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  • 1.
    Davidsson, Sabina
    et al.
    Örebro University, School of Medical Sciences. Department of Urology.
    Andrén, Ove
    Department of Urology, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
    Ohlson, Anna-Lena
    Department of Laboratory Medicine, Pathology, University Hospital Örebro, Örebro, Sweden.
    Carlsson, Jessica
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Urology.
    Andersson, Swen-Olof
    Department of Urology, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
    Giunchi, Francesca
    Department of Hematology-Oncology, Molecular Pathology Laboratory, Addarii Institute of Oncology, University of Bologna, Bologna, Italy.
    Rider, Jennifer R.
    Department of Epidemiology, Boston University School of Public Health, Boston, Massachusett, USA.
    Fiorentino, Michelangelo
    Department of Hematology-Oncology, Molecular Pathology Laboratory, Addarii Institute of Oncology, University of Bologna, Bologna, Italy.
    FOXP3+ regulatory T cells in normal prostate tissue, postatrophic hyperplasia, prostatic intraepithelial neoplasia, and tumor histological lesions in men with and without prostate cancer2018In: The Prostate, ISSN 0270-4137, E-ISSN 1097-0045, Vol. 78, no 1, 40-47 p.Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The tumor promoting or counteracting effects of the immune response to cancer development are thought to be mediated to some extent by the infiltration of regulatory T cells (Tregs ). In the present study we evaluated the prevalence of Treg populations in stromal and epithelial compartments of normal, post atrophic hyperplasia (PAH), prostatic intraepithelial neoplasia (PIN), and tumor lesions in men with and without prostate cancer.

    METHODS: Study subjects were 102 men consecutively diagnosed with localized prostate cancer undergoing radical prostatectomy and 38 men diagnosed with bladder cancer undergoing cystoprostatectomy without prostate cancer at the pathological examination. Whole mount sections from all patients were evaluated for the epithelial and stromal expression of CD4+ Tregs and CD8+ Tregs in normal, PAH, PIN, and tumor lesions. A Friedmańs test was used to investigate differences in the mean number of Tregs across histological lesions. Logistic regression was used to estimate crude and adjusted odds ratios (OR) for prostate cancer for each histological area.

    RESULTS: In men with prostate cancer, similarly high numbers of stromal CD4+ Tregs were identified in PAH and tumor, but CD4+ Tregs were less common in PIN. Greater numbers of epithelial CD4+ Tregs in normal prostatic tissue were positively associated with both Gleason score and pT-stage. We observed a fourfold increased risk of prostate cancer in men with epithelial CD4+ Tregs in the normal prostatic tissue counterpart.

    CONCLUSIONS: Our results may suggest a possible pathway through which PAH develops directly into prostate cancer in the presence of CD4+ Tregs and indicate that transformation of the anti-tumor immune response may be initiated even before the primary tumor is established.

  • 2.
    Fall, Katja
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm; Department of Epidemiology, Harvard School of Public Health, Boston, USA; Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, USA.
    Stark, J. R.
    Department of Epidemiology, Harvard School of Public Health, Boston, USA; Channing Laboratory, Department of Medicine, Brigham Women’s Hospital and Harvard Medical School, Boston, USA.
    Mucci, L. A.
    Department of Epidemiology, Harvard School of Public Health, Boston, USA; Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, USA.
    Chan, J.
    Departments of Epidemiology & Biostatistics and Urology, University of California, San Francisco, USA.
    Stampfer, M. J.
    Department of Epidemiology, Harvard School of Public Health, Boston, USA; Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, USA.
    Kurth, T.
    Department of Epidemiology, Harvard School of Public Health, Boston, USA; Division of Preventive Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, USA.
    Febbo, P. G.
    Duke University School of Medicine, Durham, USA.
    Kantoff, P.
    Division of Solid Tumor Oncology, Dana-Farber Cancer Institute, Boston, USA.
    Ma, J.
    Department of Epidemiology, Harvard School of Public Health, Boston, USA; Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, USA.
    No association between a polymorphic variant of the IRS-1 gene and prostate cancer risk2008In: The Prostate, ISSN 0270-4137, E-ISSN 1097-0045, Vol. 68, no 13, 1416-20 p.Article in journal (Refereed)
    Abstract [en]

    Objective: Insulin receptor substrate-1 (IRS-1) acts as a docking protein between the insulin-like growth factor-1 (IGF-1) receptor and intracellular signaling molecules in the IGF-1 signaling pathway. Accumulating data support a role of IGF-1 in prostate carcinogenesis. We assessed the influence of the most common IRS-1 gene polymorphism (Gly972Arg) on prostate cancer risk, alone and in combination with IGF-1 and other components in the IGF-1 signaling pathway.

    Materials and methods: In a nested case-control study within the Physicians' Health Study, the IRS-1 polymorphism was assayed from prospectively collected samples from 564 incident prostate cancer cases and 758 controls matched on age and smoking. We calculated relative risks (RR) and 95% confidence intervals (CI) using conditional logistic regression.

    Results: Among the controls, 0.8% were homozygous (AA) and 12% were heterozygous (GA) for the polymorphic allele. There was no association between carriage of the A allele and total prostate cancer risk (RR = 1.1 95% CI = 0.8-1.5), advanced disease (stage C or D or lethal prostate cancer, RR = 1.3 95% CI = 0.8-2.3), or plasma IGF-1 levels. We explored possible interactions with body mass index and components in the IGF-1 pathway including IGFBP3, PI3k, and PTEN but none of these factors influenced the relation between IRS-1 genotype and prostate cancer risk.

    Conclusions: Our data do not support an association between carriage of the variant IRS-1 gene and prostate cancer risk.

  • 3. Hedelin, Maria
    et al.
    Bälter, Katarina Augustsson
    Chang, Ellen T.
    Bellocco, Rino
    Klint, Åsa
    Johansson, Jan-Erik
    Örebro University, School of Health and Medical Sciences.
    Wiklund, Fredrik
    Thellenberg-Karlsson, Camilla
    Adami, Hans-Olov
    Grönberg, 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, 1512-1520 p.Article 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 epidemiologic 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.

  • 4.
    Markt, Sarah C.
    et al.
    Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, USA.
    Rider, Jennifer R.
    Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, USA; Brigham & Womens Hosp, Dept Med, Channing Div Network Med, Boston, USA; Harvard Univ, Sch Med, Boston, USA .
    Penney, Kathryn L.
    Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, USA; Brigham & Womens Hosp, Dept Med, Channing Div Network Med, Boston, USA; Harvard Univ, Sch Med, Boston, USA .
    Schumacher, Fredrick R.
    Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, USA.
    Epstein, Mara M.
    Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, USA; Brigham & Womens Hosp, Dept Med, Channing Div Network Med, Boston, USA; Harvard Univ, Sch Med, Boston, USA .
    Fall, Katja
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Department of Epidemiology, Harvard School of Public Health, 677 Huntington Avenue, Boston, MA, United States; Clinical Epidemiology and Biostatistics, Örebro University, Sweden.
    Sesso, Howard D.
    Brigham & Womens Hosp, Dept Med, Div Prevent Med, Boston, USA; Harvard Univ, Sch Med, Boston, USA .
    Stampfer, Meir J.
    Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, USA; Brigham & Womens Hosp, Dept Med, Channing Div Network Med, Boston, USA; Harvard Univ, Sch Med, Boston, USA .
    Mucci, Lorelei A.
    Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, USA; Brigham & Womens Hosp, Dept Med, Channing Div Network Med, Boston, USA; Harvard Univ, Sch Med, Boston, USA .
    Genetic Variation Across C-Reactive Protein and Risk of Prostate Cancer2014In: The Prostate, ISSN 0270-4137, E-ISSN 1097-0045, Vol. 74, no 10, 1034-1042 p.Article in journal (Refereed)
    Abstract [en]

    BACKGROUND. Inflammation has been hypothesized to play an important etiological role in the initiation or progression of prostate cancer. Circulating levels of the systemic inflammation marker C-reactive protein (CRP) have been associated with increased risk of prostate cancer. We investigated the role of genetic variation in CRP and prostate cancer, under the hypothesis that variants may alter risk of disease.

    METHODS. We undertook a case-control study nested within the prospective Physicians' Health Study among 1,286 men with incident prostate cancer and 1,264 controls. Four single-nucleotide polymorphisms (SNPs) were selected to capture the common genetic variation across CRP (r(2) > 0.8). We used unconditional logistic regression to assess the association between each SNP and risk of prostate cancer. Linear regression models explored associations between each genotype and plasma CRP levels.

    RESULTS. None of the CRP SNPs were associated with prostate cancer overall. Individuals with one copy of the minor allele (C) in rs1800947 had an increased risk of high-grade prostate cancer (OR: 1.7; 95% CI: 1.1-2.8), and significantly lower mean CRP levels (P-value < 0.001), however, we found no significant association with lethal disease. Mean CRP levels were significantly elevated in men with one or two copies of the minor allele in rs3093075 and rs1417939, but these were unrelated to prostate cancer risk.

