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  • 1.
    Behrens, Thomas
    et al.
    Bremen Institute of Prevention Research & Social Medicine, Bremen, Germany; Institute of Prevention & Occupational Medicine of German Social Accidents Insurance, Bochum, Germany.
    Lynge, Elsebeth
    Inst Publ Hlth, Univ Copenhagen, Copenhagen, Denmark..
    Cree, Ian
    Inst Ophthalmol, University College London (UCL), London, England.
    Lutz, Jean-Michel
    National Institute for Cancer Epidemiology and Registration (NICER), Univ Zurich, Zurich, Switzerland.
    Eriksson, Mikael
    Dept of Oncology, Lund University Hospital, Lund, Sweden..
    Guenel, Pascal
    Centre de recherche en épidémiologie et santé des populations (CESP), French National Institute of Health and Medical Research (INSERM), Villejuif, France; Univ Paris Sud, Villejuif, France.
    Merletti, Franco
    Cancer Epidemiology Unit, Univ Turin, Piemonte, Italy; ll Centro di Riferimento per l'Epidemiologia e la Prevenzione Oncologica (CPO), Piemonte, Italy.
    Morales-Suarez-Varela, Maria
    Dept of Prevention Medicine, Unit Public Health & Environmental Care, University Valencia, Valencia, Spain; CIBER Act Epidemiology & Public Health, Res Grp CIBER CB06, Valencia, Spain; Center Public Health Research CSISP, Valencia, Spain.
    Afonso, Noemia
    Med Oncol Serv, Inst Portugues Oncol Francisco Gentil, Oporto, Portugal.
    Stengrevics, Aivars
    Latvia Canc Registry, Riga, Latvia.
    Fevotte, Joelle
    Umrestte UCB Lyon 1 InVS Inrets, Lyon, France.
    Sabroe, Svend
    Dept Epidemiol, Univ Aarhus, Aarhus, Denmark..
    Llopis-Gonzalez, Agustin
    Dept Prevent Med, Unit Publ Hlth & Environm Care, Univ Valencia, Valencia, Spain; CIBER Act Epidemiol & Publ Hlth, Res Grp CIBER CB06, Valencia, Spain.
    Gorini, Giuseppe
    Environm & Occupat Epidemiol Unit, ISPO Canc Prevent & Res Inst, Florence, Italy.
    Hardell, Lennart
    Department of Oncology, Örebro University Hospital, Region Örebro län, Örebro, Sweden.
    Stang, Andreas
    Inst Clin Epidemiol, Univ Halle Wittenberg, Halle, Germany; Inst Med Informat Biometry & Epidemiol, Univ Duisburg Essen, Essen, Germany..
    Ahrens, Wolfgang
    Bremen Inst Prevent Res & Social Med, Bremen, Germany; Inst Med Informat Biometry & Epidemiol, Univ Duisburg Essen, Essen, Germany.
    Pesticide exposure in farming and forestry and the risk of uveal melanoma2012In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 23, no 1, p. 141-151Article in journal (Refereed)
    Abstract [en]

    Since pesticides are disputed risk factors for uveal melanoma, we studied the association between occupational pesticide exposure and uveal melanoma risk in a case-control study from nine European countries.

    Incident cases of uveal melanoma and population as well as hospital controls were included and frequency-matched by country, 5-year age groups and sex. Self-reported exposure was quantified with respect to duration of exposure and pesticide application method. We calculated the exposure intensity level based on application method and use of personal protective equipment. Odds ratios (OR) and 95% confidence intervals (95% CI) were estimated by unconditional logistic regression analyses and adjusted for several potential confounders.

    293 case and 3,198 control subjects were interviewed. We did not identify positive associations with activities in farming or forestry, pesticide application or pesticide mixing. No consistent positive associations were seen with exposure intensity level scores either. The only statistically significantly raised association in this study was for exposure to chemical fertilizers in forestry (OR = 8.93; 95% CI 1.73-42.13), but this observation was based on only six exposed subjects. Results did not change when we restricted analyses to morphologically verified cases and excluded proxy interviews as well as cancer controls. We did not observe effect modification by sex or eye color.

