umu.sePublications
Change search
Refine search result
234567 201 - 250 of 320
CiteExportLink to result list
Permanent link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Rows per page
  • 5
  • 10
  • 20
  • 50
  • 100
  • 250
Sort
  • Standard (Relevance)
  • Author A-Ö
  • Author Ö-A
  • Title A-Ö
  • Title Ö-A
  • Publication type A-Ö
  • Publication type Ö-A
  • Issued (Oldest first)
  • Issued (Newest first)
  • Created (Oldest first)
  • Created (Newest first)
  • Last updated (Oldest first)
  • Last updated (Newest first)
  • Disputation date (earliest first)
  • Disputation date (latest first)
  • Standard (Relevance)
  • Author A-Ö
  • Author Ö-A
  • Title A-Ö
  • Title Ö-A
  • Publication type A-Ö
  • Publication type Ö-A
  • Issued (Oldest first)
  • Issued (Newest first)
  • Created (Oldest first)
  • Created (Newest first)
  • Last updated (Oldest first)
  • Last updated (Newest first)
  • Disputation date (earliest first)
  • Disputation date (latest first)
Select
The maximal number of hits you can export is 250. When you want to export more records please use the Create feeds function.
  • 201. Robinson, David
    et al.
    Sandblom, Gabriel
    Johansson, Robert
    Garmo, Hans
    Stattin, Pär
    Umeå University, Faculty of Medicine, Surgical and Perioperative Sciences, Urology and Andrology.
    Mommsen, Sören
    Varenhorst, Eberhard
    Prediction of survival of metastatic prostate cancer based on early serial measurements of prostate specific antigen and alkaline phosphatase.2008In: J Urol, ISSN 1527-3792, Vol. 179, no 1, p. 117-22; discussion 122Article in journal (Refereed)
  • 202. Roddam, Andrew W
    et al.
    Allen, Naomi E
    Appleby, Paul
    Key, Timothy J
    Ferrucci, Luigi
    Carter, H Ballentine
    Metter, E Jeffrey
    Chen, Chu
    Weiss, Noel S
    Fitzpatrick, Annette
    Hsing, Ann W
    Lacey, James V
    Helzlsouer, Kathy
    Rinaldi, Sabina
    Riboli, Elio
    Kaaks, Rudolf
    Janssen, Joop A M J L
    Wildhagen, Mark F
    Schröder, Fritz H
    Platz, Elizabeth A
    Pollak, Michael
    Giovannucci, Edward
    Schaefer, Catherine
    Quesenberry, Charles P
    Vogelman, Joseph H
    Severi, Gianluca
    English, Dallas R
    Giles, Graham G
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology. Urologi och andrologi.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Johansson, Mattias
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Chan, June M
    Gann, Peter
    Oliver, Steven E
    Holly, Jeff M
    Donovan, Jenny
    Meyer, François
    Bairati, Isabelle
    Galan, Pilar
    Insulin-like growth factors, their binding proteins, and prostate cancer risk: analysis of individual patient data from 12 prospective studies.2008In: Ann Intern Med, ISSN 1539-3704, Vol. 149, no 7, p. 461-471Article in journal (Refereed)
  • 203. Rohrmann, S.
    et al.
    Linseisen, J.
    Allen, N.
    Bueno-de-Mesquita, H. B.
    Johnsen, N. F.
    Tjonneland, A.
    Overvad, K.
    Kaaks, R.
    Teucher, B.
    Boeing, H.
    Pischon, T.
    Lagiou, P.
    Trichopoulou, A.
    Trichopoulos, D.
    Palli, D.
    Krogh, Vittorio
    Tunnino, R.
    Ricceri, F.
    Argueelles Suarez, M. V.
    Agudo, A.
    Sanchez, M-J
    Chirlaque, M-D
    Barricarte, A.
    Larranaga, N.
    Boshuizen, H.
    van Kranen, H. J.
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Johansson, M.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences.
    Bjartell, A.
    Ulmert, D.
    Khaw, K-T
    Wareham, N. J.
    Ferrari, Pietro
    Romieux, I.
    Gunter, M. J. R.
    Riboli, Elio
    Key, T. J.
    Smoking and the risk of prostate cancer in the European Prospective Investigation into Cancer and Nutrition2013In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 108, no 3, p. 708-714Article in journal (Refereed)
    Abstract [en]

    Background: Smoking is not associated with prostate cancer incidence in most studies, but associations between smoking and fatal prostate cancer have been reported. Methods: During 1992 and 2000, lifestyle information was assessed via questionnaires and personal interview in a cohort of 145112 European men. Until 2009, 4623 incident cases of prostate cancer were identified, including 1517 cases of low-grade, 396 cases of high grade, 1516 cases of localised, 808 cases of advanced disease, and 432 fatal cases. Multivariable Cox proportional hazards regression models were used to examine the association of smoking status, smoking intensity, and smoking duration with the risk of incident and fatal prostate cancer. Results: Compared with never smokers, current smokers had a reduced risk of prostate cancer (RR = 0.90, 95% CI: 0.83-0.97), which was statistically significant for localised and low-grade disease, but not for advanced or high-grade disease. In contrast, heavy smokers (25+ cigarettes per day) and men who had smoked for a long time (40+ years) had a higher risk of prostate cancer death (RR = 1.81, 95% CI: 1.11-2.93; RR = 1.38, 95% CI: 1.01-1.87, respectively). Conclusion: The observation of an increased prostate cancer mortality among heavy smokers confirms the results of previous prospective studies.

  • 204. Rohrmann, Sabine
    et al.
    Linseisen, Jakob
    Key, Timothy J
    Jensen, Majken K
    Overvad, Kim
    Johnsen, Nina Føns
    Tjønneland, Anne
    Kaaks, Rudolf
    Bergmann, Manuela M
    Weikert, Cornelia
    Naska, Androniki
    Trichopoulou, Antonia
    Trichopoulos, Dimitrios
    Pala, Valeria
    Sacerdote, Carlotta
    Palli, Domenico
    Tumino, Rosario
    Bueno-de-Mesquita, H Bas
    Vrieling, Alina
    González, Carlos A
    Larrañaga, Nerea
    Navarro, Carmen
    Barricarte, Aurelio
    Quiros, J Ramon
    Martínez-García, Carmen
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology. Urologi och andrologi.
    Manjer, Jonas
    Wirfält, Elisabet
    Bingham, Sheila
    Khaw, Key-Tee
    Egevad, Lars
    Ferrari, Pietro
    Jenab, Mazda
    Riboli, Elio
    Alcohol consumption and the risk for prostate cancer in the European prospective investigation into cancer and nutrition.2008In: Cancer Epidemiol Biomarkers Prev, ISSN 1055-9965, Vol. 17, no 5, p. 1282-7Article in journal (Refereed)
  • 205. Scelo, G
    et al.
    Hofmann, J N
    Banks, R E
    Bigot, P
    Bhatt, R S
    Cancel-Tassin, G
    Chew, S K
    Creighton, C J
    Cussenot, O
    Davis, I J
    Escudier, B
    Frayling, T M
    Häggström, Christel
    Umeå University, Faculty of Medicine, Department of Biobank Research. Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Hildebrandt, M A T
    Holcatova, I
    Johansson, M
    Linehan, W M
    McDermott, D F
    Nathanson, K L
    Ogawa, S
    Perlman, E J
    Purdue, M P
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Swanton, C
    Vasudev, N S
    Wu, X
    Znaor, A
    Brennan, P
    Chanock, S J
    International cancer seminars: a focus on kidney cancer2016In: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 27, no 8, p. 1382-1385Article in journal (Refereed)
    Abstract [en]

    Recent years have seen important advances in our understanding of the etiology, biology and genetics of kidney cancer. To summarize important achievements and identify prominent research questions that remain, a workshop was organized by IARC and the US NCI. A series of 'difficult questions' were formulated, which should be given future priority in the areas of population, genomic and clinical research.Recent years have seen important advances in our understanding of the etiology, biology and genetics of kidney cancer. To summarize important achievements and identify prominent research questions that remain, a workshop was organized by IARC and the US NCI. A series of 'difficult questions' were formulated, which should be given future priority in the areas of population, genomic and clinical research.

