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  • 1.
    Bergström, A.
    et al.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden.
    Moradi, T.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden.
    Lindblad, Per
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden; Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    Nyren, O.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden.
    Adami, H. O.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology and Harvard Center for Cancer Prevention, Harvard School of Public Health, Boston, MA, USA.
    Wolk, A.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden.
    Occupational physical activity and renal cell cancer: a nationwide cohort study in Sweden1999In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 83, no 2, p. 186-91Article in journal (Refereed)
    Abstract [en]

    The causes of renal cell cancer remain incompletely understood. In one previous retrospective case-control study, high occupational physical activity has been associated with a decreased risk among men, but not among women. Our aim was to investigate the association between occupational physical activity and renal cell cancer in a large cohort in Sweden. A cohort of Swedish men and women was identified in the nationwide censuses in 1960 and 1970, and the reported occupations were classified into 4 levels of physical demands. Follow-up from 1971 through 1989 was accomplished through record linkages to the Swedish Cancer Registry. Multivariate Poisson regression models were used to estimate relative risk (RR) and 95% confidence intervals (CI). We found a monotonic increase in risk of renal cell cancer with decreasing level of occupational physical activity among men (p for trend <0.001). After adjustment for socio-economic status, place of residence, and calendar year of follow-up, men with long-term sedentary jobs had a 25% (RR = 1.25, 95% CI 1.02-1.53) increased risk compared to men with physically demanding occupations. Among women there was no association, the dose-risk trend was not significant (p for trend >0.50). Occupational physical activity was inversely associated with renal cell cancer among men. The absence of association among women might be due to smaller range of exposure, confounding by household work or reproductive factors, or to a difference in biological response to physical activity in men and women.

  • 2.
    Bergström, A.
    et al.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden.
    Terry, P.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden.
    Lindblad, Per
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden.
    Lichtenstein, P.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden.
    Ahlbom, A.
    The Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Feychting, M.
    The Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Wolk, A.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden.
    Physical activity and risk of renal cell cancer2001In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 92, no 1, p. 155-157Article in journal (Refereed)
    Abstract [en]

    The relation between physical activity and renal cell cancer is unclear. High occupational physical activity has been associated with a decreased risk of renal cell cancer among men-but not among women-in two previous studies, while no association has been found for leisure time physical activity. Our aim was to investigate the association between occupational and leisure time physical activity in a prospective cohort of 17,241 Swedish twins. Information on physical activity and a wide range of potential confounding factors was obtained through a mailed questionnaire. During follow-up from 1967 through 1997 we identified 102 cases of renal cell cancer. We found no evidence of an inverse association between either occupational or leisure time physical activity and risk of renal cell cancer in this prospective cohort.

  • 3.
    Dickerman, Barbra A.
    et al.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, USA.
    Torfadottir, Johanna E.
    Centre for Public Health Sciences, University of Iceland, Reykjavik, Iceland.
    Valdimarsdottir, Unnur A.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, USA; Centre for Public Health Sciences, University of Iceland, Reykjavik, Iceland; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Wilson, Kathryn M.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, USA; Centre for Public Health Sciences, University of Iceland, Reykjavik, Iceland; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Steingrimsdottir, Laufey
    Unit for Nutrition Research, University Hospital, Reykjavik, Iceland; Faculty of Food Science and Nutrition, University of Iceland, Reykjavik, Iceland.
    Aspelund, Thor
    Centre for Public Health Sciences, University of Iceland, Reykjavik, Iceland; The Icelandic Heart Association, Kopavogur, Iceland.
    Batista, Julie L.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, USA; .
    Fall, Katja
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, USA.
    Giovannucci, Edward
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, USA; Channing Division of Network Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston MA, USA; Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston MA, USA.
    Sigurdardottir, Lara G.
    Centre for Public Health Sciences, University of Iceland, Reykjavik, Iceland; Faculty of Medicine, University of Iceland, Reykjavik, Iceland; Department of Education and Prevention, The Icelandic Cancer Society, Reykjavik, Iceland.
    Tryggvadottir, Laufey
    The Icelandic Cancer Registry, Reykjavik, Iceland.
    Gudnason, Vilmundur
    The Icelandic Heart Association, Kopavogur, Iceland; Faculty of Medicine, University of Iceland, Reykjavik, Iceland.
    Markt, Sarah C.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, USA.
    Mucci, Lorelei A.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, USA; Channing Division of Network Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston MA, USA.
    Midlife metabolic factors and prostate cancer risk in later life2018In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 142, no 6, p. 1166-1173Article in journal (Refereed)
    Abstract [en]

    Metabolic syndrome is associated with several cancers, but evidence for aggressive prostate cancer is sparse. We prospectively investigated the influence of metabolic syndrome and its components on risk of total prostate cancer and measures of aggressive disease in a cohort of Icelandic men. Men in the Reykjavik Study (n = 9,097, enrolled 1967-1987) were followed for incident (n = 1,084 total; n = 378 advanced; n = 148 high-grade) and fatal (n = 340) prostate cancer until 2014. Cox regression was used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for (1) measured metabolic factors at cohort entry (body mass index (BMI), blood pressure, triglycerides, fasting blood glucose) and (2) a metabolic syndrome score (range 0-4) combining the risk factors: BMI ≥30 kg/m2 ; systolic blood pressure (SBP) ≥130 or diastolic blood pressure (DBP) ≥85 mm Hg or taking antihypertensives; triglycerides ≥150 mg/dl; fasting blood glucose ≥100 mg/dl or self-reported type 2 diabetes. Hypertension and type 2 diabetes were associated with a higher risk of total, advanced, high-grade, and fatal prostate cancer, independent of BMI. Neither BMI nor triglycerides were associated with prostate cancer risk. Higher metabolic syndrome score (3-4 vs 0) was associated with a higher risk of fatal prostate cancer (HR 1.55; 95% CI: 0.89, 2.69; p trend = 0.08), although this finding was not statistically significant. Our findings suggest a positive association between midlife hypertension and diabetes and risk of total and aggressive prostate cancer. Further, metabolic syndrome as a combination of factors was associated with an increased risk of fatal prostate cancer.

