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  • 1.
    Ahlin, Cecilia
    et al.
    Örebro University.
    Zhou, Wenjing
    Holmqvist, Marit
    Holmberg, Lars
    Nilsson, Cecilia
    Jirström, Karin
    Blomqvist, Carl
    Amini, Rose-Marie
    Fjällskog, Marie-Louise
    Cyclin A is a proliferative marker with good prognostic value in node-negative breast cancer2009In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 18, no 9, p. 2501-2506Article in journal (Refereed)
    Abstract [en]

    Background: Proliferative markers are not recommended as prognostic factors for clinical use in breast cancer due to lack of standardization in methodology. However, proliferation is driving several gene expression signatures emphasizing the need for a reliable proliferative marker IF or clinical use. Studies suggest that cyclin A is a prognostic marker with satisfying reproducibility. We investigated cyclin A as a prognostic marker in node-negative breast cancer using previously defined cutoff values. Patients and Methods: In a case-control study, we defined 190 women who died from breast cancer as cases and 190 women alive at the time for the corresponding case's death as controls. Inclusion criteria were tumor size <= 50 mm, no lymph node metastases and no adjuvant chemotherapy. Tumor tissues were immunostained for cyclin A using commercially available antibodies. Results: We found a statistically significant association between expression of cyclin A and breast cancer death in a univariate model: odds ratio for cyclin A(ave) 2.7 [95% confidence interval (CI), 1.7-4.3] and cyclin A(max) 3.4 (CI, 2.1-5.5). Corresponding odds ratio for Ki67 were Ki67(ave) 1.9 (CI, 1.2-3.1) and Ki67(max) 1.7 (CI, 1.1-2.7) and for grade 3.1 (CI, 1.8-5.1). Cyclin A was strongly correlated to Ki67 and grade why a model including all was not appropriate. Conclusions: Cyclin A is a prognostic factor for breast cancer death in node-negative patients using standardized methodology regarding scoring and cutoff values. Adding cyclin A as a proliferative marker to established clinicopathologic factors will improve the separation of low and high risk breast cancer. (Cancer Epidemiol Biomarkers Prev 2009;18(9):2501-6)

  • 2.
    Davidsson, Sabina
    et al.
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Fiorentino, Michelangelo
    Mol Pathol Lab, Addarii Inst Oncol, Dept Hematol Oncol, Univ Bologna, Bologna, Italy; Sch Med, Dana Farber Canc Inst, Dept Pathol, Brigham & Womens Hosp & Adult Oncol, Harvard Univ, Boston MA, USA.
    Andrén, Ove
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Fang, Fang
    Sch Med, Channing Lab, Dept Med, Brigham & Womens Hosp, Harvard Univ, Boston MA, USA; Dept Med Epidemiol & Biostat, Karolinska Inst, Stockholm, Sweden.
    Mucci, Lorelei A.
    Sch Publ Hlth, Dept Epidemiol, Harvard Univ, Boston MA, USA; Sch Med, Channing Lab, Dept Med, Brigham & Womens Hosp, Harvard Univ, Boston MA, USA.
    Varenhorst, Eberhard
    Dept Urol, Linköping Univ Hosp, Linköping, Sweden.
    Fall, Katja
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Rider, Jennifer R.
    Dept Urol, Örebro Univ Hosp, Örebro, Sweden; Sch Med, Dana Farber Canc Inst, Dept Pathol, Brigham & Womens Hosp & Adult Oncol, Harvard Univ, Boston MA, USA.
    Inflammation, focal atrophic lesions, and prostatic intraepithelial neoplasia with respect to risk of lethal prostate cancer2011In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 20, no 10, p. 2280-2287Article in journal (Refereed)
    Abstract [en]

    Background: A challenge in prostate cancer (PCa) management is identifying potentially lethal disease at diagnosis. Inflammation, focal prostatic atrophy, and prostatic intraepithelial neoplasia (PIN) are common in prostate tumor specimens, but it is not clear whether these lesions have prognostic significance. Methods: We conducted a case-control study nested in a cohort of men diagnosed with stage T1a-b PCa through transurethral resection of the prostate in Sweden. Cases are men who died of PCa (n = 228). Controls are men who survived more than 10 years after PCa diagnosis without metastases (n = 387). Slides were assessed for Gleason grade, inflammation, PIN, and four subtypes of focal prostatic atrophy: simple atrophy (SA), postatrophic hyperplasia (PAH), simple atrophy with cyst formation, and partial atrophy. We estimated OR and 95% CI for odds of lethal PCa with multivariable logistic regression. Results: Chronic inflammation and PIN were more frequently observed in tumors with PAH, but not SA. No specific type of atrophy or inflammation was significantly associated with lethal PCa overall, but there was a suggestion of a positive association for chronic inflammation. Independent of age, Gleason score, year of diagnosis, inflammation, and atrophy type, men with PIN were 89% more likely to die of PCa (95% CI: 1.04-3.42). Conclusion: Our data show that PIN, and perhaps presence of moderate or severe chronic inflammation, may have prognostic significance for PCa. Impact: Lesions in tumor adjacent tissue, and not just the tumor itself, may aid in identification of clinically relevant disease. Cancer Epidemiol Biomarkers Prev; 20(10); 2280-7. (C) 2011 AACR.