  • 206. Schumacher, Fredrick R.
    et al.
    Berndt, Sonja I.
    Siddiq, Afshan
    Jacobs, Kevin B.
    Wang, Zhaoming
    Lindstrom, Sara
    Stevens, Victoria L.
    Chen, Constance
    Mondul, Alison M.
    Travis, Ruth C.
    Stram, Daniel O.
    Eeles, Rosalind A.
    Easton, Douglas F.
    Giles, Graham
    Hopper, John L.
    Neal, David E.
    Hamdy, Freddie C.
    Donovan, Jenny L.
    Muir, Kenneth
    Al Olama, Ali Amin
    Kote-Jarai, Zsofia
    Guy, Michelle
    Severi, Gianluca
    Gronberg, Henrik
    Isaacs, William B.
    Karlsson, Robert
    Wiklund, Fredrik
    Xu, Jianfeng
    Allen, Naomi E.
    Andriole, Gerald L.
    Barricarte, Aurelio
    Boeing, Heiner
    Bueno-de-Mesquita, H. Bas
    Crawford, E. David
    Diver, W. Ryan
    Gonzalez, Carlos A.
    Gaziano, J. Michael
    Giovannucci, Edward L.
    Johansson, Mattias
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology. International Agency for Research on Cancer (IARC), Lyon, France.
    Le Marchand, Loic
    Ma, Jing
    Sieri, Sabina
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Stampfer, Meir J.
    Tjonneland, Anne
    Vineis, Paolo
    Virtamo, Jarmo
    Vogel, Ulla
    Weinstein, Stephanie J.
    Yeager, Meredith
    Thun, Michael J.
    Kolonel, Laurence N.
    Henderson, Brian E.
    Albanes, Demetrius
    Hayes, Richard B.
    Feigelson, Heather Spencer
    Riboli, Elio
    Hunter, David J.
    Chanock, Stephen J.
    Haiman, Christopher A.
    Kraft, Peter
    Genome-wide association study identifies new prostate cancer susceptibility loci2011In: Human Molecular Genetics, ISSN 0964-6906, E-ISSN 1460-2083, Vol. 20, no 19, p. 3867-3875Article in journal (Refereed)
    Abstract [en]

    Prostate cancer (PrCa) is the most common non-skin cancer diagnosed among males in developed countries and the second leading cause of cancer mortality, yet little is known regarding its etiology and factors that influence clinical outcome. Genome-wide association studies (GWAS) of PrCa have identified at least 30 distinct loci associated with small differences in risk. We conducted a GWAS in 2782 advanced PrCa cases (Gleason grade >= 8 or tumor stage C/D) and 4458 controls with 571 243 single nucleotide polymorphisms (SNPs). Based on in silico replication of 4679 SNPs (Stage 1, P < 0.02) in two published GWAS with 7358 PrCa cases and 6732 controls, we identified a new susceptibility locus associated with overall PrCa risk at 2q37.3 (rs2292884, P = 4.3 x 10(-8)). We also confirmed a locus suggested by an earlier GWAS at 12q13 (rs902774, P = 8.6 x 10(-9)). The estimated per-allele odds ratios for these loci (1.14 for rs2292884 and 1.17 for rs902774) did not differ between advanced and non-advanced PrCa (case-only test for heterogeneity P = 0.72 and P = 0.61, respectively). Further studies will be needed to assess whether these or other loci are differentially associated with PrCa subtypes.

  • 207. Schwartzbaum, Judith
    et al.
    Edlinger, Michael
    Zigmont, Victoria
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Rempala, Grzegorz A.
    Nagel, Gabriele
    Hammar, Niklas
    Ulmer, Hanno
    Foeger, Bernhard
    Walldius, Goran
    Manjer, Jonas
    Malmstrom, Hakan
    Feychting, Maria
    Associations between prediagnostic blood glucose levels, diabetes, and glioma2017In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 7, article id 1436Article in journal (Refereed)
    Abstract [en]

    Previous literature indicates that pre-diagnostic diabetes and blood glucose levels are inversely related to glioma risk. To replicate these findings and determine whether they could be attributed to excess glucose consumption by the preclinical tumour, we used data from the Apolipoprotein MOrtality RISk (AMORIS) (n = 528,580) and the Metabolic syndrome and Cancer project (Me-Can) cohorts (n = 269,365). We identified individuals who were followed for a maximum of 15 years after their first blood glucose test until glioma diagnosis, death, emigration or the end of follow-up. Hazard ratios (HRs), 95% confidence intervals (CIs) and their interactions with time were estimated using Cox time-dependent regression. As expected, pre-diagnostic blood glucose levels were inversely related to glioma risk (AMORIS, P-trend = 0.002; Me-Can, P-trend = 0.04) and pre-diagnostic diabetes (AMORIS, HR = 0.30, 95% CI 0.17 to 0.53). During the year before diagnosis, blood glucose was inversely associated with glioma in the AMORIS (HR = 0.78, 95% CI 0.66 to 0.93) but not the Me-Can cohort (HR = 0.99, 95% CI 0.63 to 1.56). This AMORIS result is consistent with our hypothesis that excess glucose consumption by the preclinical tumour accounts for the inverse association between blood glucose and glioma. We discuss additional hypothetical mechanisms that may explain our paradoxical findings.

  • 208.
    Shiryaeva, Liudmila
    et al.
    Umeå University, Faculty of Science and Technology, Department of Chemistry.
    Antti, Henrik
    Umeå University, Faculty of Science and Technology, Department of Chemistry.
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Kieselbach, Thomas
    Umeå University, Faculty of Science and Technology, Department of Chemistry.
    Schröder, Wolfgang P.
    Umeå University, Faculty of Science and Technology, Department of Chemistry.
    Wikström, Pernilla
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Two-dimensional difference gel electrophoresis to reveal proteins in plasma associated with high risk prostate cancerManuscript (preprint) (Other academic)
    Abstract [en]

    Prostate cancer is a common but highly variable disease. Conventional methods for prognostication are limited and needed to be complemented by novel biomarkers which could identify clinically significant tumors at a curable timepoint. With the aim to find biomarkers in plasma for high risk prostate cancer, we combined the ProteoMiner technology for protein fractionation with 2-dimentional difference gel electrophoresis (2D-DIGE). Plasma samples from patients with high risk tumors, defined to have bone metastases (M1, N=7) or locally advanced or poorly differentiated prostate cancer (M0, N=14), or benign disease (N=15) were analyzed. As a result of combined univariate and multivariate analyses (orthogonal partial least-squares discriminant analysis, OPLS-DA), 338 protein spots were found to be significantly associated with high risk prostate cancer. Ninety-eight (98) of the spots were successfully identified by LC-MS/MS, and OPLS-DA of those resulted in a reliable method for class separation; M1 vs. M0 vs. B (R2Xcum: 31.1%, R2Y cum: 59.9%, Q2cum: 41.4%, P < 0.0001). The panel of identified potential protein markers for high risk prostate cancer included highly to intermediately abundant plasma proteins involved in key processes such as lipid transport, coagulation, inflammation, and immune responses. Their putative roles for prostate cancer progression are discussed.

  • 209.
    Skytt, Åsa
    et al.
    Umeå University, Faculty of Medicine, Medical Biosciences, Pathology.
    Thysell, Elin
    Umeå University, Faculty of Science and Technology, Chemistry.
    Stattin, Pär
    Umeå University, Faculty of Medicine, Surgical and Perioperative Sciences, Urology and Andrology.
    Stenman, Ulf-Håkan
    Antti, Henrik
    Umeå University, Faculty of Science and Technology, Chemistry.
    Wikström, Pernilla
    Umeå University, Faculty of Medicine, Medical Biosciences, Pathology.
    SELDI-TOF MS versus prostate specific antigen analysis of prospective plasma samples in a nested case-control study of prostate cancer2007In: International Journal of Cancer, ISSN 0020-7136, Vol. 121, no 3, p. 615-20Article in journal (Refereed)
    Abstract [en]

    There is an urgent need for better biomarkers for detection of clinically significant prostate cancer (PCa). Recent studies suggest that surface enhanced laser desorption/ionization time-of-flight mass spectrometry (SELDI-TOF MS) analysis of serum may provide diagnostic information. The aim of this study was to investigate if PCa cases could be identified by applying predefined SELDI-TOF analysis conditions on prospectively, uniformly collected plasma samples from PCa cases and matched controls. Prospective samples from 387 incident PCa cases and an equal number of controls, matched for age and time for recruitment, were analyzed by SELDI-TOF MS (IMAC30/Cu chip) and multivariate classification analysis. Prospective prostate specific antigen levels were subjected to ROC curve analysis giving an AUC of 0.87 for the total cohort with a median lag time between blood sampling and diagnosis of 6.1 years. No markers were found by SELDI-TOF MS that significantly discriminated between cases and controls in the total cohort or in subanalysis of cases with less than 2 years between blood donation and diagnosis (n = 42). Cases with aggressive disease at the time of diagnosis who gave blood less than 4 years prior to diagnosis (n = 23) could however be separated from their controls (sensitivity 70%, specificity 83%) by a model based on SELDI-TOF MS and OPLS-DA data analysis. We were thus not able to confirm previous results with SELDI-TOF MS identifying men with PCa from healthy individuals, but we report an optimal experimental set-up for verification of markers for early detection of cancer in prospectively collected samples.

  • 210.
    Stattin, Pär
    Umeå University, Faculty of Medicine, Surgical and Perioperative Sciences, Urology and Andrology.
    Circulating testosterone and prostate cancer: A brief review2004In: Andrologie, Vol. 14, no 4, p. 375-380Article, review/survey (Other (popular science, discussion, etc.))
  • 211.
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Commentary: Fatherhood status and prostate cancer risk--the jury is still out2011In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 40, no 2, p. 488-Article in journal (Other academic)
  • 212.
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Mortality in Older Men With Low-Risk Prostate Cancer and High Comorbidity2015In: Journal of Clinical Oncology, ISSN 0732-183X, E-ISSN 1527-7755, Vol. 33, no 9, p. 1086-1087Article in journal (Other academic)
  • 213.
    Stattin, Pär
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology. Urologi och andrologi.
    Björ, Ove
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology. Onkologi.
    Ferrari, Pietro
    Nutrition and Hormones Group, International Agency for Research on Cancer-World Health Organization, Lyon, France.
    Lukanova, Annekatrin
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Lenner, Per
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology. Onkologi.
    Lindahl, Bernt
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Kaaks, Rudolf
    Division of Cancer Epidemiology, German Cancer Research Center Im Neuenheimer, Heidelberg, Germany.
    Prospective study of hyperglycemia and cancer risk.2007In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 30, no 3, p. 561-567Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: To investigate whether hyperglycemia is associated with increased cancer risk.