  • 4.
    Downer, Mary K.
    et al.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, United States; Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston MA, United States; Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston MA, United States.
    Batista, Julie L.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, United States; Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston MA, United States.
    Mucci, Lorelei A.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, United States; Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston MA, United States.
    Stampfer, Meir J.
    Epstein, Mara Meyer
    Department of Medicine and the Meyers Primary Care Institute, University of Massachusetts Medical School, Worcester MA, United States.
    Håkansson, Niclas
    The National Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Wolk, Alicja
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Johansson, Jan-Erik
    Örebro University Hospital. Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Andrén, Ove
    Örebro University Hospital. Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Fall, Katja
    Örebro University, School of Medical Sciences. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, United States; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Andersson, Swen-Olof
    Örebro University Hospital. Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Dairy intake in relation to prostate cancer survival2017In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 140, no 9, p. 2060-2069Article in journal (Refereed)
    Abstract [en]

    Dairy intake has been associated with increased risk of advanced prostate cancer. Two US cohort studies reported increased prostate cancer-specific mortality with increased high-fat milk intake. We examined whether dairy and related nutrient intake were associated with prostate cancer progression in a Swedish patient population with high dairy consumption. We prospectively followed 525 men with newly diagnosed prostate cancer (diagnosed 1989-1994). We identified and confirmed deaths through February 2011 (n = 222 prostate cancer-specific, n = 268 from other causes). Cox proportional hazards regression was used to calculate hazard ratios (HR) and 95% confidence intervals (CI) for the associations between food or nutrient intake and prostate cancer-specific death. On average, patients consumed 5.0 servings/day of total dairy products at diagnosis. In the whole population, high-fat milk intake was not associated with prostate cancer-specific death (95% CI: 0.78, 2.10; p-trend = 0.32; multivariate-adjusted model). However, among patients diagnosed with localized prostate cancer, compared to men who consumed <1 servings/day of high-fat milk, those who drank >= 3 servings/day had an increased hazard of prostate cancer mortality (HR = 6.10; 95% CI: 2.14, 17.37; p-trend = 0.004; multivariate-adjusted model). Low-fat milk intake was associated with a borderline reduction in prostate cancer death among patients with localized prostate cancer. These associations were not observed among patients diagnosed with advanced stage prostate cancer. Our data suggest a positive association between high-fat milk intake and prostate cancer progression among patients diagnosed with localized prostate cancer. Further studies are warranted to investigate this association and elucidate the mechanisms by which high-fat milk intake may promote prostate cancer progression.

  • 5.
    Flaberg, E.
    et al.
    Department of Microbiology, Tumor and Cell Biology (MTC), Center for Integrative Recognition in the Immune System (IRIS), Karolinska Institutet, Stockholm, Sweden; Department of Microbiology, Tumor and Cell Biology (MTC), Karolinska Institute, Stockholm, Sweden.
    Markasz, L.
    Department of Microbiology, Tumor and Cell Biology (MTC), Center for Integrative Recognition in the Immune System (IRIS), Karolinska Institutet, Stockholm, Sweden.
    Petranyi, Gabor
    Department of Microbiology, Tumor and Cell Biology (MTC), Center for Integrative Recognition in the Immune System (IRIS), Karolinska Institutet, Stockholm, Sweden.
    Stuber, G.
    Department of Microbiology, Tumor and Cell Biology (MTC), Center for Integrative Recognition in the Immune System (IRIS), Karolinska Institutet, Stockholm, Sweden.
    Dicsö, F.
    Division of Pediatrics, Jósa András County Hospital, Nyíregyháza, Hungary.
    Alchihabi, N.
    Division of Pediatrics, Jósa András County Hospital, Nyíregyháza, Hungary.
    Oláh, E.
    Department of Pediatrics, Medical and Health Science Center, Debrecen University, Debrecen, Hungary.
    Csízy, I.
    Department of Pediatrics, Medical and Health Science Center, Debrecen University, Debrecen, Hungary.
    Józsa, T.
    Department of Pediatrics, Medical and Health Science Center, Debrecen University, Debrecen, Hungary.
    Andrén, Ove
    Örebro University, School of Health and Medical Sciences. Clinic of Urology, Örebro County Council, Örebro, Sweden.
    Johansson, J-E
    Örebro University, School of Health and Medical Sciences. Clinic of Urology, Örebro County Council, Örebro, Sweden.
    Andersson, Swen-Olof
    Örebro University, School of Health and Medical Sciences. Clinic of Urology, Örebro County Council, Örebro, Sweden.
    Klein, G.
    Department of Microbiology, Tumor and Cell Biology (MTC), Center for Integrative Recognition in the Immune System (IRIS), Karolinska Institutet, Stockholm, Sweden.
    Szekely, L.
    Department of Microbiology, Tumor and Cell Biology (MTC), Center for Integrative Recognition in the Immune System (IRIS), Karolinska Institutet, Stockholm, Sweden.
    High-throughput live cell imaging reveals differential inhibition of tumor cell proliferation by human fibroblasts2011In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 128, no 12, p. 2793-2802Article in journal (Refereed)
    Abstract [en]

    Increasing evidence indicates that cancer development requires changes both in the precancerous cells and in their microenvironment. To study one aspect of the microenvironmental control, we departed from Michael Stoker's observation (Stroker et al, J Cell Sci 1966;1:297-310) that normal fibroblasts can inhibit the growth of admixed cancer cells (neighbour suppression). We have developed a high-throughput microscopy and image analysis system permitting the examination of live mixed cell cultures growing on 384-well plates, at the single cell level and over time. We have tested the effect of 107 samples of low passage number (<5) primary human fibroblasts from pediatric and adult donors, on the growth of six human tumor cell lines. Three of the lines were derived from prostate carcinomas, two from lung carcinomas and one was an EBV transformed lymphoblastoid line. Labeled tumor cells were grown in the presence of unlabeled fibroblasts. The majority of the tested fibroblasts inhibited the proliferation of the tumor cells, compared to the control cultures where labeled tumor cells were co-cultured with unlabeled tumor cells. The proliferation inhibiting effect of the fibroblasts differed depending on their site of origin and the age of the donor. Inhibition required direct cell contact. Mouse 3T3 fibroblasts inhibited the growth of SV40-transformed 3T3 cells and human tumor cells, showing that the inhibitory effect could prevail across the species barrier. Our high-throughput system allows the quantitative analysis of the inhibitory effect of fibroblasts on the population level and the exploration of differences depending on the source of the normal cells.

  • 6.
    Hilvo, Mika
    et al.
    Biotechnology for Health and Well-being, VTT Technical Research Centre of Finland Espoo, Espoo, Finland.
    Gade, Stephan
    German Breast Group, GBG-Forschungs GmbH, Neu-Isenburg, Germany.
    Hyötyläinen, Tuulia
    Örebro University, School of Science and Technology. Biotechnology for Health and Well-being, VTT Technical Research Centre of Finland Espoo, Espoo, Finland.
    Nekljudova, Valentina
    German Breast Group, GBG-Forschungs GmbH, Neu-Isenburg, Germany.
    Seppänen-Laakso, Tuulikki
    Biotechnology for Health and Well-being, VTT Technical Research Centre of Finland Espoo, Espoo, Finland.
    Sysi-Aho, Marko
    Biotechnology for Health and Well-being, VTT Technical Research Centre of Finland Espoo, Espoo, Finland.
    Untch, Michael
    Department of Gynecology and Obstetrics, Helios Klinikum Berlin-Buch, Berlin, Germany.
    Huober, Jens
    Department of Gynecology, University of Ulm, Ulm, Germany.
    von Minckwitz, Gunter
    German Breast Group, GBG-Forschungs GmbH, Neu-Isenburg, Germany.
    Denkert, Carsten
    Department of Gynecology and Obstetrics, Helios Klinikum Berlin-Buch, Berlin, Germany.
    Oresic, Matej
    Örebro University, School of Medical Sciences. Biotechnology for Health and Well-being, VTT Technical Research Centre of Finland Espoo, Espoo, Finland.
    Loibl, Sibylle
    German Breast Group, GBG-Forschungs GmbH, Neu-Isenburg, Germany.
    Monounsaturated fatty acids in serum triacylglycerols are associated with response to neoadjuvant chemotherapy in breast cancer patients2014In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 134, no 7, p. 1725-1733Article in journal (Refereed)
    Abstract [en]