  • 3.
    Fall, Katja
    et al.
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Örebro University Hospital, Örebro, Sweden; Harvard School of Public Health, Boston MA,USA.
    Garmo, Hans
    Regional Oncology Center, Syracuse NY, USA.
    Gudbjörnsdottir, Soffia
    Sahlgrenska University Hospital, Gothenburgh University, Göteborg, Sweden.
    Stattin, Pär
    Memorial Sloan-Kettering Cancer Center, New York City NY, USA.
    Zethelius, Björn
    Department of Public Health and Caring Sciences/Geriatrics, Uppsala University, Uppsala, Sweden; Medical Products Agency, Uppsala, Sweden.
    Diabetes Mellitus and Prostate Cancer Risk: A Nationwide Case-Control Study within PCBaSe Sweden2013In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 22, no 6, p. 1102-1109Article in journal (Refereed)
  • 4.
    Karlsson, Christina
    et al.
    Örebro University, School of Health and Medical Sciences.
    Bodin, Lennart
    Piehl-Aulin, Karin
    Örebro University, School of Health and Medical Sciences.
    Karlsson, Mats G.
    Örebro University, School of Health and Medical Sciences.
    Tissue microarray validation: a methodologic study with special reference to lung cancer2009In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 18, no 7, p. 2014-2021Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Although tissue microarray (TMA) studies of histopathologic material have been frequently reported in studies of malignant diseases, the question of sample size (i.e., the diameter and the number of tissue cylinders investigated) has been rarely discussed. This study addresses the methodologic question of sample size in a variety of tumor types.

    MATERIAL AND METHODS: Material from 29 cases of lung carcinoma (small cell, squamous cell, and adenocarcinomas) was examined immunohistochemically for Ki-67 and p53 expression in virtually constructed cylinders of different diameters. The influence of tissue sample size (i.e., different numbers of virtual cylinders) was also investigated. Results from Ki-67 evaluation were analyzed as a continuous variable, whereas p53 expression was scored. p53 evaluations based on scoring in cylinders versus scoring of whole sections were also compared. Furthermore, 10 cases of endometrial and breast carcinomas were evaluated for estrogen receptor, Ki-67, and HER2 by scoring up to five cylinders.

    RESULTS AND CONCLUSIONS: Tissue cylinders of 0.6 and 1.0 mm diameters were compared and found equally informative about Ki-67 expression (intraclass correlation, 0.96). A statistical approach considering intraindividual and interindividual variation data is presented, indicating that in this specific setting three cylinders per case is an adequate sample size for TMA studies. Further sampling yields only a small gain in accuracy as determined by Ki-67 quantification and p53 scoring (kappa-coefficient, 0.9). For endometrial and breast tissues, TMA scoring of three cylinders yielded excellent agreement (kappa, >0.75) compared with whole-section scoring.

  • 5. Larsson, Susanna C.
    et al.
    Andersson, Swen-Olof
    Örebro University, School of Health and Medical Sciences.
    Johansson, Jan-Erik
    Örebro University, School of Health and Medical Sciences.
    Wolk, Alicja
    Fruit and vegetable consumption and risk of bladder cancer: a prospective cohort study2008In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 17, no 9, p. 2519-2522Article in journal (Refereed)
    Abstract [en]

    Fruit and vegetable consumption has been inconsistently associated with risk of bladder cancer. We used data from a prospective population-based cohort study of 82,002 Swedish women and men to examine the association between fruit and vegetable consumption and bladder cancer incidence. Diet was assessed with a validated food frequency questionnaire. During a mean follow-up of 9.4 years, 485 incident cases of bladder cancer were identified in the Swedish cancer registries. We found no statistically significant association between intakes of total fruits and vegetables, total fruits, or total vegetables and bladder cancer risk after adjustment for age, sex, education, and cigarette smoking. The multivariate rate ratios (95% confidence intervals) comparing the highest with the lowest quartile of intake were 0.80 (0.60-1.05) for total fruits and vegetables, 0.93 (0.69-1.25) for fruits, and 0.89 (0.67-1.19) for vegetables. Likewise, no associations were observed for citrus fruits, cruciferous vegetables, or green leafy vegetables. The associations did not differ by sex or smoking status. In conclusion, findings from this prospective study suggest that fruit and vegetable intakes are not likely to be appreciably associated with the risk of bladder cancer.