    Risk estimates for pesticide exposures and occupational activities in agriculture and forestry were not increased and did not indicate a hormonal mechanism due to these exposures.

  • 2.
    Bergengren, Lovisa
    et al.
    Örebro University, School of Health Sciences. Deparment of Women's Health.
    Karlsson, Mats
    Örebro University, School of Medical Sciences. Deparment of Laboratory Medicine.
    Helenius, Gisela
    Örebro University, School of Medical Sciences.
    Prevalence of HPV and pathological changes among women 70 years of age, 10 years after exclusion from the Swedish cervical cancer screening program2020In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 31, no 4, p. 377-381Article in journal (Refereed)
    Abstract [en]

    PURPOSE: Örebro County introduced an updated screening program 2016 with primary HPV test for women over 30 years and prolonged screening, increasing the cut-off age from 56-60 to 64-70. The aim of this study was to investigate the prevalence of HPV genotypes and their correlation to histological changes in women, 10 years after exclusion from the screening program, due to an eventual implementation of a catch-up program including all women aged 60-70.

    METHODS: All women in Örebro County, born 1,946 (n = 1,968), were invited to a liquid-based cell sample with primary HPV screening. Samples were analyzed for hrHPV mRNA and positive samples were genotyped. hrHPV positive women were offered to do a conization.

    RESULTS: Out of 809 participants, 31 (3.8%) were hrHPV positive, of these 22 did a conization. Histologically, 5/22 (23%) had LSIL and 5/22 (23%) had HSIL. Normal histology was found in 12/22 (55%). The most prevalent genotypes were HPV 16, 33, 52, 56, and 68. Of the women with HSIL, one case of cervical cancer was confirmed in a recone biopsy after 4 months.

    CONCLUSION: The study showed considerable prevalence of hrHPV and histologically confirmed LSIL/HSIL. These data led to catch-up screening for women between 60 and 70 years when overlapping two screening strategies.

  • 3.
    Epstein, Mara M
    et al.
    Department of Epidemiology, Harvard School of Public Health, Boston MA, United States; Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston MA, United States.
    Andrén, Ove
    Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Kasperzyk, Julie L
    Department of Epidemiology, Harvard School of Public Health, Boston MA, United States; Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston MA, United States.
    Shui, Irene M
    Department of Epidemiology, Harvard School of Public Health, Boston MA, United States.
    Penney, Kathryn L
    Department of Epidemiology, Harvard School of Public Health, Boston MA, United States; Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston MA, United States.
    Fall, Katja
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Clinical Epidemiology and Biostatistics, Örebro University Hospital, Örebro, Sweden.
    Rider, Jennifer R
    Department of Epidemiology, Harvard School of Public Health, Boston MA, United States; Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston MA, United States.
    Stampfer, Meir J
    Department of Epidemiology, Harvard School of Public Health, Boston MA, United States; Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston MA, United States.
    Andersson, Swen-Olof
    Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Giovannucci, Edward
    Department of Epidemiology, Harvard School of Public Health, Boston MA, United States; Department of Nutrition, Harvard School of Public Health, Boston MA, United States.
    Mucci, Lorelei A
    Department of Epidemiology, Harvard School of Public Health, Boston MA, United States; Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston MA, United States; Centre for Public Health Services, University of Iceland, Reykjavik, Iceland.
    Seasonal variation in expression of markers in the vitamin D pathway in prostate tissue2012In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 23, no 8, p. 1359-1366Article in journal (Refereed)
    Abstract [en]

    PURPOSE: Recent studies suggest variation in genes along the vitamin D pathway, as well as vitamin D receptor (VDR) protein levels, may be associated with prostate cancer. As serum vitamin D levels vary by season, we sought to determine whether the expression of genes on the vitamin D pathway, assessed in prostate tumor tissue, do the same.