    Changes in cellular lipid metabolism are a common feature in most solid tumors, which occur already in early stages of the tumor progression. However, it remains unclear if the tumor-specific lipid changes can be detected at the level of systemic lipid metabolism. The objective of this study was to perform comprehensive analysis of lipids in breast cancer patient serum samples. Lipidomic profiling using an established analytical platform was performed in two cohorts of breast cancer patients receiving neoadjuvant chemotherapy. The analyses were performed for 142 patients before and after neoadjuvant chemotherapy, and the results before chemotherapy were validated in an independent cohort of 194 patients. The analyses revealed that in general the tumor characteristics are not reflected in the serum samples. However, there was an association of specific triacylglycerols (TGs) in patients' response to chemotherapy. These TGs containing mainly oleic acid (C18:1) were found in lower levels in those patients showing pathologic complete response before receiving chemotherapy. Some of these TGs were also associated with estrogen receptor status and overall or disease-free survival of the patients. The results suggest that the altered serum levels of oleic acid in breast cancer patients are associated with their response to chemotherapy.

  • 7. Johannesson, Marie
    et al.
    Askling, Johan
    Montgomery, Scott M.
    Örebro University, School of Health and Medical Sciences.
    Ekbom, Anders
    Bahmanyar, Shahram
    Cancer risk among patients with cystic fibrosis and their first-degree relatives2009In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 125, no 12, p. 2953-2956Article in journal (Refereed)
    Abstract [en]

    Patients with cystic fibrosis (CF) are at increased risk of some cancers. Little is known about the cancer risks among carriers heterozygous for the CF mutation and it is hypothesized this may be associated with reduced cancer risk. Using Swedish general population-based registers, we identified 884 patients with CF from 1968 to 2003 and 3,033 of their first-degree relatives The subjects were followed from birth of index persons or 1958, whichever came later, until death, emigration or 2003, whichever came first. Cancer risks were compared with the general Swedish population using standardized incidence ratios (SIR) with 95% confidence intervals (CI). Patients, followed for an average of 21 years, were at a higher overall risk of cancer. Some 26 cancer diagnoses, after excluding multiple diagnoses of nonmelanoma skin cancer in one man, produced an overall SIR of 3.2 (95% CI 2.1-4.6). We found statistically significantly increased risks for kidney, thyroid, endocrine, lymphoma and nonmelanoma skin cancer. There was no modification of cancer risk among parents and siblings, with an average of 21 years of follow-up. This study did not identify a heterozygote advantage for CF gene mutations in relation to cancer risk.

  • 8. Landgren, Ola
    et al.
    Björkholm, Magnus
    Montgomery, Scott M.
    Örebro University, Department of Clinical Medicine.
    Hjalgrim, Henrik
    Sjöberg, Jan
    Goldin, Lynn R.
    Askling, Johan
    Personal and family history of autoimmune diabetes mellitus and susceptibility to young-adult-onset Hodgkin lymphoma2006In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 118, no 2, p. 449-452Article in journal (Refereed)
    Abstract [en]

    Young-adult-onset (15-44 years of age) Hodgkin lymphoma (HL) is believed to arise as a consequence of late primary infection in susceptible individuals. The properties of this susceptibility remain little understood. We have previously reported an increased occurrence of HL in patients with rheumatoid arthritis and among their offspring, suggesting that susceptibility to autoimmunity might be of importance also in the pathogenesis of HL. To explore this hypothesis, we assessed the association of personal and family history of diabetes mellitus, with risk of subsequent HL in a population-based case-control study, including as cases all individuals diagnosed with HL above 15 years of age 1964-1999 (n = 6,873) in Sweden, and matched population controls (n = 12,565). First-degree relatives of cases and controls were identified through linkage with the Multi-generation Register. We identified discharges listing diabetes mellitus through linkage with the Inpatient Register (1964-2000). We used odds ratios (OR) as measures of relative risk. Cases with young-adult-onset HL were less likely to have a personal (OR =0.5, 95% CI 0.2-1.1) or family (OR =0.7, 95% CI 0.6-0.8) history of diabetes mellitus. In contrast, HL diagnosed at older ages was neither associated with a personal (OR =1.0) nor family (OR =1.0) history of diabetes mellitus. These findings suggests that characteristics of the immune system associated with conditions such as diabetes mellitus type I are of importance in the pathogenesis of young-adult-onset HL.

    Copyright 2005 Wiley-Liss, Inc.

  • 9.
    Lindblad, Per
    et al.
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden; Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    McLaughlin, J. K.
    National Cancer Institute, Bethesda, Maryland, United States.
    Mellemgaard, A.
    Danish Cancer Society, Danish Cancer Registry, Copenhagen, Denmark .
    Adami, H. O.
    Cancer Epidemiology Unit, University Hospital, Uppsala, Sweden; Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, United States.
    Risk of kidney cancer among patients using analgesics and diuretics: a population-based cohort study1993In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 55, no 1, p. 5-9Article in journal (Refereed)
    Abstract [en]

    The aim of this study was to determine the risk of kidney cancer in 2 cohorts defined on the basis of hospital discharge diagnoses associated with analgesic or diuretic use during the period 1965 to 1983. Patients were followed up through 1984 for cancer incidence. After excluding cancers in the first year of observation, 161 kidney cancers were observed vs. 138 expected among 54,662 patients in the analgesics cohort. The relative risk was higher for women than for men. When examined by sub-site within the kidney, risk for cancer of the renal pelvis was similar in magnitude to that for the renal parenchyma. Among 115,616 patients in the diuretics cohort, 278 kidney cancers occurred vs. 209 expected. The risk for women was higher than for men. This elevation in risk was confined to cancer of the renal parenchyma, with no significantly increased risk seen for cancer of the renal pelvis. Although we observed little excess risk among members of the analgesics cohort, the significantly elevated risk among patients using diuretics supports a number of recent studies, but inability to adjust for confounding factors such as obesity preclude drawing any conclusion regarding diuretics. Further research is warranted to assess in detail the relationship between diuretic use and cancer of the renal parenchyma.