  • 6.
    Lindblad, Per
    et al.
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden; Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    Wolk, A.
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden.
    Bergstrom, R.
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden; Department of Statistics, Uppsala University, Uppsala, Sweden.
    Adami, H. O.
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden; Department of Epidemiology, Harvard School of Public Health, Boston, MA, United States .
    Diet and risk of renal cell cancer: a population-based case-control study1997In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 6, no 4, p. 215-223Article in journal (Refereed)
    Abstract [en]

    In a few previous studies on diet and renal cell cancer, an inconsistent positive association with meat, milk, and protein and a negative association with vegetable and fruit consumption have been found. Whereas earlier studies have dealt with recent diet only, our study explored the effect of foods consumed both during the usual adult lifetime and 20 years prior to interview. The study included 379 individuals with incident histologically verified renal cell cancer and 350 control subjects residing in eight counties in Sweden between June 1989 and December 1991. Usual adult dietary intake and dietary habits 20 years prior to interview were assessed by a structured face-to-face interview and a self-administered questionnaire, respectively. Odds ratios were estimated through unconditional logistic regression. We have not observed an association of renal cell cancer with milk or total meat consumption per se; however, frequent intake of fried/sauteed meat increased the risk of renal cell cancer by about 60%; frequent consumption of poultry was also associated with an increased risk (P for trend, 0.05). A significantly protective effect on risk of renal cell cancer was observed with increasing consumption of fruit (P for trend, 0.05). When analyzed by smoking status, total fruit and especially citrus fruit consumption among nonsmokers showed an even stronger protective effect; the highest quartiles of total fruit, apple, and citrus fruit consumption entailed a 50-60% reduction in risk of renal cell cancer compared with the lowest quartiles. There was a suggestion of a protective effect of high total vegetable consumption. A protective effect of vitamin C and alpha-tocopherol was also more pronounced in nonsmokers (P for trend, 0.004 and 0.007, respectively). Our study adds to the evidence that diet may have an important role in the etiology of renal cell cancer.

  • 7.
    Lindblad, Per
    et al.
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden; Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    Wolk, A.
    Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    Bergström, R.
    Department of Urology, Sundsvall Hospital, Sundsvall, Sweden; Department of Statistics, Uppsala University, Uppsala, Sweden; Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden.
    Persson, I.
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden.
    Adami, H. O.
    Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, United States; Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden.
    The role of obesity and weight fluctuations in the etiology of renal cell cancer: a population-based case-control study1994In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 3, no 8, p. 631-9Article in journal (Refereed)
    Abstract [en]

    The causes of renal cell cancer (RCC) are poorly understood. Besides smoking, obesity remains the only risk factor that is fairly well established. The association between obesity and RCC appears stronger and more consistent in women than in men. We investigated the question of whether this apparent sex difference could be explained by repeated weight changes (weight cycling), less physical exercise, or pharmacological treatment of obesity in women. Structured face-to-face interviews were carried out with 379 (70% of all eligible) incident cases of RCC and 353 (72% of eligible) controls. The relationships between RCC and adult height, weight, and body mass index (BMI), defined as weight/height, were analyzed. Odds ratios (ORs) were estimated through logistic regression. No association was found between adult height and RCC. In men, weight and BMI appeared at most to be weakly related to risk of RCC. In women, higher adult weight and BMI (usual, highest, and lowest) and also high BMI at ages 30, 40, and 50 years were consistently associated with a significantly increased risk of RCC. Women with an usual adult BMI in the top 5% had a nearly 3-fold increased risk of RCC [OR, 2.67; 95% confidence interval (CI), 1.02-7.01]. Compared with individuals with no weight-loss periods, 2 or more such periods implied an OR of 0.96 (95% CI, 0.32-2.90) in men and 3.87 (95% CI, 1.20-12.45) in women. Physical activity at work reduced the risk of RCC in men but not women. Regular use of diet pills containing amphetamine was associated with an increased risk of RCC (OR, 4.06; 95% CI, 1.35-12.22).(ABSTRACT TRUNCATED AT 250 WORDS)