    METHODS: Our study incorporates mRNA expression data from 362 men in the Swedish Watchful Waiting cohort, diagnosed between 1977 and 1999, and 106 men enrolled in the US Physicians' Health Study (PHS) diagnosed between 1983 and 2004. We also assayed for VDR protein expression among 832 men in the PHS and Health Professionals Follow-up Study cohorts. Season was characterized by date of initial tissue specimen collection categorically and by average monthly ultraviolet radiation levels. One-way analysis of variance was used to examine variation in the expression levels of six genes on the vitamin D pathway-VDR, GC, CYP27A1, CYP27B1, RXRα, CYP24A1-and VDR protein by season, adjusted for age at diagnosis and Gleason grade. Variation was also examined separately among lethal and nonlethal cases.

    RESULTS: Tumor expression levels of the six genes did not vary significantly by season of tissue collection. No consistent patterns emerged from subgroup analyses by lethal versus nonlethal cases.

    CONCLUSIONS: Unlike circulating levels of 25(OH) vitamin D, expression levels of genes on the vitamin D pathway and VDR protein did not vary overall by season of tissue collection. Epidemiological analyses of vitamin D gene expression may not be biased by seasonality.

  • 4. Hedelin, Maria
    et al.
    Klint, Åsa
    Chang, Ellen T.
    Bellocco, Rino
    Johansson, Jan-Erik
    Örebro University, School of Health and Medical Sciences.
    Andersson, Swen-Olof
    Örebro University, School of Health and Medical Sciences.
    Heinonen, Satu-Maarit
    Adlercreutz, Herman
    Adami, Hans-Olov
    Grönberg, Henrik
    Bälter, Katarina Augustsson
    Dietary phytoestrogen, serum enterolactone and risk of prostate cancer: the cancer prostate Sweden study (Sweden)2006In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 17, no 2, p. 169-180Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: Based on evidence that phytoestrogens may protect against prostate cancer, we evaluated the associations between serum enterolactone concentration or dietary phytoestrogen intake and risk of prostate cancer. METHODS: In our Swedish population-based case-control study, questionnaire-data were available for 1,499 prostate cancer cases and 1,130 controls, with serum enterolactone levels in a sub-group of 209 cases and 214 controls. Unconditional logistic regression was performed to estimate multivariate odds ratios (ORs) and 95% confidence intervals (CIs) for associations with risk of prostate cancer. RESULTS: High intake of food items rich in phytoestrogens was associated with a decreased risk of prostate cancer. The OR comparing the highest to the lowest quartile of intake was 0.74 (95% CI: 0.57-0.95; p-value for trend: 0.01). In contrast, we found no association between dietary intake of total or individual lignans or isoflavonoids and risk of prostate cancer. Intermediate serum levels of enterolactone were associated with a decreased risk of prostate cancer. The ORs comparing increasing quartiles of serum enterolactone concentration to the lowest quartile were, respectively, 0.28 (95% CI: 0.15-0.55), 0.63 (95% CI: 0.35-1.14) and 0.74 (95% CI: 0.41-1.32). CONCLUSIONS: Our results support the hypothesis that certain foods high in phytoestrogens are associated with a lower risk of prostate cancer.

  • 5.
    Kennedy, Beatrice
    et al.
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Clinical Epidemiology and Biostatistics Unit, Örebro University Hospital, Örebro, Sweden.
    Valdimarsdóttir, Unnur
    Faculty of Medicine, School of Health Sciences, University of Iceland, Reykjavík, Iceland.
    Sundström, Karin
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Sparén, Pär
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Lambe, Mats
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Regional Cancer Centre, Uppsala University Hospital, Uppsala, Sweden.
    Fall, Katja
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Faculty of Medicine, School of Health Sciences, University of Iceland, Reykjavík, Iceland.
    Fang, Fang
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Loss of a parent and the risk of cancer in early life: a nationwide cohort study2014In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 25, no 4, p. 499-506Article in journal (Refereed)
    Abstract [en]

    Background: While early-life exposure to stress has been associated with subsequent psychiatric and cardiovascular morbidity, little is known regarding its potential role in cancer development. We hypothesized that severe emotional stress, such as the loss of a parent through death during childhood, may increase the risk of cancer in early life.