    RESEARCH DESIGN AND METHODS: In the Västerbotten Intervention Project of northern Sweden, fasting and postload plasma glucose concentrations were available for 33,293 women and 31,304 men and 2,478 incident cases of cancer were identified. Relative risk (RR) of cancer for levels of fasting and postload glucose was calculated with the use of Poisson models, with adjustment for age, year of recruitment, fasting time, and smoking status. Repeated measurements 10 years after baseline in almost 10,000 subjects were used to correct RRs for random error in glucose measurements.

    RESULTS: Total cancer risk in women increased with rising plasma levels of fasting and postload glucose, up to an RR for the top versus bottom quartile of 1.26 (95% CI 1.09-1.47) (P(trend) <0.001) and 1.31 (1.12-1.52) (P(trend) = 0.001), respectively. Correction for random error in glucose measurements increased these risks up to 1.75 (1.32-2.36) and 1.63 (1.26-2.18), respectively. For men, corresponding uncorrected RR was 1.08 (0.92-1.27) (P(trend) = 0.25) and 0.98 (0.83-1.16) (P(trend) = 0.99), respectively. Risk of cancer of the pancreas, endometrium, urinary tract, and of malignant melanoma was statistically significantly associated with high fasting glucose with RRs of 2.49 (1.23-5.45) (P(trend) = 0.006), 1.86 (1.09-3.31) (P(trend) = 0.02), 1.69 (0.95-3.16) (P(trend) = 0.049), and 2.16 (1.14-4.35) (P(trend) = 0.01), respectively. Adjustment for BMI had no material effect on risk estimates.

    CONCLUSIONS: The association of hyperglycemia with total cancer risk in women and in women and men combined for several cancer sites, independently of obesity, provides further evidence for an association between abnormal glucose metabolism and cancer.

     

  • 214.
    Stattin, Pär
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology. Urologi och andrologi.
    Bylund, Annika
    Umeå University, Faculty of Medicine, Department of Community Medicine and Rehabilitation, Geriatric Medicine. Geriatrik.
    Biessy, Carine
    Kaaks, Rudolf
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research. Näringsforskning.
    Adlercreutz, Herman
    Prospective study of plasma enterolactone and prostate cancer risk (Sweden).2004In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 15, no 10, p. 1095-1102Article in journal (Refereed)
  • 215.
    Stattin, Pär
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology. Department of Surgery, Urology Service, Memorial Sloan-Kettering Cancer Center, New York, NY.
    Carlsson, Sigrid
    Holmström, Benny
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Vickers, Andrew
    Hugosson, Jonas
    Lilja, Hans
    Jonsson, Håkan
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Prostate cancer mortality in areas with high and low prostate cancer incidence2014In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 106, no 3, p. dju007-Article in journal (Refereed)
    Abstract [en]

    The effect of prostate-specific antigen (PSA) screening on prostate cancer mortality remains debated, despite evidence from randomized trials. We investigated the association between prostate cancer incidence, reflecting uptake of PSA testing, and prostate cancer mortality. The study population consisted of all men aged 50 to 74 years residing in eight counties in Sweden with an early increase in prostate cancer incidence and six counties with a late increase during two time periods. Incidence of metastatic prostate cancer was investigated in the period from 2000 to 2009, and prostate cancerspecific mortality and excess mortality were investigated in the period from 1990 to 1999 and the period from 2000 to 2009 by calculating rate ratios for high- vs low-incidence counties and rate ratios for the period from 2000 to 2009 vs the period from 1990 to 1999 within these two groups. All statistical tests were two-sided. There were 4528134 person-years at risk, 1577 deaths from prostate cancer, and 1210 excess deaths in men with prostate cancer in high-incidence counties and 2471373 person-years at risk, 985 prostate cancer deaths, and 878 excess deaths in low-incidence counties in the period from 2000 to 2009. Rate ratios in counties with high vs low incidence adjusted for time period were 0.81 (95% confidence interval [CI] 0.73 to 0.90) for prostate cancer specific mortality and 0.74 (95% CI 0.64 to 0.86) for excess mortality, and the rate ratio of metastatic prostate cancer was 0.85 (95% CI 0.79 to 0.92). The lower prostate cancer mortality in high-incidence counties reflecting a high PSA uptake suggests that more-intense as compared with less-intense opportunistic PSA screening reduces prostate cancer mortality.

  • 216.
    Stattin, Pär
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Carlsson, Sigrid
    Jonsson, Håkan
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    RE: Prostate Cancer Mortality in Areas With High and Low Prostate Cancer Incidence Response2014In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 106, no 10, p. dju293-Article in journal (Refereed)
  • 217.
    Stattin, Pär
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Garmo, H
    Steineck, G
    Bill-Axelson, A
    Re: Immediate risk of suicide and cardiovascular death after a prostate cancer diagnosis2010In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 102, no 18, p. 1447-1448; author reply 1448Article in journal (Other academic)
  • 218.
    Stattin, Pär
    et al.
    Umeå University, Faculty of Medicine, Surgical and Perioperative Sciences, Urology and Andrology.
    Holmberg, Erik
    Bratt, Ola
    Adolfsson, Jan
    Johansson, Jan-Erik
    Hugosson, Jonas
    Surveillance and deferred treatment for localized prostate cancer. Population based study in the National Prostate Cancer Register of Sweden.2008In: J Urol, ISSN 1527-3792, Vol. 180, no 6, p. 2423-9; discussion 2429Article in journal (Refereed)
  • 219.
    Stattin, Pär
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Holmberg, Erik
    Johansson, Jan-Erik
    Holmberg, Lars
    Adolfsson, Jan
    Hugosson, Jonas
    Outcomes in localized prostate cancer: National Prostate Cancer Register of Sweden follow-up study2010In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 102, no 13, p. 950-958Article in journal (Refereed)
    Abstract [en]

    Background Treatment for localized prostate cancer remains controversial. To our knowledge, there are no outcome studies from contemporary population-based cohorts that include data on stage, Gleason score, and serum levels of prostate-specific antigen (PSA).

    Methods In the National Prostate Cancer Register of Sweden Follow-up Study, a nationwide cohort, we identified 6849 patients aged 70 years or younger. Inclusion criteria were diagnosis with local clinical stage T1–2 prostate cancer from January 1, 1997, through December 31, 2002, a Gleason score of 7 or less, a serum PSA level of less than 20 ng/mL, and treatment with surveillance (including active surveillance and watchful waiting, n = 2021) or curative intent (including radical prostatectomy, n = 3399, and radiation therapy, n = 1429). Among the 6849 patients, 2686 had low-risk prostate cancer (ie, clinical stage T1, Gleason score 2-6, and serum PSA level of <10 ng/mL). The study cohort was linked to the Cause of Death Register, and cumulative incidence of death from prostate cancer and competing causes was calculated.

    Results For the combination of low- and intermediate-risk prostate cancers, calculated cumulative 10-year prostate cancer–specific mortality was 3.6% (95% confidence interval [CI] = 2.7% to 4.8%) in the surveillance group and 2.7% (95% CI = 2.1% to 3.45) in the curative intent group. For those with low-risk disease, the corresponding values were 2.4% (95% CI = 1.2% to 4.1%) among the 1085 patients in the surveillance group and 0.7% (95% CI = 0.3% to 1.4%) among the 1601 patients in the curative intent group. The 10-year risk of dying from competing causes was 19.2% (95% CI = 17.2% to 21.3%) in the surveillance group and 10.2% (95% CI = 9.0% to 11.4%) in the curative intent group.

    Conclusion A 10-year prostate cancer–specific mortality of 2.4% among patients with low-risk prostate cancer in the surveillance group indicates that surveillance may be a suitable treatment option for many patients with low-risk disease.