  • 8.
    Lu, Donghao
    et al.
    Department of Medical Epidemiology & Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Carlsson, Jessica
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Penney, Kathryn L.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, USA; Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston MA, USA.
    Davidsson, Sabina
    Örebro University Hospital. Örebro University, School of Medical Sciences. Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Andersson, Swen-Olof
    Department of Urology, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
    Mucci, Lorelei A.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, USA; Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston MA, USA.
    Valdimarsdóttir, Unnur
    Department of Medical Epidemiology & Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, USA; Faculty of Medicine, Center of Public Health Sciences, School of Health Sciences, University of Iceland, Reykjavík, Iceland.
    Andrén, Ove
    Örebro University, School of Medical Sciences. Department of Urology, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
    Fang, Fang
    Department of Medical Epidemiology & Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fall, Katja
    Örebro University, School of Medical Sciences. Department of Medical Epidemiology & Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Expression and Genetic Variation in Neuroendocrine Signaling Pathways in Lethal and Nonlethal Prostate Cancer among Men Diagnosed with Localized Disease2017In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 26, no 12, p. 1781-1787Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Recent data suggest that neuroendocrine signaling pathways may play a role in the progression of prostate cancer, particularly for early-stage disease. We aimed to explore whether expression of selected genes in the adrenergic, serotoninergic, glucocorticoid, and dopaminergic pathways differs in prostate tumor tissue from men with lethal disease compared to men with nonlethal disease.

    METHODS: Based on the Swedish Watchful Waiting Cohort, we included 511 men diagnosed with incidental prostate cancer through TURP during 1977-1998 with follow-up up to 30 years. For those with tumor tissue (N=262), we measured mRNA expression of 223 selected genes included in neuroendocrine pathways. Using DNA from normal prostate tissue (N=396), we genotyped 36 SNPs from 14 receptor genes. Lethal prostate cancer was the primary outcome in analyses with pathway gene expression and genetic variants.

    RESULTS: Differential expression of genes in the serotoninergic pathway was associated with risk of lethal prostate cancer (P=0.007); similar but weaker associations were noted for the adrenergic (P=0.014) and glucocorticoid (P=0.020) pathways. Variants of the HTR2A (rs2296972; P=0.002) and NR3CI (rs33388; P=0.035) genes (within the serotoninergic and glucocorticoid pathways) were associated with lethal cancer in over-dominant models. These genetic variants were correlated with expression of several genes in corresponding pathways (P<0.05).

    CONCLUSIONS: Our findings lend support to hypothesis that the neuroendocrine pathways, particularly serotoninergic pathway, are associated with lethal outcome in the natural course of localized prostate cancer.

    IMPACT: The current study provides evidence of the role of neuroendocrine pathways in prostate cancer progression which may have clinical utility.

  • 9. Mucci, Lorelei A.
    et al.
    Pawitan, Yudi
    Demichelis, Francesca
    Fall, Katja
    Stark, Jennifer R.
    Adami, Hans-Olov
    Andersson, Swen-Olof
    Örebro University, School of Health and Medical Sciences.
    Andrén, Ove
    Eisenstein, Anna
    Holmberg, Lars
    Huang, Wei
    Kantoff, Philip W.
    Kim, Robert
    Perner, Sven
    Stampfer, Meir J.
    Johansson, Jan-Erik
    Örebro University, School of Health and Medical Sciences.
    Rubin, Mark A.
    Testing a multigene signature of prostate cancer death in the Swedish Watchful Waiting Cohort2008In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 17, no 7, p. 1682-1688Article in journal (Refereed)
    Abstract [en]

    Although prostate cancer is a leading cause of cancer death, most men die with and not from their disease, underscoring the urgency to distinguish potentially lethal from indolent prostate cancer. We tested the prognostic value of a previously identified multigene signature of prostate cancer progression to predict cancer-specific death. The Örebro Watchful Waiting Cohort included 172 men with localized prostate cancer of whom 40 died of prostate cancer. We quantified protein expression of the markers in tumor tissue by immunohistochemistry and stratified the cohort by quintiles according to risk classification. We accounted for clinical variables (age, Gleason, nuclear grade, and tumor volume) using Cox regression and calculated receiver operator curves to compare discriminatory ability. The hazard ratio of prostate cancer death increased with increasing risk classification by the multigene model, with a 16-fold greater risk comparing highest-risk versus lowest-risk strata, and predicted outcome independent of clinical factors (P = 0.002). The best discrimination came from combining information from the multigene markers and clinical data, which perfectly classified the lowest-risk stratum where no one developed lethal disease; using the two lowest-risk groups as reference, the hazard ratio (95% confidence interval) was 11.3 (4.0-32.8) for the highest-risk group and difference in mortality at 15 years was 60% (50-70%). The combined model provided greater discriminatory ability (area under the curve = 0.78) than the clinical model alone (area under the curve = 0.71; P = 0.04). Molecular tumor markers can add to clinical variables to help distinguish lethal and indolent prostate cancer and hold promise to guide treatment decisions. 