  • 10.
    Lindblad, Per
    et al.
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden; Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    Mellemgaard, A.
    Danish Cancer Society, Copenhagen, Denmark .
    Schlehofer, B.
    Deutsches Krebsforschungszentrum, Heidelberg, Germany.
    Adami, H. O.
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden; Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, United States.
    McCredie, M.
    Cancer Epidemiology Research Unit, NSW Cancer Council, Sydney, Australia.
    McLaughlin, J. K.
    International Epidemiology Institute, Rockville, Maryland, United States.
    Mandel, J. S.
    Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis, Minnesota, United States .
    International renal-cell cancer study. V. Reproductive factors, gynecologic operations and exogenous hormones1995In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 61, no 2, p. 192-198Article in journal (Refereed)
    Abstract [en]

    The relationships between reproductive factors, exogenous hormones and renal-cell cancer were examined in an international, multicenter, population-based, case-control study undertaken in 1989-1991. Data from 5 centers situated in Australia, Denmark, Germany, Sweden and the United States included for analysis 608 women with renal-cell cancer and 766 female controls. A significant trend in risk (p = 0.002) was associated with number of births, with an 80% excess risk for 6 or more births [RR = 1.8, 95% confidence interval (CI) = 1.1 to 2.9] compared with one birth. A decreasing risk was seen for increasing age at first birth, although this was confounded by body-mass index and number of births. A suggestive reduction of risk was also seen for increasing age at menarche. Age at menopause was unrelated to risk of renal-cell cancer. An increased risk was observed for women having had both a hysterectomy and an oophorectomy. Use of oral contraceptives in non-smoking women reduced the risk of renal-cell cancer (RR = 0.5, 95% CI = 0.4 to 0.8); this reduction increased with longer duration of use. No association was observed for estrogen replacement therapy. Our results indicate that certain hormonal and reproductive variables may be related to risk of renal-cell cancer and deserve further investigation, both epidemiologically and experimentally.

  • 11.
    Lindblad, Per
    et al.
    Department of Urology Epidemiology Unit, University Hospital, Uppsala, Sweden; Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden.
    Zack, M.
    Centers for Disease Control, Atlanta, United States.
    Adami, H. O.
    Department of Cancer Epidemiology Unit, University Hospital, Uppsala, Sweden.
    Ericson, A.
    National Board of Health and Welfare, Stockholm, Sweden.
    Maternal and perinatal risk factors for Wilms' tumor: a nationwide nested case-control study in Sweden1992In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 51, no 1, p. 38-41Article in journal (Refereed)
    Abstract [en]

    This report describes maternal and perinatal risk factors for Wilms' tumor analyzed in a case-control study nested in a nationwide cohort in Sweden. The Swedish National Cancer Registry ascertained 110 cases from among successive birth cohorts from 1973 through 1984, identified by the Swedish Medical Birth Registry, the latter based on medical records. From the Birth Registry, we matched 5 controls without cancer to each case by sex and date of birth. Wilms'-tumor children were more likely to have mothers who had been exposed to penthrane (methoxyflurane) anesthesia during delivery than mothers of controls (odds ratio (OR) = 2.4; 95% confidence interval (CI) 1.1 to 5.1); this excess risk was higher in females than males and increased with age at diagnosis. Wilms'-tumor cases were also more likely to have had physiologic jaundice (OR = 2.3; 95% CI 1.1 to 5.0). Higher parity of the mother decreased the risk of Wilms' tumor among females (OR = 0.7; 95% CI 0.5 to 1.0). We were unable to confirm the reported increased risks of Wilms' tumor for those with high birth weights or with a maternal history of hypertension or fluid retention during pregnancy, nor did we find any association with mother's age at delivery, previous stillbirth, previous live birth, gestational length or height of the child.

  • 12.
    Ludvigsson, Jonas F.
    et al.
    Clinical Epidemiology Unit, Department of Medicine, Karolinska University Hospital and Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden.
    West, Joe
    Division of Epidemiology and Public Health, University of Nottingham, Nottingham City Hospital, Nottingham, United Kingdom.
    Ekbom, Anders
    Clinical Epidemiology Unit, Department of Medicine, Karolinska University Hospital and Karolinska Institutet, Stockholm, Sweden.
    Stephansson, Olof
    Clinical Epidemiology Unit, Department of Medicine, Karolinska University Hospital and Karolinska Institutet, Stockholm, Sweden; Department of Women's and Children's Health, Karolinska University Hospital and Institutet, Stockholm, Sweden.
    Reduced risk of breast, endometrial and ovarian cancer in women with celiac disease2012In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 131, no 3, p. E244-E250Article in journal (Refereed)
    Abstract [en]

    Women with celiac disease (CD) may be at decreased risk of female hormone-related cancers given the observed reduction in breast cancer seen in some cohorts. Using biopsy data from all 28 pathology departments in Sweden, we identified 17,852 women with CD who were diagnosed between 1969 and 2007. We used Cox regression model to estimate their risk of breast, endometrial and ovarian cancer and then compared them with 88,400 age- and sex-matched controls. The results indicate that individuals with CD were at a lower risk for all three outcomes: breast cancer (hazard ratio, HR = 0.85; 95% CI = 0.721.01), endometrial cancer (HR = 0.60; 95% CI =0.410.86) and ovarian cancer (HR = 0.89; 95% CI =0.591.34). This inverse relationship was strengthened when we excluded the first year of follow-up beyond CD diagnosis (breast: HR = 0.82; 95% CI =0.680.99; endometrial: HR = 0.58; 0.390.87; ovarian cancer: HR = 0.72; 0.451.15). In conclusion, CD seems to be inversely related not only to breast cancer but also to endometrial and ovarian cancer. Potential explanations include shared risk factors and early menopause.

  • 13.
    Mandel, J. S.
    et al.
    School of Public Health, University of Minnesota, Minneapolis, Minnesota, United States.
    McLaughlin, J. K.
    National Cancer Institute, Division of Cancer Etiology, Bethesda, Maryland, United States.
    Schlehofer, B.
    German Cancer Research Center, Division of Epidemiology, Heidelberg, Germany.
    Mellemgaard, A.
    Danish Cancer Society, Copenhagen, Denmark.
    Helmert, U.
    Bremer Institute for Prevention and Social Medicine, Bremen, Germany.
    Lindblad, Per
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden.
    McCredie, M.
    Cancer Epidemiology Research Unit, New South Wales Cancer Council, Sydney, Australia .
    Adami, H. O.
    Uppsala University, Uppsala, Sweden .
    International renal-cell cancer study. IV. Occupation1995In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 61, no 5, p. 601-605Article in journal (Refereed)
    Abstract [en]