  • 220.
    Stattin, Pär
    et al.
    Umeå University, Faculty of Medicine, Surgical and Perioperative Sciences, Urology and Andrology.
    Johansson, Robert
    Lodnert, Ronald
    Umeå University, Faculty of Medicine, Surgical and Perioperative Sciences, Urology and Andrology.
    Andrén, Ove
    Bill-Axelsson, Anna
    Bratt, Ola
    Damber, Jan-Erik
    Hellström, Magnus
    Hugosson, Jonas
    Lundgren, Rolf
    Törnblom, Magnus
    Varenhorst, Eberhard
    Johansson, Jan-Erik
    Geographical variation in incidence of prostate cancer in Sweden.2005In: Scand J Urol Nephrol, ISSN 0036-5599, Vol. 39, no 5, p. 372-9Article in journal (Refereed)
  • 221.
    Stattin, Pär
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology. Department of Surgery, Urology Service, Memorial Sloan-Kettering Cancer Centre, New York, NY, USA.
    Loeb, Stacy
    Department of Urology, New York University and Manhattan Veterans Affairs Medical Centre, New York, NY, USA.
    "To Measure Is To Know. If You Cannot Measure It, You Cannot Improve It'': Statistical Modeling Cannot Compensate for Unmeasured Bias2014In: European Urology, ISSN 0302-2838, E-ISSN 1873-7560, Vol. 65, no 4, p. 701-703Article in journal (Other academic)
  • 222.
    Stattin, Pär
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Lukanova, Annekatrin
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Biessy, Carine
    Söderberg, Stefan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Palmqvist, Richard
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Kaaks, Rudolf
    Olsson, Tommy
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Jellum, Egil
    Obesity and colon cancer: does leptin provide a link?2004In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 109, no 1, p. 149-152Article in journal (Refereed)
    Abstract [en]

    Obesity, a risk factor for colorectal cancer, is associated with elevated serum levels of leptin, the adipocyte-derived hormone, and insulin. Experimental and epidemiologic studies have indicated a role for insulin in the pathogenesis of colon cancer, and recent experimental studies have suggested a similar role for leptin. In a case-control study nested in the Janus Biobank, Norway, we measured serum levels of leptin and C-peptide (a marker of pancreatic insulin secretion) in cryopreserved prediagnostic sera from men (median age, 45 years) who were diagnosed with cancer of the colon (n = 235) or rectum (n = 143) after blood collection (median time, 17 years), and among 378 controls matched for age and date of blood collection. Conditional logistic regression analyses showed an approximately 3-fold increase in colon cancer risk with increasing concentrations of leptin up to an odds ratio (OR) of 2.72 (95% CI = 1.44-5.12) for top vs. bottom quartile (p(trend) = 0.008). The corresponding OR for C-peptide was 1.81 (95% CI = 0.67-4.86; p(trend) = 0.19). The risk estimates remained unchanged after mutual adjustment. No association of hormone levels with rectal cancer risk was found. Reproducibility of hormone measurements assessed by intraclass coefficients (ICCs) for paired samples taken 1 year apart was high for leptin (ICC = 0.82) but lower for C-peptide (ICC = 0.30). Our results suggest that leptin is a risk factor for colon cancer, and that leptin may provide a link between obesity and colon cancer. Leptin may be directly involved in colon tumorigenesis or it may serve as a sensitive and robust marker of an obesity-induced adverse endocrine environment. Only weak support for an association of insulin with colon cancer was found.

  • 223.
    Stattin, Pär
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Lukanova, Annekatrin
    Lindahl, Bernt
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Kaaks, Rudolf
    Prospective study of hyperglycemia and cancer risk: Response to Bowker and Johnson2007In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 30, no 7, p. e78-Article in journal (Refereed)
  • 224.
    Stattin, Pär
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology. Urologi och andrologi.
    Lumme, Sonja
    Tenkanen, Leena
    Alfthan, Henrik
    Jellum, Egil
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Thoresen, Steinar
    Hakulinen, Timo
    Luostarinen, Tapio
    Lehtinen, Matti
    Dillner, Joakim
    Stenman, Ulf-Håkan
    Hakama, Matti
    High levels of circulating testosterone are not associated with increased prostate cancer risk: a pooled prospective study.2004In: International Journal of Cancer, ISSN 0020-7136, Vol. 108, no 3, p. 418-24Article in journal (Refereed)
  • 225.
    Stattin, Pär
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology. Urologi och andrologi.
    Rinaldi, Sabina
    Biessy, Carine
    Stenman, Ulf-Håkan
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Kaaks, Rudolf
    High levels of circulating insulin-like growth factor-I increase prostate cancer risk: a prospective study in a population-based nonscreened cohort.2004In: Journal of Clinical Oncology, ISSN 0732-183X, Vol. 22, no 15, p. 3104-12Article in journal (Refereed)
  • 226.
    Stattin, Pär
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Robinson, David
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Lambe, Mats
    Uppsala University Hospital, Regional Cancer Center, Uppsala, Sweden; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Re: Giorgio Gandaglia, Freddie Bray, Matthew R. Cooperberg, et al.: Prostate Cancer Registries: Current Status and Future Directions. Eur Urol. In press. http://dx.doi.org/10.1016/j.eururo.2015.05.0462015In: European Urology, ISSN 0302-2838, E-ISSN 1873-7560, Vol. 68, no 5, p. E110-E110Article in journal (Refereed)
  • 227.
    Stattin, Pär
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology. Department of Surgical Sciences, Uppsala University, Uppsala, Sweden.
    Sandin, Fredrik
    Birkebæk Thomsen, Frederik
    Garmo, Hans
    Robinson, David
    Franck Lissbrant, Ingela
    Jonsson, Håkan
    Umeå University, Faculty of Medicine, Department of Radiation Sciences.
    Bratt, Ola
    Association of Radical Local Treatment with Mortality in Men with Very High-risk Prostate Cancer: A Semiecologic, Nationwide, Population-based Study2017In: European Urology, ISSN 0302-2838, E-ISSN 1873-7560, Vol. 72, no 1, p. 125-134Article in journal (Refereed)
    Abstract [en]

    Background: Current guidelines recommend androgen deprivation therapy only for men with very high-risk prostate cancer (PCa), but there is little evidence to support this stance.

    Objective: To investigate the association between radical local treatment and mortality in men with very high-risk PCa.

    Design, setting, and participants: Semiecologic study of men aged <80 yr within the Prostate Cancer data Base Sweden, diagnosed in 1998–2012 with very high-risk PCa (local clinical stage T4 and/or prostate-specific antigen [PSA] level 50–200 ng/ml, any N, and M0). Men with locally advanced PCa (local clinical stage T3 and PSA level <50 ng/ml, any N, and M0) were used as positive controls.

    Intervention: Proportion of men who received prostatectomy or full-dose radiotherapy in 640 experimental units defined by county, diagnostic period, and age at diagnosis.

    Outcome measurements and statistical analysis: PCa and all-cause mortality rate ratios (MRRs).

    Results and limitations: Both PCa and all-cause mortality were half as high in units in the highest tertile of exposure to radical local treatment compared with units in the lowest tertile (PCa MRR: 0.51; 95% confidence interval [CI], 0.28–0.95; and all-cause MRR: 0.56; 95% CI, 0.33–0.92). The results observed for locally advanced PCa for highest versus lowest tertile of exposure were in agreement with results from randomized trials (PCa MRR: 0.75; 95% CI, 0.60–0.94; and all-cause MRR: 0.85; 95% CI, 0.72–1.00). Although the semiecologic design minimized selection bias on an individual level, the effect of high therapeutic activity could not be separated from that of high diagnostic activity.

    Conclusions: The substantially lower mortality in units with the highest exposure to radical local treatment suggests that radical treatment decreases mortality even in men with very high-risk PCa for whom such treatment has been considered ineffective.

    Patient summary: Men with very high-risk prostate cancer diagnosed and treated in units with the highest exposure to surgery or radiotherapy had a substantially lower mortality.

  • 228.
    Stattin, Pär
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Sandin, Fredrik
    Reg Canc Ctr, Uppsala, Sweden.
    Hugosson, Jonas
    Univ Gothenburg, Inst Clin Sci, Sahlgrenska Acad, Gothenburg, Sweden.
    Reply from authors re: Urs E. Studer, Peter C. Albertsen. It's Time to Change the Treatment Paradigm for Prostate Cancer! Eur Urol 2013;63:97-9 PCBaSe Sweden combines the National Prostate Cancer Register of Sweden with Health Care Registers and Demographic Databases: A useful tool for observational studies2013In: European Urology, ISSN 0302-2838, E-ISSN 1873-7560, Vol. 63, no 1, p. 99-100Article in journal (Other academic)
  • 229.
    Stattin, Pär
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Sandin, Fredrik
    Ortqvist, David
    Damber, Lena
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Holmberg, Erik
    Cederberg, Hakan
    Lambe, Mats
    ONLINE REPORT IN REAL TIME FROM THE NATIONAL PROSTATE CANCER REGISTER (NPCR) OF SWEDEN, A NEW AND EFFICIENT TOOL FOR QUALITY ASSURANCE2014In: BMJ Quality and Safety, ISSN 2044-5415, E-ISSN 2044-5423, Vol. 23, no 4, p. 350-350Article in journal (Other academic)
  • 230.
    Stattin, Pär
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology. Urologi och andrologi.
    Söderberg, Stefan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology. Medicin.
    Biessy, Carine
    Lenner, Per
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology. Onkologi.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Kaaks, Rudolf
    Olsson, Tommy
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine. Medicin.
    Plasma leptin and breast cancer risk: a prospective study in northern Sweden2004In: Breast Cancer Res Treat, ISSN 0167-6806, Vol. 86, no 3, p. 191-196Article in journal (Refereed)
    Abstract [en]

    Chronic burnout refers to a syndrome caused by chronic stress. Clinical observations indicate that chronic burnout is associated with impaired cognitive functioning. However, there have been no systematic studies of the cognitive performance in chronic burnout patients. We have evaluated general cognitive ability, memory, and attention in 67 female patients treated for chronic burnout. The patients and 15 healthy control subjects were tested with standardized tests of verbal and nonverbal cognitive ability (WAIS), verbal (Claeson-Dahl) and nonverbal (Rey complex figures) memory, and visual and auditory attention (IVA). Significant reductions in nonverbal memory and auditory and visual attention were found for the patient group. These results indicate that patients with chronic burnout have specific cognitive impairments, which should be emphasized in the evaluation of symptoms and treatment regimes in this disorder.