  • 10. Mucci, Lorelei A.
    et al.
    Pawitan, Yudi
    Demichelis, Francesca
    Fall, Katja
    Stark, Jennifer R.
    Adami, Hans-Olov
    Andersson, Swen-Olof
    Örebro University, School of Health and Medical Sciences.
    Andrén, Ove
    Örebro University, School of Health and Medical Sciences.
    Eisenstein, Anna S.
    Holmberg, Lars
    Huang, Wei
    Kantoff, Philip W.
    Perner, Sven
    Stampfer, Meir J.
    Johansson, Jan-Erik
    Örebro University, School of Health and Medical Sciences.
    Rubin, Mark A.
    Nine-gene molecular signature is not associated with prostate cancer death in a watchful waiting cohort2008In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 17, no 1, p. 249-251Article in journal (Refereed)
    Abstract [en]

    Tumor molecular markers hold promise to distinguish potentially lethal from indolent prostate cancer and to guide treatment choices. A previous study identified a nine-gene molecular signature in tumors associated with prostate-specific antigen relapse after prostatectomy. We examined this molecular model in relation to prostate cancer death among 172 men with initially localized disease. We quantified protein expression of the nine genes in tumors to classify progression risk. Accounting for clinical prognostic factors, the nine-gene model did not provide discrimination to predict lethal and indolent prostate cancer.

  • 11. Rubin, Mark A.
    et al.
    Bismar, Tarek A.
    Andrén, Ove
    Örebro University, School of Health and Medical Sciences.
    Mucci, Lorelei
    Kim, Robert
    Shen, Ronglai L.
    Ghosh, Debashis
    Wei, John T.
    Chinnaiyan, Arul M.
    Adami, Hans-Olov
    Kantoff, Philip W.
    Johansson, Jan-Erik
    Decreased alpha-methylacyl CoA racemase expression in localized prostate cancer is associated with an increased rate of biochemical recurrence and cancer-specific death2005In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 14, no 6, p. 1424-1432Article in journal (Refereed)
    Abstract [en]

    alpha-Methylacyl CoA racemase (AMACR) is overexpressed in prostate cancer relative to benign prostatic tissue. AMACR expression is highest in localized prostate cancer and decreases in metastatic prostate cancer. Herein, we explored the use of AMACR as a biomarker for aggressive prostate cancer. AMACR protein expression was determined by immunohistochemistry using an image analysis system on two localized prostate cancer cohorts consisting of 204 men treated by radical prostatectomy and 188 men followed expectantly. The end points for the cohorts were time to prostate-specific antigen (PSA) failure (i.e., elevation > 0.2 ng/mL) and time to prostate cancer death in the watchful waiting cohort. Using a regression tree method, optimal AMACR protein expression cutpoints were determined to best differentiate prostate cancer outcome in each of the cohorts separately. Cox proportional hazard models were then employed to examine the effect of the AMACR cutpoint on prostate cancer outcome, and adjusted for clinical variables. Lower AMACR tissue expression was associated with worse prostate cancer outcome, independent of clinical variables (hazard ratio, 3.7 for PSA failure; P = 0.018; hazard ratio, 4.1 for prostate cancer death, P = 0.0006). Among those with both low AMACR expression and high Gleason score, the risk of prostate cancer death was 18-fold higher (P = 0.006). The AMACR cutpoint developed using prostate cancer-specific death as the end point predicted PSA failures independent of Gleason score, PSA, and margin status. This is the first study to show that AMACR expression is significantly associated with prostate cancer progression and suggests that not all surrogate end points may be optimal to define biomarkers of aggressive prostate cancer.

  • 12.
    Sigurdardottir, Lara G.
    et al.
    Center of Public Health Sciences, University of Iceland, Reykjavik, Iceland; Faculty of Medicine, University of Iceland, Reykjavik, Iceland; The Icelandic Cancer Society, Reykjavik, Iceland.
    Valdimarsdottir, Unnur A.
    Center of Public Health Sciences, University of Iceland, Reykjavik, Iceland; Faculty of Medicine, University of Iceland, Reykjavik, Iceland; Clinical Epidemiology Unit, Örebro University Hospital, Örebro, Sweden; Örebro University, Örebro, Sweden; Department of Epidemiology, Harvard School of Public Health, Boston MA, USA.
    Fall, Katja
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Center of Public Health Sciences, University of Iceland, Reykjavik, Iceland; Clinical Epidemiology Unit, Örebro University Hospital, Örebro, Sweden; Department of Epidemiology, Harvard School of Public Health, Boston MA, USA.
    Rider, Jennifer R.
    Department of Epidemiology, Harvard School of Public Health, Boston MA, USA; Channing Laboratory, Harvard Medical School, Boston MA, USA.
    Lockley, Steven W.
    Division of Sleep Medicine, Department of Medicine, Brigham and Women’s Hospital, Boston MA, USA; Division of Sleep Medicine, Harvard Medical School, Boston MA, USA.
    Schernhammer, Eva S.
    Department of Epidemiology, Harvard School of Public Health, Boston MA, USA; Channing Laboratory, Harvard Medical School, Boston MA, USA.
    Mucci, Lorelei A.
    Center of Public Health Sciences, University of Iceland, Reykjavik, Iceland; Department of Epidemiology, Harvard School of Public Health, Boston MA, USA; Channing Laboratory, Harvard Medical School, Boston MA, USA.
    Circadian disruption, sleep loss, and prostate cancer risk: a systematic review of epidemiologic studies2012In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 21, no 7, p. 1002-1011Article, review/survey (Refereed)
    Abstract [en]