    CONCLUSION. Our findings suggest that SNPs in the CRP gene are not associated with risk of overall or lethal prostate cancer. Polymorphisms in CRP rs1800947 may be associated with higher grade disease, but our results require replication in other cohorts.

  • 5. Shui, Irene M
    et al.
    Stark, Jennifer R
    Penney, Kathryn L
    Schumacher, Fredrick R
    Epstein, Mara M
    Pitt, Michael J
    Stampfer, Meir J
    Tamimi, Rulla M
    Lindstrom, Sara
    Sesso, Howard D
    Fall, Katja
    Department of Epidemiology, Harvard School of Public Health, Boston, MA, United States: Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden.
    Ma, Jing
    Kraft, Peter
    Giovannucci, Edward
    Mucci, Lorelei A
    Genetic variation in the toll-like receptor 4 and prostate cancer incidence and mortality2012In: The Prostate, ISSN 0270-4137, E-ISSN 1097-0045, Vol. 72, no 2, 209-216 p.Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Common genetic variants in the Toll-like receptor 4 (TLR4), which is involved in inflammation and immune response pathways, may be important for prostate cancer.

    METHODS: In a large nested case-control study of prostate cancer in the Physicians' Health Study (1982-2004), 10 single nucleotide polymorphisms (SNPs) were selected and genotyped to capture common variation within the TLR4 gene as well as 5 kb up and downstream. Unconditional logistic regression was used to assess associations of these SNPs with total prostate cancer incidence, and with prostate cancers defined as advanced stage/lethal (T3/T4, M1/N1(T1-T4), lethal) or high Gleason grade (7 (4 + 3) or greater). Cox-proportional hazards regression was used to assess progression to metastases and death among prostate cancer cases.

    RESULTS: The study included 1,267 controls and 1,286 incident prostate cancer cases, including 248 advanced stage/lethal and 306 high grade cases. During a median follow-up of 10.6 years, 183 men died of prostate cancer or developed distant metastases. No statistically significant associations between the TLR4 SNPs were found for total prostate cancer incidence, including SNPs for which an association was reported in other published studies. Additionally, there were no significant associations with TLR4 SNPS and the incidence of advanced stage/lethal, or high grade cancers; nor was there evidence among prostate cancer cases for associations of TLR4 SNPs with progression to prostate cancer specific mortality or bony metastases.

    CONCLUSIONS: Results from this prospective nested case-control study suggest that genetic variation across TLR4 alone is not strongly associated with prostate cancer risk or mortality.

  • 6. Xu, Jianfeng
    et al.
    Sun, Jielin
    Kader, A. Karim
    Lindström, Sara
    Wiklund, Fredrik
    Hsu, Fang-Chi
    Johansson, Jan-Erik
    Örebro University, School of Health and Medical Sciences.
    Zheng, S. Lilly
    Thomas, Gilles
    Hayes, Richard B.
    Kraft, Peter
    Hunter, David J.
    Chanock, Stephen J.
    Isaacs, William B.
    Grönberg, Henrik
    Estimation of absolute risk for prostate cancer using genetic markers and family history2009In: The Prostate, ISSN 0270-4137, E-ISSN 1097-0045, Vol. 69, no 14, 1565-1572 p.Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Multiple DNA sequence variants in the form of single-nucleotide polymorphisms (SNPs) have been found to be reproducibly associated with prostate cancer (PCa) risk. METHODS: Absolute risk for PCa among men with various numbers of inherited risk alleles and family history of PCa was estimated in a population-based case-control study in Sweden (2,893 cases and 1,781 controls), and a nested case-control study from the Prostate, Lung, Colon and Ovarian (PLCO) Cancer Screening Trial in the U.S. (1,172 cases and 1,157 controls). RESULTS: Increased number of risk alleles and positive family history were independently associated with PCa risk. Considering men with 11 risk alleles (mode) and negative family history as having baseline risk, men who had >or=14 risk alleles and positive family history had an odds ratio (OR) of 4.92 [95% confidence interval (CI): 3.64-6.64] in the Swedish study. These associations were confirmed in the U.S. population. Once a man's SNP genotypes and family history are known, his absolute risk for PCa can be readily calculated and easily interpreted. For example, 55-year-old men with a family history and >or=14 risk alleles have a 52% and 41% risk of being diagnosed with PCa in the next 20 years in the Swedish and U.S. populations, respectively. In comparison, without knowledge of genotype and family history, these men had an average population absolute risk of 13%. CONCLUSION: This risk prediction model may be used to identify men at considerably elevated PCa risk who may be selected for chemoprevention.

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