  • 231.
    Stattin, Pär
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Vickers, Andrew J.
    New York, NY, USA.
    Sjoberg, Daniel D.
    New York, NY, USA.
    Johansson, Robert
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Granfors, Torvald
    Stockholm, Sweden.
    Johansson, Mattias
    Section of Genetics, The International Agency for Research on Cancer, Lyon, France.
    Pettersson, Kim
    Turku, Finland.
    Scardino, Peter T.
    New York, NY, USA.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research. Umeå University, Faculty of Medicine, Department of Biobank Research.
    Lilja, Hans
    New York, NY, USA; Headington, Oxford, UK; Malmö, Sweden.
    Improving the Specificity of Screening for Lethal Prostate Cancer Using Prostate-specific Antigen and a Panel of Kallikrein Markers: a Nested Case-Control Study2015In: European Urology, ISSN 0302-2838, E-ISSN 1873-7560, Vol. 68, no 2, p. 207-213Article in journal (Refereed)
    Abstract [en]

    Background: A disadvantage of prostate-specific antigen (PSA) for the early detection of prostate cancer (PCa) is that many men must be screened, biopsied, and diagnosed to prevent one death. Objective: To increase the specificity of screening for lethal PCa at an early stage. Design, setting, and participants: We conducted a case-control study nested within a population-based cohort. PSA and three additional kallikreins were measured in cryopreserved blood from a population-based cohort in Vasterbotten, Sweden. Of 40 379 men providing blood at ages 40, 50, and 60 yr from 1986 to 2009, 12 542 men were followed for > 15 yr. From this cohort, the Swedish Cancer Registry identified 1423 incident PCa cases, 235 with distant metastasis. Outcome measurements and statistical analysis: Risk of distant metastasis for different PSA levels and a prespecified statistical model based on the four kallikrein markers. Results and limitations: Mostmetastatic cases occurred in men with PSA in the top quartile at age 50 yr (69%) or 60 yr (74%), whereas 20-yr risk of metastasis for men with PSA below median was low (<= 0.6%). Among men with PSA > 2 ng/ml, a prespecified model based on four kallikrein markers significantly enhanced the prediction of metastasis compared with PSA alone. About half of all men with PSA > 2 ng/ml were defined as low risk by this model and had a <= 1% 15-yr risk of metastasis. Conclusions: Screening at ages 50-60 yr should focus on men with PSA in the top quartile. A marker panel can aid biopsy decision making. Patient summary: For men in their fifties, screening should focus on those in the top 10% to 25% of PSA values because the majority of subsequent cases of distant metastasis are found among these men. Testing of four kallikrein markers in men with an elevated PSA could aid biopsy decision making.

  • 232.
    Stenman, Katarina
    et al.
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Diagnostic Radiology.
    Hauksson, Jón
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Radiation Physics.
    Gröbner, Gerhard
    Umeå University, Faculty of Science and Technology, Department of Chemistry.
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Bergh, Anders
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Riklund, Katrine
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Diagnostic Radiology.
    Detection of polyunsaturated omega-6 fatty acid in human malignant prostate tissue by 1D and 2D high-resolution magic angle spinning NMR spectroscopy2009In: Magnetic Resonance Materials in Physics, Biology and Medicine, ISSN 0968-5243, E-ISSN 1352-8661, Vol. 22, no 6, p. 327-331Article in journal (Refereed)
    Abstract [en]

    OBJECT: Polyunsaturated omega-6 fatty acids (PUFAs) have been shown to promote prostate cancer. Here, we describe the use of HRMAS NMR spectroscopy to detect omega-6 PUFA species in prostate tissues. MATERIALS AND METHODS: Samples originating from non-malignant (n = 54) and malignant (n = 27) prostate tissues (from 27 prostatectomized men) were studied by 1D (1)H, 2D (1)H-(1)H and (1)H-(13)C HRMAS NMR spectroscopy followed by histopathological characterization. RESULTS: HRMAS NMR proved to be a powerful, non-destructive method to identify and characterize PUFAs. The omega-6 PUFA was found in 15% of examined human prostate tumors. CONCLUSION: It is possible to detect PUFAs in prostate tissues using our NMR-based spectroscopic approach.

  • 233.
    Stenman, Katarina
    et al.
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Diagnostic Radiology.
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Stenlund, Hans
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Global Health.
    Riklund, Katrine
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Diagnostic Radiology.
    Gröbner, Gerhard
    Umeå University, Faculty of Science and Technology, Department of Chemistry.
    Bergh, Anders
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    1H HRMAS NMR Derived Bio-markers Related to Tumor Grade, Tumor Cell Fraction, and Cell Proliferation in Prostate Tissue Samples2011In: Biomarker Insights, ISSN 1177-2719, E-ISSN 1177-2719, Vol. 6, p. 39-47Article in journal (Refereed)
    Abstract [en]

    A high-resolution magic angle spinning NMR spectroscopic approach is presented for evaluating the occurrence, amount and aggressiveness of cancer in human prostate tissue samples. Using this technique, key metabolites in malignant and non-malignant samples (n = 149) were identified, and patterns of their relative abundance were analyzed by multivariate statistical methods. Ratios of various metabolites – including (glycerophophorylcholine + phosphorylcholine)/creatine, myo-inositol/scyllo-inositol, scyllo-inositol/creatine, choline/creatine, and citrate/creatine – correlated with: i) for non-malignant tissue samples, the distance to the nearest tumor and its Gleason score and; ii) the fraction of tumor cells present in the sample; and iii) tumor cell proliferation (Ki67 labelling index). This NMR-based approach allows the extraction of information that could be useful for developing novel diagnostic methods for prostate cancer.

  • 234.
    Stenman, Katarina
    et al.
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Diagnostic Radiology.
    Surowiec, Izabella
    Umeå University, Faculty of Science and Technology, Department of Chemistry.
    Antti, Henrik
    Umeå University, Faculty of Science and Technology, Department of Chemistry.
    Riklund, Katrine
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Diagnostic Radiology.
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Bergh, Anders
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Gröbner, Gerhard
    Umeå University, Faculty of Science and Technology, Department of Chemistry.
    Detection of local prostate metabolites by HRMAs NMR spectroscopy: a comparative study of human and rat prostate tissues2010In: Magnetic Resonance Insights, ISSN 1178-623X, Vol. 4, p. 27-41Article in journal (Refereed)
    Abstract [en]

    The use of magnetic resonance spectroscopy (MRS) for the detection of in-vivo metabolic perturbations is increasing in popularity in Prostate Cancer (PCa) research on both humans and rodent models. However, there are distinct metabolic differences between species and prostate areas; a fact making general conclusions about PCa difficult. Here, we use High Resolution Magic Angle Spinning Nuclear Magnetic Resonance (HRMAS NMR) spectroscopy to provide tissue specific identification of metabolites and their relative ratios; information useful in providing insight into the biochemical pathways of the prostate. As our NMR-based approach reveals, human and rat prostate tissues have different metabolic signatures as reflected in numerous key metabolites, including citrate and choline compounds, but also aspartate, lysine, taurine, glutamate, glutamine, creatine and inositol. In general, distribution of these metabolites is not only highly dependent on the species (human versus rat), but also on the location (lobe/zone) in the prostate tissue and the sample pathology; an observation making HRMAS NMR of intact tissue samples a promising method for extracting differences and common features in various experimental prostate cancer models.

  • 235.
    Stocks, Tanja
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology. Department of Clinical Sciences in Malmö, Diabetes and Cardiovascular Diseases, Genetic Epidemiology, Lund University, Lund, Sweden.
    Björge, Tone
    Bergen, Norway; Oslo, Norway.
    Ulmer, Hanno
    Innsbruck, Austria.
    Manjer, Jonas
    Lund University, Malmö, Sweden.
    Häggström, Christel
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology. Umeå University, Faculty of Medicine, Department of Biobank Research.
    Nagel, Gabriele
    Ulm, Germany; Oslo, Norway.
    Engeland, Anders
    Oslo, Norway; Bergen, Norway.
    Johansen, Dorthe
    Lund University, Malmö, Sweden.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research. Umeå University, Faculty of Medicine, Department of Biobank Research.
    Selmer, Randi
    Oslo, Norway.
    Concin, Hans
    Bregenz, Austria.
    Tretli, Steinar
    Oslo, Norway.
    Jonsson, Håkan
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Metabolic risk score and cancer risk: pooled analysis of seven cohorts2015In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 44, no 4, p. 1353-1387Article in journal (Refereed)
    Abstract [en]

    Background: There are few data on the joint influence of metabolic factors on risk of separate cancers. Methods: We analysed data on body mass index, blood pressure and plasma levels of glucose, total cholesterol and triglycerides from seven European cohorts comprising 564 596 men and women with a mean age of 44 years. We weighted those factors equally into a standardized metabolic risk score [MRS, mean = 0, standard deviation (SD) = 1], with an individual's level indicated as SDs from the sex-and cohort-specific means. Cancer hazard ratios were calculated by Cox regression with age as timescale and with relevant adjustments including smoking status. All statistical tests were two-sided. Results: During a mean follow-up of 12 years, 21 593 men and 14 348 women were diagnosed with cancer. MRS was linearly and positively associated with incident cancer in total and at sites (P<0.05). In men, risk per SD MRS was increased by 43% (95% confidence interval: 27-61) for renal cell cancer, 43% (16-76) for liver cancer, 29% (20-38) for colon cancer, 27% (5-54) for oesophageal cancer, 20% (9-31) for rectal cancer, 19% (4-37) for leukaemias, 15% (1-30) for oral cancer and 10% (2-19) for bladder cancer. In women, risk increases per SD MRS were 56% (42-70) for endometrial cancer, 53% (29-81) for pancreatic cancer, 40% (16-67) for renal cell cancer, 27% (9-47) for cervical cancer and 17% (3-32) for rectal cancer. Conclusion: This largest study to date on the joint influence of metabolic factors on risk of separate cancers showed increased risks for several cancers, in particular renal cell and liver cancer in men and endometrial and pancreatic cancer in women.