    Disruption of the circadian system has been hypothesized to increase cancer risk, either because of direct disruption of the molecular machinery generating circadian rhythms or because of disruption of parameters controlled by the clock such as melatonin levels or sleep duration. This hypothesis has been studied in hormone-dependent cancers among women, but data are sparse about potential effects of circadian disruption on the risk of prostate cancer. This review systematically examines available data evaluating the effects of light at night, sleep patterns, and night shift work on prostate cancer risk.

  • 13. Sigurdardottir, Lara G.
    et al.
    Valdimarsdottir, Unnur A.
    Mucci, Lorelei A.
    Fall, Katja
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Rider, Jennifer R.
    Schernhammer, Eva
    Czeisler, Charles A.
    Launer, Lenore
    Harris, Tamara
    Stampfer, Meir J.
    Gudnason, Vilmundur
    Lockley, Steven W.
    Sleep disruption among older men and risk of prostate cancer2013In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 22, no 5, p. 872-879Article in journal (Refereed)
    Abstract [en]

    Background: Although positive associations have consistently been reported between sleep disruption and breast cancer, less is known about its potential role in prostate cancer.

    Methods: Within the prospective AGES-Reykjavik cohort study, we followed 2,102 men recruited in 20022006 until the end of 2009. Participants answered questions on sleep disruption. Information on the occurrence of prostate cancer was obtained through record linkages across the Icelandic Cancer Registry. We used Cox regression models with 95% confidence intervals (CI) to estimate HRs of prostate cancer by symptoms of sleep disruption.

    Results: During follow-up, 135 men (6.4%) were diagnosed with prostate cancer. Compared with men without sleep disruption, those with problems falling and staying asleep were at significantly increased risk of prostate cancer [HR, 1.7 (95% CI, 1.0-2.9) and 2.1 (95% CI, 1.2-3.7)], respectively, with increasing sleep disruption severity. When restricted to advanced prostate cancer (>= stage T3 or lethal disease), these associations became even stronger [HR 2.1 (95% CI, 0.7-6.2) and 3.2 (95% CI, 1.1-9.7)]. The results did not change after excluding from the analyses men who woke up during the night, indicative of nocturia, suggesting limited risk of reverse association.

    Conclusions: Our data suggest that certain aspects of sleep disruption may confer an increased risk of prostate cancer and call for additional, larger studies with longer follow-up times.

    Impact: Prostate cancer is one of the leading public health concerns in men; if confirmed in future studies, the association between sleep disruption and prostate cancer risk may open new avenues for prevention.

  • 14.
    Udumyan, Ruzan
    et al.
    Örebro University, School of Medical Sciences.
    Montgomery, Scott
    Örebro University, School of Medical Sciences.
    Fang, Fang
    Department of Medical Epidemiology & Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Valdimarsdóttir, Unnur
    Faculty of Medicine, Center of Public Health Sciences, School of Health Sciences, University of Iceland, Reykjavik, Iceland.
    Fall, Katja
    Örebro University, School of Medical Sciences.
    Stress resilience in late adolescence and survival among cancer patients: a Swedish register-based cohort study2018In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Chronic stress has been suggested to play a role in cancer progression, but few studies have so far examined the potential influence of stress susceptibility. This national register-based cohort study utilizes a unique data source to investigate whether a stress resilience measure is associated with survival in cancer patients.

    METHODS: The cohort includes 9,318 Swedish male cancer patients born during 1952-1956 who had their stress resilience evaluated at a semi-structured interview with a psychologist during mandatory conscription examination in late adolescence.

    RESULTS: Over a median of 3 years of follow-up from cancer diagnosis, a total of 2,541 patients died (2,322 from cancer). Overall, low (23%) compared with high (25%) stress resilience was associated with increased mortality (adjusted hazard ratio estimated by Cox regression 1.45; 95% confidence interval 1.28-1.65), particularly among men with carcinomas of the oropharynx (2.62, 1.24-5.56), upper respiratory tract (4.64, 1.05-20.41), and prostate (2.20, 1.04-4.62), as well as with Hodgkin's lymphoma (3.52, 1.40-8.86). An association was evident both for cancer types associated with smoking (1.35, 1.10-1.66) and malignancies without an established smoking aetiology (1.32, 1.12-1.56). The association between low stress resilience and mortality could partly be explained by tumour stage, marital status, and psychiatric comorbidity at cancer diagnosis.