    The relationship between renal-cell cancer (RCC) and occupation was investigated in an international multicenter population-based case-control study. Study centers in Australia, Denmark, Germany, Sweden and the United States interviewed 1732 incident RCC cases and 2309 controls. Significant associations were found with employment in the blast-furnace or the coke-oven industry [relative risk (RR), 1.7; 95% confidence interval (CI), 1.1-2.7], the iron and steel industry (RR, 1.6; 95% CI, 1.2-2.2) and exposure to asbestos (RR, 1.4; 95% CI, 1.1-1.8), cadmium (RR, 2.0; 95% CI, 1.0-3.9), dry-cleaning solvents (RR, 1.4; 95% CI, 1.1-1.7), gasoline (RR, 1.6; 95% CI, 1.2-2.0) and other petroleum products (RR, 1.6; 95% CI, 1.3-2.1). Asbestos, petroleum products and dry-cleaning solvents appear to merit further investigation, in view of the relationship between risk and duration of employment or exposure and after adjustment for confounding. There was a negative association between RCC and education, but it was not consistent across all centers. Overall, the results of our multicenter case-control study suggest that occupation may be more important in the etiology of RCC than indicated by earlier studies.

  • 14.
    McCredie, M.
    et al.
    Cancer Epidemiology Research Unit, NSW Cancer Council, Sydney, Australia.
    Pommer, W.
    Humboldt Hospital, Berlin, Germany.
    McLaughlin, J. K.
    Biostatistics Branch, National Cancer Institute, Bethesda, Maryland, United States .
    Stewart, J. H.
    Western Clinical School, University of Sydney, Sydney, Australia.
    Lindblad, Per
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden.
    Mandel, J. S.
    School of Public Health, University of Minnesota, Minneapolis, Minnesota, United States .
    Mellemgaard, A.
    Copenhagen, Denmark.
    Schlehofer, B.
    Division of Epidemiology, German Cancer Research Centre, Heidelberg, Germany.
    Niwa, S.
    Westat Inc., Rockville, Maryland, United States.
    International renal-cell cancer study. II. Analgesics1995In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 60, no 3, p. 345-349Article in journal (Refereed)
    Abstract [en]

    There has been concern about the role of analgesics in the development of renal-cell cancer, although a few studies have reported moderately elevated risks with regular or long-term use. In a large international case-control study of renal-cell cancer we examined, among other hypotheses, the effect of phenacetin-containing and of other types of analgesics: paracetamol (acetaminophen), salicylates (mainly aspirin) and pyrazolones (e.g., antipyrine or phenazone). Relative risks, adjusted for the effects of age, sex, body-mass index, tobacco smoking and study centre, were not significantly increased with intake of phenacetin, either when lifetime consumption was categorized at the level of > or = 0.1 kg or when subjects were subdivided further by amount. Nor were paracetamol, salicylates or pyrazolones linked with renal-cell cancer. No consistently increasing risks with consumption level was found. The lack of association was not altered by restricting analgesic use to that which occurred 5 or 10 years before the defined "cut-off" date or when analysis was restricted to exclusive users of a particular type of analgesic. Neither was the risk influenced by the rate of consumption or whether the consumption had occurred at a young age. Our study provides clear evidence that aspirin is unrelated to renal-cell cancer risk, and our findings do not support the hypothesis that analgesics containing phenacetin or paracetamol increase the risk, although the number of "regular" users and the amount of these types of analgesic consumed were too small to confidently rule out a minor carcinogenic effect of phenacetin and paracetamol.

  • 15.
    McLaughlin, J. K.
    et al.
    National Cancer Institute, Bethesda, Maryland, United States; International Epidemiology Institute, Rockville, Maryland, United States.
    Chow, W. H.
    National Cancer Institute, Bethesda, Maryland, United States.
    Mandel, J. S.
    Division of Environmental Health, School of Public Health, University of Minnesota, Minneapolis, Minnesota, United States.
    Mellemgaard, A.
    Danish Cancer Society, Copenhagen, Denmark.
    McCredie, M.
    Cancer Epidemiology Research Unit, New South Wales Cancer Council, Kings Cross, Australia .
    Lindblad, Per
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden.
    Schlehofer, B.
    Division of Cancer Epidemiology, German Cancer Research Center, Heidelberg, Germany.
    Pommer, W.
    Division of Cancer Epidemiology, German Cancer Research Center, Heidelberg, Germany.
    Niwa, S.
    Westat Inc., Rockville, Maryland, United States .
    Adami, H. O.
    Division of Cancer Epidemiology, German Cancer Research Center, Heidelberg, Germany .
    International renal-cell cancer study. VIII. Role of diuretics, other anti-hypertensive medications and hypertension1995In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 63, no 2, p. 216-221Article in journal (Refereed)
    Abstract [en]

    Risk of renal-cell cancer in relation to use of diuretics, other anti-hypertensive medications and hypertension was assessed in a multi-center, population-based, case-control study conducted in Australia, Denmark, Germany, Sweden and the United States, using a shared protocol and questionnaire. A total of 1,732 histologically confirmed cases and 2,309 controls, frequency-matched to cases by age and sex, were interviewed. The association between renal-cell cancer and the drugs was estimated by relative risks (RRs) and 95% confidence intervals (CIs). Risks were increased among users of diuretics and other anti-hypertensive medications. After adjustment for hypertension, risk for diuretics was reduced to unity, except among long-term (15+ years) users. Risk for use of non-diuretic anti-hypertensive drugs remained significantly elevated and increased further with duration of use. Overall risk was not enhanced when both classes of medications were used. Excess risk was not restricted to any specific type of diuretic or anti-hypertensive drug and no trend was observed with estimated lifetime consumption of any particular type of product. The RR for hypertension after adjustment for diuretics and other anti-hypertensive medications was 1.4 (95% CI = 1.2-1.7), although among non-users of any anti-hypertensive medications, there was little excess risk associated with a history of hypertension. Exclusion of drug use that first occurred within 5 years of cancer diagnosis or interview did not alter the associations. Our findings suggest small effects on renal-cell cancer risk associated with hypertension and use of diuretics and other anti-hypertensive medications. However, because of potential misclassifications of these highly correlated variables, it is difficult to distinguish the effect of treatment from its indication, hypertension.