  • 236.
    Stocks, Tanja
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Borena, Wegene
    Innsbruck Medical University, Austria.
    Strohmaier, Susanne
    Innsbruck Medical University, Austria.
    Bjorge, Tone
    University of Bergen, Norway.
    Manjer, Jonas
    Malmö University Hospital.
    Engeland, Anders
    University of Bergen, Norway.
    Johansen, Dorthe
    Malmö University Hospital.
    Selmer, Randi
    Norwegian Institute of Public Health.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Rapp, Kilian
    Ulm University, Germany.
    Concin, Hans
    Agency for Preventive and Social Medicine, Austria.
    Jonsson, Håkan
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Ulmer, Hanno
    Innsbruck Medical University, Austria.
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Cohort profile: the metabolic syndrome and cancer project (Me-Can)2010In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 39, no 3, p. 660-667Article in journal (Refereed)
  • 237.
    Stocks, Tanja
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Hergens, Maria-Pia
    Englund, Anders
    Ye, Weimin
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Blood pressure, body size and prostate cancer risk in the Swedish Construction Workers cohort.2010In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 127, no 7, p. 1660-1668Article in journal (Refereed)
    Abstract [en]

    Data from prospective studies on blood pressure and prostate cancer risk are limited, and results are inconclusive. Baseline measurements of height, weight and blood pressure were available in 336,159 men in the Swedish Construction Workers cohort. During an average of 22.2 years of follow-up, 10,002 incident cases and 2,601 fatal cases of prostate cancer were identified in National registers. For 5,219 cases, tumor characteristics were available; 2,817 tumors were classified as nonaggressive and 2,402 as aggressive. Relative risks of disease were estimated from Cox regression models, using attained age as time-scale, and adjusting for birth year, smoking status and body mass index (BMI). Top compared to bottom quintile level of systolic or diastolic blood pressure was associated with a significant 15-20% decreased risk of incident prostate cancer (p for trend: systolic < 0.0001, diastolic = 0.3), but blood pressure was not significantly associated with risk of fatal prostate cancer. BMI was not associated with prostate cancer incidence, but was positively associated with fatal prostate cancer; men in the top quintile had a 30% increased risk (p for trend = 0.0004). The associations between blood pressure and BMI and nonaggressive tumors were similar to those of incident prostate cancer, and associations with aggressive tumors were similar to those of fatal prostate cancer. Data from our study suggest that hypertension is associated with a decreased risk of incident prostate cancer, but the explanation for this finding is unclear. Our study support a positive association between overweight and risk of fatal prostate cancer.

  • 238.
    Stocks, Tanja
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Lindahl, Bernt
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    [Healthy life style seems to reduce the risk of cancer. New support for the hypothesis that overweight and high blood glucose increase the cancer risk]2007In: Lakartidningen, ISSN 0023-7205, Vol. 104, no 51-52, p. 3867-70Article in journal (Other academic)
  • 239.
    Stocks, Tanja
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology. Urologi och andrologi.
    Lukanova, A
    Johansson, Mattias
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology. Urologi och andrologi.
    Rinaldi, S
    Palmqvist, Richard
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology. Patologi.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Kaaks, R
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology. Urologi och andrologi.
    Components of the metabolic syndrome and colorectal cancer risk: a prospective study2008In: International Journal of Obesity, ISSN 0307-0565, E-ISSN 1476-5497, Vol. 32, no 2, p. 304-314Article in journal (Refereed)
    Abstract [en]

    Objective: To examine the relation of well-known factors of the metabolic syndrome (MetS) as well as related circulating factors, with risk of colorectal cancer.

    Methods: We performed a case control study of 306 colorectal cancer cases and 595 matched controls nested in the Northern Sweden Health and Disease Cohort. Levels of C-peptide, glycated haemoglobin (HbA1c), leptin and adiponectin were measured in cryopreserved samples. Body mass index (BMI), systolic and diastolic blood pressure and fasting and post-load plasma glucose, had been measured in a subcohort. Conditional logistic regression was used to calculate odds ratios (OR) of disease, including risk assessments for the MetS factors: obesity (BMI>30 kg m-2), hypertension (blood pressure 140/90 mmHg or use of anti-hypertensive drugs) and hyperglycaemia (fasting glucose 6.1 mmol l-1 or post-load glucose in capillary plasma 8.9 mmol l-1).

    Results: None of the studied variables were significantly associated with risk across quartiles. Presence of obesity, hypertension and hyperglycaemia significantly increased the risk of colorectal cancer; OR for three vs null factors was 2.57 (95% Confidence Interval [CI] 1.20–5.52; P trend=0.0021), as compared to a 30 to 70% increased risk for the factors in single. Similarly, top decile levels of C-peptide, HbA1c and leptin/adiponectin ratio were associated with an increased risk; ORs for top vs deciles 1–9 were 1.56 (95% CI 0.93–2.62; P=0.090), 1.83 (95% CI 1.00–3.36; P=0.051) and 1.50 (95% CI 0.83–2.71; P=0.18), respectively.

    Conclusions: Our study support the view that components of the MetS increase risk of colorectal cancer, and further suggests that only very high levels of metabolic factors confer an increased risk.

  • 240.
    Stocks, Tanja
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Lukanova, Annekatrin
    German Cancer Research Center, Germany.
    Björge, Tone
    University of Bergen, Norway.
    Ulmer, Hanno
    Innsbruck Medical University, Austria.
    Manjer, Jonas
    Malmö University Hospital.
    Almquist, Martin
    Malmö University Hospital.
    Concin, Hans
    Agency for Preventive and Social Medicine.
    Engeland, Anders
    University of Bergen, Norway.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Nagel, Gabriele
    Ulm University, Germany.
    Tretli, Steinar
    The Cancer Registry of Norway, Norway.
    Veierod, Marit
    University of Oslo, Norway.
    Jonsson, Håkan
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Metabolic factors and risk of colorectal cancer in the metabolic syndrome and cancer project (Me-Can)2011In: Cancer, ISSN 0008-543X, E-ISSN 1097-0142, Vol. 117, no 11, p. 2398-2407Article in journal (Refereed)
    Abstract [en]

    Background

    The metabolic syndrome (MetS) has been related to an increased risk of colorectal cancer in some small studies, but it is unknown which factors in the MetS that are most strongly related to risk, and if there is an interaction between factors.

    Methods and Findings

    In the Metabolic syndrome and Cancer project (Me-Can), data on body mass index (BMI), blood pressure, and blood levels of glucose, cholesterol, and triglycerides were available in 289,866 men and 288,834 women. Mean age at baseline was 44.0 years and mean follow-up time was 12.0 years. During follow-up, 2,834 men and 1,861 women were diagnosed with colorectal cancer. We used Cox regression models to calculate relative risk (RR) of colorectal cancer by exposures transformed into Z scores (mean = 0, standard deviation = 1), and for a MetS Z score, and used regression calibration to correct exposure levels for random error in measurement. Significant increases in risk per one unit increment of factors were observed in men for BMI, RR 1.07 (95% confidence interval, 1.02-1.13), blood pressure, RR 1.10 (1.02-1.18), and triglycerides, RR 1.17 (1.06-1.28), and in women for BMI, RR 1.08 (1.01-1.15). The RR of colorectal cancer per one unit increment of the MetS Z score was 1.24 (1.18-1.31) in men, and 1.14 (1.06-1.22) in women. There was no significant positive interaction for any combination of two metabolic factors. Associations between metabolic factors and risk of fatal colorectal cancer were similar to those for incident cancer.

    Conclusions

    Our data add further evidence for an association between factors in the MetS, in single and combined, and risk of colorectal cancer. Our data do not support an interaction between factors in the MetS on risk.