    Method: Based on the Swedish Multi-Generation Register, we identified a cohort of 4,219,691 individuals who had both parents identifiable in the same register and followed the cohort from birth to the age of 40 years between 1961 and 2006. Through information retrieved from the Swedish Causes of Death and Cancer Registers, we ascertained death among the parents and cancer diagnosis among the cohort individuals. We used Poisson regression to calculate the relative risks (RRs) and 95 % confidence intervals (CIs).

    Results: Parental death was not associated with total cancer risk. However, parental death during childhood was associated with a higher risk of human papillomavirus (HPV) infection-related cancers (RR 1.4; 95 % CI 1.2-1.7), and loss during early adulthood (>18 years) entailed a higher risk of cancers of the stomach (RR 1.8; 95 % CI 1.3-2.6), lung (RR 1.7; 95 % CI 1.1-2.4), rectum (RR 1.4; 95 % CI 1.0-2.0), and breast (RR 1.1; 95 % CI 1.0-1.3). A significant association was observed for pancreatic cancer for both loss during childhood (RR 2.6; 95 % CI 1.6-4.2) and afterward (RR 2.8; 95 % CI 1.9-4.3).

    Conclusion: Our results suggest that severe psychological stress in early life may be associated with premature development of certain malignancies, particularly cancers related to smoking and HPV infection.

  • 6. Larsson, Susanna C.
    et al.
    Johansson, Jan-Erik
    Örebro University, School of Health and Medical Sciences.
    Andersson, Swen-Olof
    Örebro University, School of Health and Medical Sciences.
    Wolk, Alicja
    Meat intake and bladder cancer risk in a Swedish prospective cohort2009In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 20, no 1, p. 35-40Article in journal (Refereed)
    Abstract [en]

    Background  High meat consumption could potentially increase the risk of bladder cancer, but findings from epidemiologic studies are inconsistent. We prospectively examined the association between meat intake and bladder cancer risk in a population-based cohort study. Methods  We prospectively followed 82,002 Swedish women and men who were free from cancer and completed a food-frequency questionnaire in 1997. Incident cases of bladder cancer were identified in the Swedish cancer registries. Cox proportional hazards models were used to calculate hazard ratios (HR) with 95% confidence intervals (CI), adjusted for age, sex, education, smoking status, pack-years of smoking, and total energy intake. Results  During a mean follow-up of 9.4 years, 485 incident cases of bladder cancer (76 women and 409 men) were ascertained in the cohort. We observed no association between the intake of total or any specific type of meat and the risk of bladder cancer. The multivariate HRs (95% CIs) comparing the highest and the lowest category of intake were 1.05 (0.71–1.55) for total meat, 1.00 (0.71–1.41) for red meat, 1.01 (0.80–1.28) for processed meats, 0.96 (0.70–1.30) for chicken/poultry, and 0.92 (0.65–1.30) for fried meats/fish. The associations did not vary by sex or smoking status. Conclusions  These results do not support the hypothesis that intake of red meat, processed meat, poultry, or fried meats/fish is associated with the risk of developing bladder cancer.

  • 7.
    Lin, Yulan
    et al.
    Unit Upper Gastrointestinal Research, Dept Molecular Medicine & Surgery, Karolinska Institute, Stockholm, Sweden.
    Yngve, Agneta
    Dept Bioscienc & Nutrition, Huddinge Hospital, Karolinska Institute, Stockholm, Sweden.
    Lagergren, Jesper
    Div Canc Studies, Kings Coll London, London, England.
    Lu, Yunxia
    Unit Upper Gastrointestinal Res, Dept Molecular Medicin & Surgery, Karolinska Institute, Stockholm, Sweden.
    Dietary intake of lignans and risk of adenocarcinoma of the esophagus and gastroesophageal junction2012In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 23, no 6, p. 837-844Article in journal (Refereed)
    Abstract [en]