  • 16.
    McLaughlin, J. K.
    et al.
    National Cancer Institute, Division of Cancer Etiology, Bethesda, Maryland, United States; International Epidemiology Institute, Rockville, Maryland, United States .
    Lindblad, Per
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden.
    Mellemgaard, A.
    Danish Cancer Society, Copenhagen, Denmark.
    McCredie, M.
    Cancer Epidemiology Research Unit, New South Wales Cancer Council, Kings Cross, Australia.
    Mandel, J. S.
    Division of Environmental Health, School of Public Health, University of Minnesota, Minneapolis, Minnesota, United States.
    Schlehofer, B.
    Division of Epidemiology, German Cancer Research Center, Heidelberg, Germany .
    Pommer, W.
    Humboldt Hospital, Berlin, Germany .
    Adami, H. O.
    Danish Cancer Society, Copenhagen, Denmark.
    International renal-cell cancer study. I. Tobacco use1995In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 60, no 2, p. 194-198Article in journal (Refereed)
    Abstract [en]

    The relationship between renal-cell cancer (RCC) and tobacco use was investigated in an international, multicenter, population-based case-control study. Coordinated studies were conducted in Australia, Denmark, Germany, Sweden and the United States using a shared protocol and questionnaire. A total of 1,732 cases (1,050 men, 682 women) and 2,309 controls (1,429 men, 880 women) were interviewed for the study. No association was observed between risk and use of cigars, pipes or smokeless tobacco. A statistically significant association was observed for cigarette smoking, with current smokers having a 40% increase in risk [relative risk (RR) = 1.4, 95% confidence interval (CI) 1.2-1.7]. Risk increased with intensity (number of cigarettes) and duration (years smoked). Among current smokers the RR for pack-years rose from 1.1 (95% CI 0.8-1.5) for < 15.9 pack years to 2.0 (95% CI 1.6-2.7) for > 42 pack years (p for trend < 0.001). Long-term quitters (> 15 years) experienced a reduction in risk of about 15-25% relative to current smokers. Those who started smoking late (> 24 years of age) had about two-thirds the risk of those who started young (< or = 12 years of age). Overall, the findings of this pooled analysis confirm that cigarette smoking is a causal factor in the etiology of RCC.

  • 17.
    Mellemgaard, A.
    et al.
    Danish Cancer Society, Division of Cancer Epidemiology, Copenhagen, Denmark.
    Lindblad, Per
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden; Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    Schlehofer, B.
    Division of Cancer Epidemiology, German Cancer Research Center, Heidelberg, Germany.
    Bergström, R.
    Dept. of Statistics, University of Uppsala, Uppsala, Sweden.
    Mandel, J. S.
    Division of Environmental Health, School of Public Health, University of Minnesota, Minnesota, United States.
    McCredie, M.
    Cancer Epidemiology Research Unit, NSW Cancer Council, Sydney, Australia .
    McLaughlin, J. K.
    National Cancer Institute, Division of Cancer Etiology, Rockville, Maryland, United States .
    Niwa, S.
    WESTAT Inc, Rockville, Maryland, United States.
    Odaka, N.
    WESTAT Inc, Rockville, Maryland, United States .
    Pommer, W.
    Humbolt Hospital, Berlin, Germany .
    International renal-cell cancer study. III. Role of weight, height, physical activity, and use of amphetamines1995In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 60, no 3, p. 350-354Article in journal (Refereed)
    Abstract [en]

    Although numerous studies have identified obesity or high relative weight as a risk factor for renal-cell cancer in women, the degree to which this effect is present in men remains unclear. A multicenter population-based case-control study concerning incident cases of histologically verified renal-cell cancer (n = 1,732) and age- and sex-matched controls (n = 2,309) was conducted in Australia, Denmark, Germany (2 centers), Sweden and the United States. Relative weight was estimated by the body mass index, and the association between this factor and other factors, such as height, physical activity and use of amphetamines, was measured by the relative risk estimated in logistic regression models. Body mass index was found to be a risk factor among women and, to a lesser extent, among men. A 3-fold increased risk (RR = 3.6, 95% CI = 2.3-5.7) was observed for women with a relative weight in the top 5% compared with those in the lowest quartile. Rate of weight change (estimated as weight change per annum in kilograms) appeared to be an independent risk factor among women but not among men. Physical activity and height were unrelated to risk of renal-cell cancer regardless of level of BMI, while use of amphetamines was associated with an increased risk among men, although no dose or duration effect was seen. Our findings verify the link between high relative weight and risk of renal-cell cancer, particularly among women. The mechanism that underlies this association is, however, still unclear, although the rate of weight change may play a role.

  • 18.
    Mucci, L. A.
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA.
    Lindblad, Per
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    Steineck, G.
    Clinical Cancer Epidemiology, Department of Oncology and Pathology, Karolinska Institutet, Stockholm, Sweden.
    Adami, H. O.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA.
    Dietary acrylamide and risk of renal cell cancer2004In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 109, no 5, p. 774-776Article in journal (Refereed)
    Abstract [en]

    The detection of acrylamide, classified as a probable human carcinogen, in commonly consumed foods created public health alarm. Thus far, only 2 epidemiologic studies have examined the effect of dietary acrylamide on cancer risk. Presently, we reanalyzed data from a large population-based Swedish case-control study of renal cell cancer. Food frequency data were linked with national food databases on acrylamide content, and daily acrylamide intake was estimated for participants. The risk of renal cell cancer was evaluated for intake of food items with elevated acrylamide levels and for total daily acrylamide dose. Adjusting for potential confounders, there was no evidence that food items with elevated acrylamide, including coffee (OR(highest vs. lowest quartile) = 0.7; 95% CI = 0.4-1.1), crisp breads (OR(highest vs. lowest quartile) = 1.0; 95% CI = 0.6-1.6) and fried potatoes (OR(highest vs. lowest quartile) = 1.1; 95% CI = 0.7-1.7), were associated with a higher risk of renal cell cancer risk. Furthermore, there was no association between estimated daily acrylamide intake through diet and cancer risk (OR(highest vs. lowest quartile) = 1.1; 95% CI = 0.7-1.8; p for trend = 0.8). The results of this study are in line with the 2 previous studies examining dietary acrylamide and suggest there is no association between dietary acrylamide and risk of renal cell cancer.

  • 19.
    Rashidkhani, B.
    et al.
    Division of Nutritional Epidemiology, The National Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Lindblad, Per
    Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    Wolk, A.
    Division of Nutritional Epidemiology, The National Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Fruits, vegetables and risk of renal cell carcinoma: a prospective study of Swedish women2005In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 113, no 3, p. 451-455Article in journal (Refereed)
    Abstract [en]

    Findings of epidemiologic studies on the relationship between fruit and vegetable consumption and renal cell carcinoma (RCC) risk have been inconclusive. To study the association between fruits and vegetables and risk of RCC in a population-based prospective cohort study of Swedish women, we collected dietary information from 61,000 women age 40-76 years by a food-frequency questionnaire. During 13.4 years of follow-up 122 women developed RCC. Cox proportional hazards models were used to estimate relative risks (RR) with 95% confidence interval (CI). Women consuming 5 or more servings of fruit and vegetables daily had a relative risk of 0.59 (95% CI = 0.26-1.34) in comparison to them consuming less than once daily. When fruits and vegetables were examined separately, those who consumed more than 75 servings per month of fruits or vegetables had multivariate relative risk of 0.59 (95% CI = 0.27-1.25) and 0.60 (95% CI = 0.31-1.17) respectively, compared to those consuming 11 or less servings per month. Within the group of fruits, the strongest inverse association was observed for banana (p = 0.07 by Wald test). The risk of RCC increased monotonically with increasing intake frequencies of fruit juice (p-value for trend = 0.10). Within the group of vegetables, the strongest inverse association was observed for root vegetables (p = 0.03 by Wald test). The risk of RCC decreased with increasing consumption frequencies of white cabbage (p for trend = 0.07). Frequent consumption of salad vegetables (once or more per day) decreased the risk by 40% (RR = 0.60; 95% CI = 0.30-1.22), in comparison to no consumption. Our results suggested that high consumption of fruits and vegetables might be associated with reduced risk of RCC.

  • 20.
    Rashidkhani, B.
    et al.
    Division of Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Åkesson, A.
    Division of Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Lindblad, Per
    Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    Wolk, A.
    Division of Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Alcohol consumption and risk of renal cell carcinoma: a prospective study of Swedish women2005In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 117, no 5, p. 848-853Article in journal (Refereed)
    Abstract [en]

    Previous literature, although not consistent, suggests that moderate alcohol consumption might be associated with decreased risk of renal cell carcinoma (RCC) in women. Thus, we examined the association between alcohol intake and the incidence of RCC by analyzing data from the Swedish Mammography Cohort, a population-based prospective cohort of 59,237 women, aged 40-76 years, who, at baseline in 1987-1990, were cancer free and had completed a food-frequency questionnaire including questions about alcohol consumption. Through June 30, 2004, 132 incident cases of RCC were diagnosed. We used the Cox proportional hazards model to estimate age and body mass index (BMI) adjusted rate ratios (RRs) and their 95% confidence intervals (CIs). Women who consumed >4.3 grams per day of alcohol (ethanol) had nonsignificantly lower risk of RCC than did women who consumed <2.5 g/d (RR = 0.71, 95% CI 0.42-1.19); among women > or = 55 years of age at entry into the cohort, corresponding risk estimates were RR = 0.33, 95% CI 0.10-1.05, p for trend = 0.04 and among women with BMI >25 kg/m2, RR = 0.30, 95% CI 0.09-0.97, p for trend = 0.04. Consistent with these findings, women who drank 1 or more servings of total alcoholic beverages per week had lower RCC risk than did women who drank less (RR = 0.62, 95% CI 0.41-0.94); the corresponding estimate for women > or = 55 years of age was RR = 0.44, 95% CI 0.22-0.88. Results from our prospective cohort study of middle-aged and elderly women indicate that moderate alcohol consumption may be associated with decreased risk of RCC.

  • 21.
    Schlehofer, B.
    et al.
    Division of Epidemiology, German Cancer Research Centre, Heidelberg, Germany; .
    Pommer, W.
    Humboldt Hospital, Berlin, Germany.
    Mellemgaard, A.
    Danish Cancer Registly, Danish Cancer Society, Copenhagen, Denmark.
    Stewart, J. H.
    Western Clinical School, University of Sydney, sydney, Australia.
    McCredie, M.
    Cancer Epidemiology Research Unit, NSW Cancer Council, Sydney, Australia.
    Niwa, S.
    Westat Inc., Rockville, MD, USA.
    Lindblad, Per
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden.
    Mandel, J. S.
    School of Public Health, University of Minnesota, Minneapolis, MN, USA.
    McLaughlin, J. K.
    BiostatisticsB ranch, National Cancer Institute, Bethesda, MD, USA.
    Wahrendorf, J.
    Division of Epidemiology, German Cancer Research Centre, Heidelberg, Germany.
    International renal-cell-cancer study. VI. the role of medical and family history1996In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 66, no 6, p. 723-726Article in journal (Refereed)
    Abstract [en]

    A number of medical conditions have been linked with renal-cell cancer, although the evidence is not consistent in every case. In a large international case-control study of renal-cell cancer, we examined, among other hypotheses, associations with a personal history of certain medical conditions and a family history of cancer of the kidney or thyroid. Relative risks (RR), adjusted for the effects of age, gender, body-mass index, tobacco smoking and study centre, were significantly increased by a history of kidney stones or thyroid or kidney disease. The RR were not altered by additional adjustment for hypertension, or when diagnoses were restricted to those made at least 5 or 10 years before 1987 (the usual "cut-off" date). The link with kidney injury is particularly likely to be affected by recall bias. Increased RR of borderline significance were found for kidney infection (RR, 1.2) and diabetes (RR, 1.4). Having one first-degree relative with kidney cancer was associated with a significantly increased risk of renal-cell cancer (RR, 1.6; 95% Cl, 1.1-2.4). Seven cases reported 2 first-degree relatives with kidney cancer. No controls had first-degree relatives with kidney cancer. None of our participants reported having von Hippel-Lindau disease. The data suggests that a few conditions of the kidney are strongly associated with renal-cell cancer and that heredity plays a role in a small proportion of cases.

  • 22.
    Shaikhibrahim, Zaki
    et al.
    Dept Prostate Canc Res, Univ Hosp, Bonn, Germany; Inst Pathol, Univ Hosp, Bonn, Germany .
    Menon, Roopika
    Dept Prostate Canc Res, Univ Hosp, Bonn, Germany; Inst Pathol, Univ Hosp, Bonn, Germany .
    Braun, Martin
    Dept Prostate Canc Res, Univ Hosp, Bonn, Germany; Inst Pathol, Univ Hosp, Bonn, Germany .
    Offermann, Anne
    Dept Prostate Canc Res, Univ Hosp, Bonn, Germany; Inst Pathol, Univ Hosp, Bonn, Germany .
    Queisser, Angela
    Dept Prostate Canc Res, Univ Hosp, Bonn, Germany; Inst Pathol, Univ Hosp, Bonn, Germany .
    Boehm, Diana
    Dept Prostate Canc Res, Univ Hosp, Bonn, Germany; Inst Pathol, Univ Hosp, Bonn, Germany .
    Vogel, Wenzel
    Dept Prostate Canc Res, Univ Hosp, Bonn, Germany; Inst Pathol, Univ Hosp, Bonn, Germany.
    Rueenauver, Kerstin
    Dept Prostate Canc Res, Univ Hosp, Bonn, Germany; Inst Pathol, Univ Hosp, Bonn, Germany .
    Ruiz, Christian
    Inst Pathol, Univ Basel Hosp, Basel, Switzerland.
    Zellweger, Tobias
    Dept Urol, St Clara Hosp, Basel, Switzerland.
    Svensson, Maria
    Örebro University Hospital. Dept Urol, Örebro University Hospital, Örebro, Sweden.
    Andrén, Ove
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Örebro University Hospital. Dept Urol, Örebro University Hospital, Örebro, Sweden.
    Kristiansen, Glen
    Inst Pathol, Univ Hosp, Bonn, Germany.
    Wernert, Nicolas
    Inst Pathol, Univ Hosp, Bonn, Germany.
    Bubendorf, Lukas
    Inst Pathol, Univ Basel Hosp, Basel, Switzerland.
    Kirfel, Jutta
    Inst Pathol, Univ Hosp, Bonn, Germany.
    Biskup, Saskia
    Ctr Genom & Transcript, CeGaT GmbH, Tubingen, Germany.
    Perner, Sven
    Dept Prostate Canc Res, Univ Hosp, Bonn, Germany; Inst Pathol, Univ Hosp, Bonn, Germany .
    MED15, encoding a subunit of the mediator complex, is overexpressed at high frequency in castration-resistant prostate cancer2014In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 135, no 1, p. 19-26Article in journal (Refereed)
    Abstract [en]

    The mediator complex is an evolutionary conserved key regulator of transcription of protein-coding genes and an integrative hub for diverse signaling pathways. In this study, we investigated whether the mediator subunit MED15 is implicated in castration-resistant prostate cancer (CRPC). MED15 expression and copy number/rearrangement status were assessed by immunohistochemistry (IHC) and fluorescence in situ hybridization (FISH), respectively on 718 prostate cancer (PCa) specimens and sequenced by Sanger on a subset. Furthermore, SMAD3 phosphorylation, androgen receptor (AR) and proliferation markers were evaluated by IHC. In PCa cells, siRNA/shRNA knockdown of MED15 was followed by proliferation assays with/without dihydrotestosterone (DHT), and treatments with recombinant TGF-beta 3. Our results show that MED15 is overexpressed in 76% of distant metastatic CRPC (CRPCMET) and 70% of local-recurrent CRPC (CRPCLOC), in contrast to low frequencies in androgen-sensitive PCa, and no expression in benign prostatic tissue. Furthermore, MED15 overexpression correlates with worse clinical outcome thus defining a highly lethal phenotype. Moreover, TGF-beta signaling activation associates with MED15 overexpression in PCa tissues, and leads to increased expression of MED15 in PCa cells. MED15 knockdown effects phosphorylation and shuttling of p-SMAD3 to the nucleus as well as TGF-beta-enhanced proliferation. In PCa tissues, MED15 overexpression associates with AR overexpression/amplification and correlates with high proliferative activity. MED15 knockdown decreases both androgen-dependent and -independent proliferation in PCa cells. Taken together, these findings implicate MED15 in CRPC, and as MED15 is evolutionary conserved, it is likely to emerge as a lethal phenotype in other therapeutic-resistant diseases, and not restricted to our disease model.

  • 23.
    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.
    Andrén, Ove
    Örebro University, School of Medical Sciences. Department of Urology, School of Medical Sciences, Örebro University Hospital, 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, UK.
    Davidsson, Sabina
    Örebro University, School of Medical Sciences. Department of Urology, School of Medical Sciences, Örebro University, Örebro, Sweden.
    Fall, Katja
    Örebro University, School of Medical Sciences. Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden.
    Acne in late adolescence and risk of prostate cancer2018In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, p. 1580-1585Article in journal (Refereed)
    Abstract [en]

    Accumulating evidence suggest that Propionibacterium acnes may play a role in prostate carcinogenesis, but data are so far limited and inconclusive. The aim of this population-based cohort study was therefore to test whether presence of acne vulgaris during late adolescence is associated with an increased risk of prostate cancer later in life. We identified a large cohort of young men born in Sweden between 1952 and 1956, who underwent mandatory assessment for military conscription around the age of 18 (n= 243,187). Test information along with health data including medical diagnoses at time of conscription was available through the Swedish Military Conscription Register and the National Patient Register. The cohort was followed through linkages to the Swedish Cancer Register to identify the occurrence of prostate cancer until December 31st 2009. We used Cox regression to calculate adjusted hazard ratios (HR) and 95% confidence intervals (95% CI) for the association between acne in adolescence and prostate cancer risk. A total of 1,633 men were diagnosed with prostate cancer during a median follow-up of 36.7 years. A diagnosis of acne was associated with a statistically significant increased risk for prostate cancer (adjusted HR: 1.43 95%; CI: 1.06-1.92), particularly for advanced stage disease (HR: 2.37 95%; CI 1.19-4.73). A diagnosis of acne classified as severe conferred a 6-fold increased risk of prostate cancer (HR: 5.70 95% CI 1.42-22.85). Data from this large prospective population-based cohort add new evidence supporting a role of P acnes infection in prostate cancer.

  • 24.
    Wolk, A.
    et al.
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden.
    Gridley, G.
    National Cancer Institute, Epidemiology and Biostatistics Program, Rochville, MD USA.
    Niwa, S.
    WESTAT Inc, Rockville, MD, USA.
    Lindblad, Per
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden; Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    McCredie, M.
    Tamer Epidemiology Research Unit, NS W Cancer Council, Sydney, Australia.
    Mellemgaard, A.
    6Danish Cancer Society, Division of Cancer Epidemiology, Copenhagen, Denmark.
    Mandel, J. S.
    School of Public Health, University of Minnesota, Minneapolis MN USA.
    Wahrendorf, J.
    Division of Epidemiology, German Cancer Research Center, Heidelberg, Germany.
    McLaughlin, J. K.
    1ntemational Epidemiology Institute, Rockville, MD, USA.
    Adami, H. O.
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden; ODepartment of Epidemiology, Harvard School of Public Health, Boston, M, USA.
    International renal cell cancer study. VII. Role of diet1996In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 65, no 1, p. 67-73Article in journal (Refereed)
    Abstract [en]

    We investigated the role of diet in the etiology of renal cell cancer (RCC) in a multi-center, population-based case-control study conducted in Australia, Denmark, Sweden and the United States, using a shared protocol. A total of 1,185 incident histopathologically confirmed cases (698 men, 487 women) and 1,526 controls (915 men, 611 women) frequency-matched to cases by sex and age were included in the analyses. The association between RCC and diet was estimated by relative risks (RR) and 95% confidence intervals (CI) adjusted for age, sex, study center, body mass index and smoking. A statistically significant positive association was observed for total energy intake (RR = 1.7, 95% CI = 1.4-2.2 for the highest vs. lowest quartile, p value for trend < 0.00001), while the hypothesis that protein and fat are risk factors independent of energy was not supported. Fried meats were associated with increased RCC risk, while vegetables and fruits were protective, with the strongest effect observed for the highest quartile of consumption of orange/dark green vegetables but not vitamin C or beta carotene. Increased risk was associated with low intake (lowest decile) of vitamin E and magnesium. We observed an apparent protective effect of alcohol confined to women and probably due to chance. Our findings indicate an important role of nutrition in the development of RCC. The apparent positive association of energy intake with risk of RCC needs further investigation in a prospective cohort study to exclude the possible impact of differences in recall between cases and controls.

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