  • 241.
    Stocks, Tanja
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Lukanova, Annekatrin
    German Cancer Research Center, Germany.
    Rinaldi, Sabina
    International Agency for Research on Cancer, France.
    Biessy, Carinne
    International Agency for Research on Cancer, France.
    Dossus, Laure
    German Cancer Research Center, Germany.
    Lindahl, Bernt
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Kaaks, Rudolf
    German Cancer Research Center, Germany.
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Insulin resistance is inversely related to prostate cancer: a prospective study in Northern Sweden2007In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 120, no 12, p. 2678-2686Article in journal (Refereed)
    Abstract [en]

    Factors related to insulin resistance have been implicated in prostate cancer development, however, few analytical studies support such an association. We performed a case control study on 392 prostate cancer cases and 392 matched controls nested in a prospective cohort in Northern Sweden. Plasma concentrations of C-peptide, leptin, glycated haemoglobin (HbA1c) and fasting and post-load glucose were analysed and homeostatic model assessment of insulin resistance (HOMA-IR) was calculated. Conditional logistic regression analyses were used to calculate odds ratios (OR) of prostate cancer. High levels of C-peptide, HOMA-IR, leptin and HbA1c were associated with significant decreases in risk of prostate cancer, with ORs for top vs. bottom quartile for C-peptide of 0.59 (95% Confidence Interval [CI], 0.40-0.89; ptrend = 0.008), HOMA-IR 0.60 (95% CI, 0.38-0.94; ptrend = 0.03), leptin 0.55 (95% CI, 0.36-0.84; ptrend = 0.006) and HbA1c 0.56 (95% CI, 0.35-0.91; ptrend = 0.02). All studied factors were strongly inversely related to risk among men less than 59 years of age at blood sampling, but not among older men, with a significant heterogeneity between the groups for leptin (pheterogeneity = 0.006) and fasting glucose (pheterogeneity = 0.03). C-peptide and HOMA-IR were strongly inversely related to non-aggressive cancer but were non-significantly positively related to risk of aggressive disease (pheterogeneity = 0.007 and 0.01, respectively). Our data suggest that androgens, which are inversely associated with insulin resistance, are important in the early prostate cancer development, whereas insulin resistance related factors may be important for tumour progression.

  • 242.
    Stocks, Tanja
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Rapp, Kilian
    Ulm University, Germany.
    Bjorge, Tone
    University of Bergen.
    Manjer, Jonas
    Malmö University Hospital.
    Ulmer, Hanno
    Innsbruck Medical University.
    Selmer, Randi
    Norwegian Institute of Public Health, Norway.
    Lukanova, Annekatrin
    German Cancer Research Center, Germany.
    Johansen, Dorthe
    Malmö University Hospital.
    Concin, Hans
    Agency for Preventive and Social Medicine, Austria.
    Tretli, Steinar
    The Cancer Registry of Norway, Norway.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Jonsson, Håkan
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Blood glucose and risk of incident and fatal cancer in the metabolic syndrome and cancer project (Me-Can): analysis of six prospective cohorts.2009In: PLoS Medicine, ISSN 1549-1277, E-ISSN 1549-1676, Vol. 6, no 12, p. e1000201-Article in journal (Refereed)
    Abstract [en]

     Background

    Prospective studies have indicated that elevated blood glucose levels may increase the risk of cancer, but the strength of the association is unclear. We examined the association between blood glucose and cancer risk in a prospective study of six European cohorts. Methods and Findings The Metabolic syndrome and Cancer project (Me-Can) includes cohorts from Norway, Austria, and Sweden; the current study included 274,126 men and 275,818 women. Mean age at baseline was 44.8 years and mean follow-up time was 10.4 years. Excluding the first year of follow-up, 18,621 men and 11,664 women were diagnosed with cancer, and 6,973 men and 3,088 women died of cancer. We used Cox regression models to calculate relative risk (RR) for glucose levels, and included adjustment for body mass index (BMI) and smoking  status in the analyses. RRs were corrected for regression dilution ratio of glucose. RR (95% confidence interval) per 1 mmol/l increment of glucose for overall incident cancer was 1.05 (1.01-1.10) in men and 1.11 (1.05-1.16) in women, and corresponding RRs for fatal cancer were 1.15 (1.07-1.22) and 1.21 (1.11-1.33), respectively. Significant increases in risk among men were found for incident and fatal cancer of the liver, gallbladder and respiratory tract, for incident thyroid cancer and multiple myeloma, and for fatal rectal cancer. In women, significant associations were found for incident and fatal cancer of the pancreas, for incident urinary bladder cancer, and for fatal cancer of the uterine corpus, cervix uteri, and stomach.

    Conclusions

    Data from our study indicate that abnormal glucose metabolism, independently of BMI, is associated with an increased risk of cancer overall and at several cancer sites. Our data showed stronger associations among women than among men, and for fatal cancer compared to incident cancer.

     

  • 243.
    Stocks, Tanja
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Van Hemelrijck, Mieke
    Manjer, Jonas
    Bjørge, Tone
    Ulmer, Hanno
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research. Umeå University, Faculty of Medicine, Department of Biobank Research.
    Lindkvist, Björn
    Selmer, Randi
    Nagel, Gabriele
    Tretli, Steinar
    Concin, Hans
    Engeland, Anders
    Jonsson, Håkan
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Blood pressure and risk of cancer incidence and mortality in the metabolic syndrome and cancer project2012In: Hypertension, ISSN 0194-911X, E-ISSN 1524-4563, Vol. 59, no 4, p. 802-810Article in journal (Refereed)
    Abstract [en]

    Observational studies have shown inconsistent results for the association between blood pressure and cancer risk. We investigated the association in 7 cohorts from Norway, Austria, and Sweden. In total, 577799 adults with a mean age of 44 years were followed for, on average, 12 years. Incident cancers were 22184 in men and 14744 in women, and cancer deaths were 8724 and 4525, respectively. Cox regression was used to calculate hazard ratios of cancer per 10-mmHg increments of midblood pressure, which corresponded with 0.7 SDs and, for example, an increment of systolic/diastolic blood pressure of 130/80 to 142/88 mmHg. All of the models used age as the time scale and were adjusted for possible confounders, including body mass index and smoking status. In men, midblood pressure was positively related to total incident cancer (hazard ratio per 10 mmHg increment: 1.07 [95% CI: 1.04-1.09]) and to cancer of the oropharynx, colon, rectum, lung, bladder, kidney, malignant melanoma, and nonmelanoma skin cancer. In women, midblood pressure was not related to total incident cancer but was positively related to cancer of the liver, pancreas, cervix, uterine corpus, and malignant melanoma. A positive association was also found for cancer mortality, with HRs per 10-mmHg increment of 1.12 (95% CI: 1.08-1.15) for men and 1.06 (95% CI: 1.02-1.11) for women. These results suggest a small increased cancer risk overall in men with elevated blood pressure level and a higher risk for cancer death in men and women.

  • 244. Strohmaier, Susanne
    et al.
    Edlinger, Michael
    Manjer, Jonas
    Stocks, Tanja
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Bjorge, Tone
    Borena, Wegene
    Häggström, Christel
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Engeland, Anders
    Nagel, Gabriele
    Almquist, Martin
    Selmer, Randi
    Tretli, Steinar
    Concin, Hans
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research. Umeå University, Faculty of Medicine, Department of Biobank Research.
    Jonsson, Håkan
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Ulmer, Hanno
    Total Serum Cholesterol and Cancer Incidence in the Metabolic Syndrome and Cancer Project (Me-Can)2013In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 8, no 1, p. e54242-Article in journal (Refereed)
    Abstract [en]

    Objective: To investigate the association between total serum cholesterol (TSC) and cancer incidence in the Metabolic syndrome and Cancer project (Me-Can).

    Methods: Me-Can consists of seven cohorts from Norway, Austria, and Sweden including 289,273 male and 288,057 female participants prospectively followed up for cancer incidence (n = 38,978) with a mean follow-up of 11.7 years. Cox regression models with age as the underlying time metric were used to estimate hazard ratios (HR) and their 95% confidence intervals (CI) for quintiles of cholesterol levels and per 1 mmol/l, adjusting for age at first measurement, body mass index (BMI), and smoking status. Estimates were corrected for regression dilution bias. Furthermore, we performed lag time analyses, excluding different times of follow-up, in order to check for reverse causation.

    Results: In men, compared with the 1st quintile, TSC concentrations in the 5th quintile were borderline significantly associated with decreasing risk of total cancer (HR = 0.94; 95% CI: 0.88, 1.00). Significant inverse associations were observed for cancers of the liver/intrahepatic bile duct (HR = 0.14; 95% CI: 0.07, 0.29), pancreas cancer (HR = 0.52, 95% CI: 0.33, 0.81), non-melanoma of skin (HR = 0.67; 95% CI: 0.46, 0.95), and cancers of the lymph-/hematopoietic tissue (HR = 0.68, 95% CI: 0.54, 0.87). In women, hazard ratios for the 5th quintile were associated with decreasing risk of total cancer (HR = 0.86, 95% CI: 0.79, 0.93) and for cancers of the gallbladder (HR = 0.23, 95% CI: 0.08, 0.62), breast (HR = 0.70, 95% CI: 0.61, 0.81), melanoma of skin (HR = 0.61, 95% CI: 0.42, 0.88), and cancers of the lymph-/hematopoietic tissue (HR = 0.61, 95% CI: 0.44, 0.83).

    Conclusion: TSC was negatively associated with risk of cancer overall in females and risk of cancer at several sites in both males and females. In lag time analyses some associations persisted, suggesting that for these cancer sites reverse causation did not apply.