    The strong male predominance in esophageal and gastroesophageal junctional adenocarcinoma remains unexplained. Sex hormonal influence has been suggested, but not proven. A protective role of dietary phytoestrogen lignans was hypothesized. A Swedish nationwide population-based case-control study was conducted in 1995-1997, including 181 cases of esophageal adenocarcinoma, 255 cases of gastroesophageal junctional adenocarcinoma, 158 cases of esophageal squamous cell carcinoma, and 806 control subjects. Data on various exposures, including dietary data, were collected through personal interviews and questionnaires. Dietary intake of lignans was assessed using a food frequency questionnaire and categorized into quartiles based on the consumption among the control participants. Unconditional logistic regression was used to calculate odds ratios (ORs) with 95 % confidence intervals (CIs), including adjustment for all established risk factors. Participants in the highest quartile of intake of lignans compared with the lowest quartile were at a decreased risk of esophageal adenocarcinoma (OR, 0.65; 95 % CI, 0.38-1.12; for trend =0.03), gastroesophageal junctional adenocarcinoma (OR, 0.37; 95 % CI, 0.23-0.58; for trend < 0.0001), and these adenocarcinomas combined (OR, 0.45; 95 % CI, 0.31-0.67; for trend < 0.0001). No clear associations were found between lignan intake and risk of esophageal squamous cell carcinoma. This population-based study indicates that a high dietary intake of lignans decreases the risk of adenocarcinoma of the esophagus and gastroesophageal junction.

  • 8. Torfadottir, Johanna E.
    et al.
    Valdimarsdottir, Unnur A.
    Mucci, Lorelei
    Stampfer, Meir
    Kasperzyk, Julie L.
    Fall, Katja
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Centre of Public Health Sciences, University of Iceland, Reykjavik, Iceland; Örebro University Hospital, Örebro, Sweden.
    Tryggvadottir, Laufey
    Aspelund, Thor
    Olafsson, Orn
    Harris, Tamara B.
    Jonsson, Eirikur
    Tulinius, Hrafn
    Adami, Hans-Olov
    Gudnason, Vilmundur
    Steingrimsdottir, Laufey
    Rye bread consumption in early life and reduced risk of advanced prostate cancer2012In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 23, no 6, p. 941-950Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: To determine whether consumption of whole-grain rye bread, oatmeal, and whole-wheat bread, during different periods of life, is associated with risk of prostate cancer (PCa).

    METHODS: From 2002 to 2006, 2,268 men, aged 67-96 years, reported their dietary habits in the AGES-Reykjavik cohort study. Dietary habits were assessed for early life, midlife, and current life using a validated food frequency questionnaire. Through linkage to cancer and mortality registers, we retrieved information on PCa diagnosis and mortality through 2009. We used regression models to estimate odds ratios (ORs) and hazard ratios (HRs) for PCa according to whole-grain consumption, adjusted for possible confounding factors including fish, fish liver oil, meat, and milk intake.

    RESULTS: Of the 2,268 men, 347 had or were diagnosed with PCa during follow-up, 63 with advanced disease (stage 3+ or died of PCa). Daily rye bread consumption in adolescence (vs. less than daily) was associated with a decreased risk of PCa diagnosis (OR = 0.76, 95 % confidence interval (CI): 0.59-0.98) and of advanced PCa (OR = 0.47, 95 % CI: 0.27-0.84). High intake of oatmeal in adolescence (≥5 vs. ≤4 times/week) was not significantly associated with risk of PCa diagnosis (OR = 0.99, 95 % CI: 0.77-1.27) nor advanced PCa (OR = 0.67, 95 % CI: 0.37-1.20). Midlife and late life consumption of rye bread, oatmeal, or whole-wheat bread was not associated with PCa risk.

    CONCLUSION: Our results suggest that rye bread consumption in adolescence may be associated with reduced risk of PCa, particularly advanced disease.

