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  • 1.
    Cantarutti, Anna
    et al.
    Univ Milano Bicocca, Dept Stat & Quantitat Methods, I-20126 Milan, Italy.;Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Bonn, Stephanie E.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Adami, Hans-Olov
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Gronberg, Henrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Bellocco, Rino
    Univ Milano Bicocca, Dept Stat & Quantitat Methods, I-20126 Milan, Italy.;Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Body mass index and mortality in men with prostate cancer2015In: The Prostate, ISSN 0270-4137, E-ISSN 1097-0045, Vol. 75, no 11, p. 1129-1136Article in journal (Refereed)
    Abstract [en]

    BACKGROUNDBody Mass index (BMI) has been shown to affect risk and mortality of several cancers. Prostate cancer and obesity are major public health concerns for middle-aged and older men. Previous studies of pre-diagnostic BMI have found an increased risk of prostate cancer mortality in obese patients. OBJECTIVETo study the associations between BMI at time of prostate cancer diagnosis and prostate cancer specific and overall mortality. METHODSBMI was analyzed both as a continuous variable and categorized into four groups based on the observed distribution in the cohort (BMI<22.5, 22.5<25, 25<27.5 and 27.5kg/m(2)). The association between BMI and mortality was assessed using stratified Cox proportional hazards models and by fitting regression splines for dose response analysis in 3,161 men diagnosed with prostate cancer. After 11 years of follow up via linkage to the population-based cause of death registry, we identified 1,161 (37%) deaths off which 690 (59%) were due to prostate cancer. RESULTSHigh BMI (BMI27.5kg/m(2)) was associated with a statistically significant increased risk of prostate cancer specific mortality (HR:1.44, 95%CI: 1.09-1.90) and overall mortality (HR:1.33, 95%CI: 1.09-1.63) compared to the reference group (BMI 22.5<25kg/m(2)). Additionally, men with a low BMI (<22.5kg/m(2)), had a statistically significant increased risk of prostate cancer specific mortality (HR:1.33, 95%CI: 1.02-1.74) and overall mortality (HR:1.36, 95%CI: 1.11-1.67) compared to the reference. However, this effect disappeared when men who died within the first two years of follow-up were excluded from the analyses while the increased risk of prostate cancer specific mortality and overall mortality remained statistically significant for men with a BMI27.5kg/m(2) (HR:1.44, 95%CI: 1.09-1.90 and HR: 1.33, 95%CI: 1.09-1.63, respectively). CONCLUSIONThis study showed that a high BMI at time of prostate cancer diagnosis was associated with increased overall mortality. Prostate 75: 1129-1136, 2015. (c) 2015 Wiley Periodicals, Inc.

  • 2. Hedelin, Maria
    et al.
    Bälter Augustsson, Katarina
    Karolinska institutet, Sweden.
    Chang, Ellen T.
    Bellocco, Rino
    Klint, Asa
    Johansson, Jan-Erik
    Wiklund, Fredrik
    Thellenberg-Karlsson, Camilla
    Adami, Hans-Olov
    Gronberg, Henrik
    Dietary intake of phytoestrogens, estrogen receptor-beta polymorphisms and the risk of prostate cancer2006In: The Prostate, ISSN 0270-4137, E-ISSN 1097-0045, Vol. 66, no 14, p. 1512-1520Article in journal (Refereed)
    Abstract [en]

    BACKGROUND. The causes of prostate cancer are poorly understood, but genetic factors may be more important than for many other malignancies, and dietary phytoestrogens may be protective. Because phytoestrogens bind tightly to the estrogen receptor-beta, we conducted an epiderniologic investigation of synergistic effects between phytoestrogen intake and estrogen receptor-beta gene polymorphisms. METHODS. We performed a population-based case-control study in Sweden. All participants reported their phytoestrogen intake and donated a blood sample. We identified four haplotype-tagging single nucleotide polymorphisms (htSNPs) and genotyped these htSNPs in 1314 prostate cancer patients and 782 controls. Odds ratios were estimated by multivariate logistic regression. Interactions between phytoestrogen intake and estrogen receptor-beta SNPs on prostate cancer risk were evaluated considering both multiplicative and additive effect scales. RESULTS. We found a significant multiplicative interaction (P = 0.04) between dietary intake of phytoestrogens and a promoter SNP in the estrogen receptor-beta gene (rs 2987983-13950), but not with any of the three other htSNPs (P = 0.11, 0.69, 0.85). Among carriers of the variant promoter alleles, we found strong inverse associations with increasing intake of total phytoestrogens (odds ratio for highest vs. lowest quartile = 0.43; P for trend < 0.001), isoflavonoids (odds ratio = 0.63; P for trend = 0.05), and coumestrol (odds ratio = 0.57; P for trend = 0.003). We found no association between phytoestrogens and prostate cancer among carriers homozygous for the wild-type allele (TT). CONCLUSIONS. Our study provides strong evidence that high intake of phytoestrogens substantially reduce prostate cancer risk among men with specific polymorphic variation in the promoter region of the estrogen receptor-beta gene.