  • 245. Sun, Jielin
    et al.
    Chang, Bao-Li
    Isaacs, Sarah D
    Wiley, Kathleen E
    Wiklund, Fredrik
    Stattin, Pär
    Umeå University, Faculty of Medicine, Surgical and Perioperative Sciences, Urology and Andrology.
    Duggan, David
    Carpten, John D
    Trock, Bruce J
    Partin, Alan W
    Walsh, Patrick C
    Grönberg, Henrik
    Xu, Jianfeng
    Isaacs, William B
    Zheng, S Lilly
    Cumulative effect of five genetic variants on prostate cancer risk in multiple study populations.2008In: Prostate, ISSN 0270-4137, Vol. 68, no 12, p. 1257-62Article in journal (Refereed)
  • 246. Sun, Jielin
    et al.
    Zheng, Siqun Lilly
    Wiklund, Fredrik
    Isaacs, Sarah D
    Li, Ge
    Wiley, Kathleen E
    Kim, Seong-Tae
    Zhu, Yi
    Zhang, Zheng
    Hsu, Fang-Chi
    Turner, Aubrey R
    Stattin, Pär
    Umeå University, Faculty of Medicine, Surgical and Perioperative Sciences, Urology and Andrology.
    Liu, Wennuan
    Kim, Jin Woo
    Duggan, David
    Carpten, John
    Isaacs, William
    Grönberg, Henrik
    Xu, Jianfeng
    Chang, Bao-Li
    Sequence variants at 22q13 are associated with prostate cancer risk.2009In: Cancer research, ISSN 1538-7445, Vol. 69, no 1, p. 10-5Article in journal (Refereed)
    Abstract [en]

    To search for genetic variants that are associated with prostate cancer risk in the genome, we combined the data from our genome-wide association study (GWAS) in a population-based case-control study in Sweden with publicly available GWAS data from the Cancer Genetic Markers of Susceptibility (CGEMS) study. We limited the cases to those with aggressive disease in an attempt to identify risk variants that are associated with this most clinically relevant form of the disease. Among the most likely candidate single nucleotide polymorphisms (SNP) identified from the two GWAS, we sequentially confirmed one SNP at 22q13 in two independent study populations: the remaining subjects in Cancer of the Prostate in Sweden and a hospital-based case-control study at Johns Hopkins Hospital. Association of aggressive prostate cancer with the SNP at 22q13 was also observed in the publicly available data of four additional study populations from the second stage of the CGEMS study. In all seven study populations examined, the frequency of allele "C" of rs9623117 at 22q13 was consistently higher in aggressive cases than in controls. The combined allelic test was highly significant, with P = 5.0 x 10(-7). The odds ratio (OR) of allele C for aggressive prostate cancer was estimated to be 1.18 [95% confidence interval (95% CI), 1.11-1.26]. However, the SNP was also associated with nonaggressive prostate cancer, with an estimated OR of 1.11 (95% CI, 1.04-1.19; P = 0.004). The risk-associated variants are located within the genomic region of TNRC6B, a gene involved in miRNA-mediated mRNA degradation. Additional studies are warranted to further confirm the association.

  • 247. Sun, Jielin
    et al.
    Zheng, Siqun Lilly
    Wiklund, Fredrik
    Isaacs, Sarah D
    Purcell, Lina D
    Gao, Zhengrong
    Hsu, Fang-Chi
    Kim, Seong-Tae
    Liu, Wennuan
    Zhu, Yi
    Stattin, Pär
    Umeå University, Faculty of Medicine, Surgical and Perioperative Sciences, Urology and Andrology.
    Adami, Hans-Olov
    Wiley, Kathleen E
    Dimitrov, Latchezar
    Sun, Jishan
    Li, Tao
    Turner, Aubrey R
    Adams, Tamara S
    Adolfsson, Jan
    Johansson, Jan-Erik
    Lowey, James
    Trock, Bruce J
    Partin, Alan W
    Walsh, Patrick C
    Trent, Jeffrey M
    Duggan, David
    Carpten, John
    Chang, Bao-Li
    Grönberg, Henrik
    Isaacs, William B
    Xu, Jianfeng
    Evidence for two independent prostate cancer risk-associated loci in the HNF1B gene at 17q12.2008In: Nat Genet, ISSN 1546-1718, Vol. 40, no 10, p. 1153-5Article in journal (Refereed)
  • 248. Suzuki, Reiko
    et al.
    Allen, Naomi E
    Key, Timothy J
    Appleby, Paul N
    Tjønneland, Anne
    Johnsen, Nina Føns
    Jensen, Majken K
    Overvad, Kim
    Boeing, Heiner
    Pischon, Tobias
    Kaaks, Rudolf
    Rohrmann, Sabine
    Trichopoulou, Antonia
    Misirli, Gesthimani
    Trichopoulos, Dimitrios
    Bueno-de-Mesquita, H Bas
    van Duijnhoven, Fränzel
    Sacerdote, Carlotta
    Pala, Valeria
    Palli, Domenico
    Tumino, Rosario
    Ardanaz, Eva
    Quirós, José Ramón
    Larrañaga, Nerea
    Sánchez, Maria-José
    Tormo, María-José
    Jakszyn, Paula
    Johansson, Ingegerd
    Umeå University, Faculty of Medicine, Odontology.
    Stattin, Pär
    Umeå University, Faculty of Medicine, Surgical and Perioperative Sciences, Urology and Andrology.
    Berglund, Göran
    Manjer, Jonas
    Bingham, Sheila
    Khaw, Kay-Tee
    Egevad, Lars
    Ferrari, Pietro
    Jenab, Mazda
    Riboli, Elio
    A prospective analysis of the association between dietary fiber intake and prostate cancer risk in EPIC.2009In: International journal of cancer. Journal international du cancer, ISSN 1097-0215, Vol. 124, no 1, p. 245-9Article in journal (Refereed)
    Abstract [en]

    Few studies have examined the association between dietary fiber intake and prostate cancer risk. We evaluated the association between dietary fiber intake and the risk of prostate cancer among 142,590 men in the European Prospective Investigation into Cancer and Nutrition (EPIC). Consumption of dietary fiber (total, cereal, fruit and vegetable fiber) was estimated by validated dietary questionnaires and calibrated using 24-hr dietary recalls. Incidence rate ratios were estimated using Cox regression and adjusted for potential confounding factors. During an average of 8.7 years follow-up, prostate cancer was diagnosed in 2,747 men. Overall, there was no association between dietary fiber intake (total, cereal, fruit or vegetable fiber) and prostate cancer risk, although calibrated intakes of total fiber and fruit fiber were associated with nonstatistically significant reductions in risk. There was no association between fiber derived from cereals or vegetables and risk and no evidence for heterogeneity in any of the risk estimates by stage or grade of disease. Our results suggest that dietary fiber intake is not associated with prostate cancer risk.

  • 249. Szulkin, Robert
    et al.
    Holmberg, Erik
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Xu, Jianfeng
    Zheng, Sigun
    Palmgren, Juni
    Grönberg, Henrik
    Wiklund, Fredrik
    Prostate cancer risk variants are not associated with disease progression2012In: The Prostate, ISSN 0270-4137, E-ISSN 1097-0045, Vol. 72, no 1, p. 30-39Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Currently used prognostic markers are limited in their ability to accurately predict disease progression among patients with localized prostate cancer. We examined 23 reported prostate cancer susceptibility variants for association with disease progression. METHODS: Disease progression was explored among 4,673 Swedish patients treated for clinically localized prostate cancer between 1997 and 2002. Prostate cancer progression was defined according to primary treatment as a composed event reflecting termination of deferred treatment, biochemical recurrence, local progression, or presence of distant metastasis. Association between single variants, and all variants combined, were performed in Cox regression analysis assuming both log-additive and co-dominant genetic models. RESULTS: Three of the 23 genetic variants explored were nominally associated with prostate cancer progression; rs9364554 (P = 0.041) on chromosome 6q25 and rs10896449 (P = 0.029) on chromosome 11q13 among patients treated with curative intent; and rs4054823 (P = 0.008) on chromosome 17p12 among patients on surveillance. However, none of these associations remained statistically significant after correction for multiple testing. The combined effect of all susceptibility variants was not associated with prostate cancer progression neither among patients receiving treatment with curative intent (P = 0.14) nor among patients on surveillance (P = 0.92). CONCLUSIONS: We observed no evidence for an association between any of 23 established prostate cancer genetic risk variants and disease progression. Accumulating evidence suggests separate genetic components for initiation and progression of prostate cancer. Future studies systematically searching for genetic risk variants associated with prostate cancer progression and prognosis are warranted. Prostate © 2011 Wiley-Liss, Inc.

  • 250. Teo, J. S. M.
    et al.
    Gnanapragasam, V. J.
    Bratt, O.
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences.
    Huang, H. H.
    Muir, K.
    Lophatananon, A.
    Lee, L. S.
    External validation of a new clinical prognostic grouping to improve prediction of disease mortality at diagnosis in primary non-metastatic prostate cancer2017In: BJU International, ISSN 1464-4096, E-ISSN 1464-410X, Vol. 120, p. 9-10Article in journal (Other academic)
234567 201 - 250 of 320
CiteExportLink to result list
Permanent link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf