univ, Dept Mat & Environm Chem, S-10405 Stockholm, Sweden..
    Wilson, Kathryn M.
    Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.;Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA..
    Paulsson, Birgit
    Stockholm Univ, Dept Mat & Environm Chem, S-10405 Stockholm, Sweden..
    Athanassiadis, Ioannis
    Stockholm Univ, Dept Mat & Environm Chem, S-10405 Stockholm, Sweden..
    Gronberg, Henrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Adami, Hans-Olov
    Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.;Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Adolfsson, Jan
    Karolinska Inst, CLINTEC, Oncol Ctr, Stockholm, Sweden..
    Mucci, Lorelei A.
    Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.;Brigham & Womens Hosp, Channing Lab, Boston, MA 02115 USA..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Tornqvist, Margareta
    Stockholm Univ, Dept Mat & Environm Chem, S-10405 Stockholm, Sweden..
    Alcohol influence on acrylamide to glycidamide metabolism assessed with hemoglobin-adducts and questionnaire data2010Ingår i: Food and Chemical Toxicology, ISSN 0278-6915, E-ISSN 1873-6351, Vol. 48, nr 3, s. 820-824Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Our purpose was to investigate whether alcohol (ethanol) consumption could have an influence on the metabolism of acrylamide to glycidamide in humans exposed to acrylamide through food. We studied a subsample from a population-based case-control study of prostate cancer in Sweden (CAPS). Questionnaire data for alcohol intake estimates was compared to the ratio of hemoglobin-adduct levels for acrylamide and glycidamide, used as a measure of individual differences in metabolism. Data from 161 nonsmoking men were processed with regard to the influence of alcohol on the metabolism of acrylamide to glycidamide. A negative, linear trend of glycidamide-adduct to acrylamide-adduct-level ratios with increasing alcohol intake was observed and the strongest association (p-value for trend = 0.02) was obtained in the group of men with the lowest adduct levels (<= 47 pmol/g globin) when alcohol intake was stratified by acrylamide-adduct levels. The observed trend is likely due to a competitive effect between ethanol and acrylamide as both are substrates for cytochrome P450 2E1. Our results, strongly indicating that ethanol influence metabolism of acrylamide to glycidamide, partly explain earlier observations of only low to moderate associations between questionnaire data on dietary acrylamide intake and hemoglobin-adduct levels. (C) 2009 Elsevier Ltd. All rights reserved.

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