  • 3. 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 pathway2006In: The Prostate, ISSN 0270-4137, E-ISSN 1097-0045, Vol. 66, no 16, p. 1729-1743Article, review/survey (Refereed)
    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.

  • 4.
    Olsson, Mats
    et al.
    Karolinska Univ Hosp, Dept Urol, SE-14186 Stockholm, Sweden..
    Lindstrom, Sara
    Umea Univ, Dept Radiat Sci, Umea, Sweden..
    Haggkvist, Benjamin
    Umea Univ Hosp, Ctr Oncol, S-90185 Umea, Sweden..
    Adami, Hans-Olov
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.;Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Stattin, Par
    Umea Univ, Dept Surg & Perioperat Sci, Umea, Sweden..
    Ask, Birgitta
    Karolinska Univ Hosp, Dept Lab Med, Karolinska Inst, Stockholm, Sweden..
    Rane, Anders
    Karolinska Univ Hosp, Dept Lab Med, Karolinska Inst, Stockholm, Sweden..
    Ekstrom, Lena
    Karolinska Univ Hosp, Dept Lab Med, Karolinska Inst, Stockholm, Sweden..
    Gronberg, Henrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    The UGT2B17 gene deletion is not associated with prostate cancer risk2008In: The Prostate, ISSN 0270-4137, E-ISSN 1097-0045, Vol. 68, no 5, p. 571-575Article in journal (Refereed)
    Abstract [en]

    BACKGROUND. Deletion polymorphism of the UDP-glucuronosyltransferase 2B17 (UG'T2B17) gene has been associated with an increased prostate cancer risk in two previous independent studies. Here we determine the risk in a large-scale population-based case-control study. METHODS. Genotyping was conducted with a 5'-nuclease activity assay to distinguish those with one or two UGT2B17 gene copies (ins/del and ins/ins) from individuals homozygous for the deletion (del/del) allele. RESULTS. In contrast to previous findings, no association between the UGT2B17 deletion polymorphism and prostate cancer risk was found. Furthermore the UGT2B17 gene deletion did not affect the risk for prostate cancer specific death. CONCLUSION. The UGT2B17 deletion polymorphism does not play a major role in prostate cancer susceptibility as previously indicated.

  • 5. Zheng, S. Lilly
    et al.
    Liu, Wennuan
    Wiklund, Fredrik
    Dimitrov, Latchezar
    Bälter, Katarina
    Karolinska institutet, Sweden.
    Sun, Jielin
    Adami, Hans-Olov
    Johansson, Jan-Erik
    Sun, Jishan
    Chang, Baoli
    Loza, Matthew
    Turner, Aubrey R.
    Bleecker, Eugene R.
    Meyers, Deborah A.
    Carpten, John D.
    Duggan, David
    Isaacs, William B.
    Xu, Jianfeng
    Gronberg, Henrik
    A comprehensive association study for genes in inflammation pathway provides support for their roles in prostate cancer risk in the CAPS study2006In: The Prostate, ISSN 0270-4137, E-ISSN 1097-0045, Vol. 66, no 14, p. 1556-1564Article in journal (Refereed)
    Abstract [en]

    BACKGROUND. Recently identified associations of prostate cancer risk with several genes involved in innate immunity support a role of inflammation in the etiology of prostate cancer. Considering inflammation is regulated by a complex system of gene products, we hypothesize sequence variants in many other genes of this pathway are associated with prostate cancer. METHODS. We evaluated 9,275 SNPs; in 1,086 genes of the inflammation pathway using a MegAlleleTM genotyping system among 200 familial cases and 200 unaffected controls selected from a large Swedish case-control population (CAPS). RESULTS. We found that significantly more than the expected numbers of SNPs were significant at a nominal P-value of 0.01, 0.05, and 0.1, providing overall support for our hypothesis. The excess was largest when using a more liberal nominal P-value (0.1); we observed 992 significant SNPs compared with the 854 significant SNPs expected by chance, and this difference was significant based on a permutation test (P = 0.0025). We also began the effort of differentiating true associated SNPs by selecting a small subset of significant SNPs (N = 26) and genotyped these in an independent sample of similar to 1,900 CAPS1 subjects. We were able to confirm 3 of these 26 SNPs. It is expected that many more true associated SNPs will be confirmed among the 992 significant SNPs identified in our pathway screen. CONCLUSIONS. Our study provides the first objective support for an association between prostate cancer and multiple modest-effect genes in inflammatory pathways.

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