  • 9.
    Wilson, Kathryn M.
    et al.
    Sch Publ Hlth, Dept Epidemiol, Harvard Univ, Boston MA, USA; Sch Med, Brigham & Womens Hosp, Channing Div Network Med, Harvard Univ, Boston MA, USA.
    Balter, Katarina
    Dept Med Epidemiol & Biostat, Karolinska Inst, Stockholm, Sweden.
    Moller, Elisabeth
    Dept Med Epidemiol & Biostat, Karolinska Inst, Stockholm, Sweden.
    Adami, Hans-Olov
    Sch Publ Hlth, Dept Epidemiol, Harvard Univ, Boston MA, USA; Dept Med Epidemiol & Biostat, Karolinska Inst, Stockholm, Sweden.
    Andrén, Ove
    Örebro University Hospital.
    Andersson, Swen-Olof
    Örebro University Hospital.
    Gronberg, Henrik
    Dept Med Epidemiol & Biostat, Karolinska Inst, Stockholm, Sweden.
    Mucci, Lorelei A.
    Sch Publ Hlth, Dept Epidemiol, Harvard Univ, Boston MA, USA; Sch Med, Brigham & Womens Hosp, Channing Div Network Med, Harvard Univ, Boston MA, USA.
    Coffee and risk of prostate cancer incidence and mortality in the Cancer of the Prostate in Sweden Study2013In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 24, no 8, p. 1575-1581Article in journal (Refereed)
    Abstract [en]

    Coffee intake has recently been associated with significantly lower risk of lethal and advanced prostate cancer in a US population. We studied the association between coffee and prostate cancer risk in the population-based case-control study Cancer of the Prostate in Sweden. Dietary data were available for 1,499 cases and 1,112 controls. We calculated odds ratios (ORs) for the risk of prostate cancer in high versus low categories of coffee intake using logistic regression. We studied overall prostate cancer risk as well as risk of fatal, advanced, localized, high-grade, grade 7, and low-grade disease. Mean coffee intake was 3.1 cups per day among both cases and controls. Coffee intake was not associated with overall prostate cancer risk. Risk of fatal prostate cancer was inversely, but not statistically significantly, associated with coffee intake, with an odds ratio of 0.64 [95 % confidence interval (CI) 0.34-1.19, p value for linear trend = 0.81] for men consuming greater than 5 cups per day compared to men drinking less than 1 cup per day. The highest intake of coffee was associated non-significantly with lower risk of advanced disease (OR = 0.73, 95 % CI 0.41-1.30, p trend = 0.98) and associated significantly with lower risk of high-grade cancer (Gleason 8-10; OR = 0.50, 95 % CI 0.26-0.98, p trend = 0.13). Risk of localized, grade 7, and low-grade cancers was not associated with coffee intake. This study provides some support of an inverse association between coffee and lethal and high-grade prostate cancer.

  • 10.
    Wolk, A.
    et al.
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden; Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden; Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden.
    Lindblad, Per
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden; Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden.
    Adami, H. O.
    Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden; Department of Cancer Epidemiology, University Hospital, Uppsala, Sweden; Department of Epidemiology, Harvard School of Public Health, Boston, MA, United States.
    Nutrition and renal cell cancer1996In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 7, no 1, p. 5-18Article in journal (Refereed)
    Abstract [en]

    Epidemiologic evidence on the relation between nutrition and renal cell cancer is reviewed. Kidney cancer, comprising 1.7 percent of all malignant diseases diagnosed worldwide, shows about a 20-fold international variation in the incidence in men and 10-fold in women. This substantial variation indicates an important causal role of environmental factors. Renal cell (parenchymal) cancer (RCC) accounts for about 80 percent of all kidney cancers. While the etiology of RCC is incompletely understood, analytic epidemiologic studies provide consistent support for a positive association of obesity with risk of RCC; the dose-response observed supports a causal relationship. Only a few prospective studies, all of them limited in size, have been published, while ecologic and case-control studies suggest that diet may be important in the etiology of RCC. However, contradictory results and methodologic limitations in some case-control studies prevent definite conclusions concerning diet and RCC. A positive association of protein and fat intake, as well as their main food sources (meat, milk, fats), with risk of RCC-as suggested by ecologic studies-has no clear support in analytic epidemiologic studies. A protective effect of vegetables and fruits has been observed in most case-control studies, while the majority do not show an association between alcohol, coffee, and risk of RCC. Recent reports indicated an increased risk of RCC associated with consumption of fried/sauteed meat and low intakes of magnesium or vitamin E. An apparent positive association with total energy intake, perhaps due to bias, needs further investigation.

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