    CONCLUSIONS: We observed an association between low stress resilience and mortality among men diagnosed with cancer, particularly, oropharyngeal cancer, upper respiratory tract cancers, prostate cancer and Hodgkin's lymphoma.

    IMPACT: These results suggest that individual variation in stress resilience may influence survival among men with some cancer types.

  • 15.
    Ugge, Henrik
    et al.
    Örebro University, School of Medical Sciences. Department of Urology, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Udumyan, Ruzan
    Örebro University, School of Medical Sciences.
    Carlsson, Jessica
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Davidsson, Sabina
    Örebro University, School of Medical Sciences.
    Andrén, Ove
    Örebro University, School of Medical Sciences. Department of Urology, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Montgomery, Scott
    Örebro University, School of Medical Sciences. Clinical Epidemiology Unit, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology and Public Health, University College London, London, United Kingdom.
    Fall, Katja
    Örebro University, School of Medical Sciences.
    Appendicitis before age 20 years is associated with an increased risk of later prostate cancer2018In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 27, no 6, p. 660-664Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Appendicitis before age 20 years has been observed to influence the risk of several inflammatory conditions, possibly through underlying immunological mechanisms. Inflammation has further been suggested to be involved in prostate cancer development. We therefore hypothesized that immunological characteristics signaled by appendicitis before late adolescence might influence the risk of later prostate cancer, and aimed to evaluate this association in a population-based study.

    METHODS: We identified a large cohort of Swedish men who underwent assessment for military conscription around the age of 18 years (n= 242,573). Medical diagnoses at time of conscription were available through the Swedish Military Conscription Register. The Swedish Cancer Register was used to identify diagnoses of prostate cancer. Multivariable adjusted Cox regression analyses were used to estimate hazard ratios (HR) and 95% confidence intervals (95% CI) for the association between appendicitis and prostate cancer.

    RESULTS: During a median of 36.7 years of follow-up, 1,684 diagnoses of prostate cancer occurred. We found a statistically significant association between appendicitis and overall prostate cancer (adjusted HR: 1.70; 95% CI: 1.08-2.67). The risk was notably increased for advanced (HR: 4.42; 95% CI: 1.74-11.22) and lethal (HR: 8.95; 95% CI: 2.98-26.91) prostate cancer.

    CONCLUSION: These results suggest that a diagnosis of appendicitis before adulthood potentially signals underlying immune characteristics and a pattern of inflammatory response relevant to prostate cancer risk.

    IMPACT: The study lends support to the proposed role of inflammation in prostate carcinogenesis, and adds another area of investigation potentially relevant to prostate cancer development.

  • 16.
    Zareba, Piotr
    et al.
    Division of Urology, McMaster University, Hamilton ON, Canada.
    Flavin, Richard
    Department of Pathology, Dana-Farber Cancer Institute, Harvard Medical School, Boston MA, United States; Department of Pathology, Trinity College Dublin, Dublin, Ireland.
    Isikbay, Masis
    Harvard Medical School, Boston Massachusetts, United States.
    Rider, Jennifer R.
    Department of Epidemiology, Boston University School of Public Health, Boston MA, United States; Harvard T.H. Chan School of Public Health, Boston MA, United States.
    Gerke, Travis A.
    Harvard T.H. Chan School of Public Health, Boston MA, United States; Department of Cancer Epidemiology, Moffitt Cancer Center, Tampa FL, United States.
    Finn, Stephen
    Department of Pathology, Dana-Farber Cancer Institute, Harvard Medical School, Boston MA, United States; Department of Pathology, Trinity College Dublin, Dublin, Ireland.
    Pettersson, Andreas
    Harvard T.H. Chan School of Public Health, Boston MA, United States; Clinical Epidemiology Unit, Department of Medicine, Karolinska Universitetssjukhuset, Stockholm, Sweden.
    Giunchi, Francesca
    Pathology Unit, Addarii Institute, S. Orsola-Malpighi Hospital, Bologna, Italy.
    Unger, Robert H.
    Harvard T.H. Chan School of Public Health, Boston MA, United States.
    Tinianow, Alex M.
    Harvard T.H. Chan School of Public Health, Boston MA, United States.
    Andersson, Swen-Olof
    Örebro University Hospital. Department of Urology, Örebro University Hospital, Örebro, Sweden; School of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Andrén, Ove
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Fall, Katja
    Örebro University, School of Medical Sciences. Harvard T.H. Chan School of Public Health, Boston MA, United States.
    Fiorentino, Michelangelo
    Department of Pathology, Dana-Farber Cancer Institute, Harvard Medical School, Boston MA, United States; Pathology Unit, Addarii Institute, S. Orsola-Malpighi Hospital, Bologna, Italy.
    Mucci, Lorelei A.
    Harvard T.H. Chan School of Public Health, Boston MA, United States; Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston MA, United States; Division of Public Health Sciences, University of Iceland, Reykjavik, Iceland.
    Perineural Invasion and Risk of Lethal Prostate Cancer2017In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 26, no 5, p. 719-726Article in journal (Refereed)
    Abstract [en]

    Background: Prostate cancer has a propensity to invade and grow along nerves, a phenomenon called perineural invasion (PNI). Recent studies suggest that the presence of PNI in prostate cancer has been associated with cancer aggressiveness.

    Methods: We investigated the association between PNI and lethal prostate cancer in untreated and treated prostate cancer cohorts: the Swedish Watchful Waiting Cohort of 615 men who underwent watchful waiting, and the U.S. Health Professionals Follow-Up Study of 849 men treated with radical prostatectomy. One pathologist performed a standardized histopathologic review assessing PNI and Gleason grade. Patients were followed from diagnosis until metastasis or death.

    Results: The prevalence ofPNI was7% and 44% in the untreated and treated cohorts, respectively. PNI was more common in high Gleason grade tumors in both cohorts. PNI was associated with enhanced tumor angiogenesis, but not tumor proliferation or apoptosis. In the Swedish study, PNI was associated with lethal prostate cancer [OR 7.4; 95% confidence interval (CI), 3.6-16.6; P < 0.001]. A positive, although not statistically significant, associationpersisted after adjustment for age, Gleason grade, and tumor volume (OR 1.9; 95% CI, 0.8-5.1; P = 0.17). In the U.S. study, PNI predicted lethal prostate cancer independent of clinical factors (HR 1.8; 95% CI, 1.0, 3.3; P = 0.04).

    Conclusions: These data support the hypothesis that perineural invasion creates a microenvironment that promotes cancer aggressiveness. Impact: Our findings suggest that PNI should be a standardized component of histopathologic review, and highlights a mechanism underlying prostate cancer metastasis. (C) 2017 AACR.

  • 17. Zheng, S. Lilly
    et al.
    Stevens, Victoria L.
    Wiklund, Fredrik
    Isaacs, Sarah D.
    Sun, Jielin
    Smith, Shelly
    Pruett, Kristen
    Wiley, Kathleen E.
    Kim, Seong-Tae
    Zhu, Yi
    Zhang, Zheng
    Hsu, Fang-Chi
    Turner, Aubrey R.
    Johansson, Jan-Erik
    Örebro University, School of Health and Medical Sciences.
    Liu, Wennuan
    Kim, Jin Woo
    Chang, Bao-Li
    Duggan, David
    Carpten, John
    Rodriguez, Carmen
    Isaacs, William
    Grönberg, Henrik
    Xu, Jianfeng
    Two independent prostate cancer risk-associated Loci at 11q132009In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 18, no 6, p. 1815-1820Article in journal (Refereed)
    Abstract [en]

    Single nucleotide polymorphisms (SNP) at 11q13 were recently implicated in prostate cancer risk by two genome-wide association studies and were consistently replicated in multiple study populations. To explore prostate cancer association in the regions flanking these SNPs, we genotyped 31 tagging SNPs in a approximately 110 kb region at 11q13 in a Swedish case-control study (Cancer of the Prostate in Sweden), including 2,899 cases and 1,722 controls. We found evidence of prostate cancer association for the previously implicated SNPs including rs10896449, which we termed locus 1. In addition, multiple SNPs on the centromeric side of the region, including rs12418451, were also significantly associated with prostate cancer risk (termed locus 2). The two groups of SNPs were separated by a recombination hotspot. We then evaluated these two representative SNPs in an additional approximately 4,000 cases and approximately 3,000 controls from three study populations and confirmed both loci at 11q13. In the combined allelic test of all four populations, P = 4.0 x 10(-11) for rs10896449 at locus 1 and P = 1.2 x 10(-6) for rs12418451 at locus 2, and both remained significant after adjusting for the other locus and study population. The prostate cancer association at these two 11q13 loci was unlikely confounded by prostate-specific antigen (PSA) detection bias because neither SNP was associated with PSA levels in controls. Unlike locus 1, in which no known gene is located, several putative mRNAs are in close proximity to locus 2. Additional confirmation studies at locus 2 and functional studies for both loci are needed to advance our knowledge on the etiology of prostate cancer.

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