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  • 1. Adami, Johanna
    et al.
    Nyrén, Olof
    Bergström, Reinhold
    Uppsala University, Disciplinary Domain of Humanities and Social Sciences, Faculty of Social Sciences, Department of Statistics.
    Ekbom, Anders
    Engholm, Göran
    Englund, Anders
    Glimelius, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology.
    Smoking and the risk of leukemia, lymphoma, and multiple myeloma (Sweden)1998In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 9, no 1, p. 49-56Article in journal (Refereed)
    Abstract [en]

    While several epidemiologic studies have indicated a link between smoking and the risk of developing hematolymphoproliferative cancers (chiefly leukemias, lymphomas, and multiple myelomas), in particular myeloid leukemia, the role of tobacco in the etiology of these neoplasms remains unclear. To evaluate the potential impact of tobacco use on development of leukemia, lymphoma, and multiple myeloma, we conducted a cohort study of 334,957 Swedish construction workers using prospectively collected exposure-information with complete long-term follow-up. A total of 1,322 incident neoplasms occurred during the study period, 1971-91. We found no significant association between smoking status, number of cigarettes smoked, or duration of smoking and the risk of developing leukemias, lymphomas, or multiple myeloma. There was a suggestion of a positive association between smoking and the risk of developing Hodgkin's disease, although the rate ratios were not significantly elevated, except for young current smokers. No positive dose-risk trends emerged. Our study provides no evidence that smoking bears any major relationship to the occurrence of leukemias, non-Hodgkin's lymphomas, or multiple myeloma.

  • 2.
    Alexeyev, Oleg
    et al.
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology. Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Virology.
    Bergh, Johanna
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Marklund, Ingrid
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Virology.
    Thellenberg Karlsson, Camilla
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Wiklund, Fredrik
    Grönberg, Henrik
    Bergh, Anders
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Elgh, Fredrik
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Virology.
    Association between the presence of bacterial 16S RNA in prostate specimens taken during transurethral resection of prostate and subsequent risk of prostate cancer (Sweden)2006In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 17, no 9, p. 1127-1133Article in journal (Refereed)
    Abstract [en]

    Objective: To study bacterial 16S RNA in archival prostate samples from 352 patients with benign prostate hyperplasia (BPH) and evaluate whether the presence of bacterial DNA was different in those who later developed prostate cancer (n = 171) and in the matched controls that did not progress to cancer (n = 181).

    Methods: 16S DNA PCR followed by cloning and sequencing the positive samples.

    Results: In 96/352 (27%) of the prostate tissue specimens 16S RNA were detected. Sequence analysis revealed Propionibacterium acnes as the predominant microorganism (23% of 16S RNA positive patients). The second most frequent isolate—Escherichia coli was found in 12 (12%) patients. The other isolates included Pseudomonas sp. (3 patients), Actinomyces sp. (2), Streptococcus mutans (1), Corynebacterium sp. (2),Nocardioides sp. (1), Rhodococcus sp. (1) Veillonella sp. (2). In P. acnes positive samples 62% exhibited severe histological inflammation versus 50% in the bacteria-negative group (p = 0.602). The presence of P. acnes in the prostate was associated with prostate cancer development (OR 2.17, 95% CI 0.77–6.95).

    Conclusions: This study has revealed P. acnes as the most common bacteria in the prostate in BPH. Further studies are needed to clarify its role in contributing to the development of prostatic inflammation and prostate cancer.

  • 3. Almquist, Martin
    et al.
    Johansen, Dorthe
    Björge, Tone
    Ulmer, Hanno
    Lindkvist, Björn
    Stocks, Tanja
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Engeland, Anders
    Rapp, Kilian
    Jonsson, Håkan
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Selmer, Randi
    Diem, Guenter
    Häggström, Christel
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Tretli, Steinar
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Manjer, Jonas
    Metabolic factors and risk of thyroid cancer in the Metabolic syndrome and Cancer project (Me-Can)2011In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 22, no 5, p. 743-751Article in journal (Refereed)
    Abstract [en]

    Objective  To investigate metabolic factors and their possible impact on risk of thyroid cancer. Methods  A prospective cohort study was conducted based on seven population-based cohorts in Norway, Austria, and Sweden, in the Metabolic syndrome and Cancer project (Me-Can). Altogether 578,700 men and women with a mean age of 44.0 years at baseline were followed for on average 12.0 years. Relative risk of incident thyroid cancer was assessed by levels of BMI, blood pressure, and blood levels of glucose, cholesterol, triglycerides, and by a combined metabolic syndrome (MetS) score. Risk estimates were investigated for quintiles, and a z score distribution of exposures was analyzed using Cox proportional hazards regression. Results  During follow-up, 255 women and 133 men were diagnosed with thyroid cancer. In women, there was an inverse association between glucose and thyroid cancer risk, with adjusted RR: 95% CI was 0.61 (0.41–0.90), p trend = 0.02 in the fifth versus the first quintile, and a positive association between BMI and thyroid cancer risk with a significant trend over quintiles. There was no association between the other metabolic factors, single or combined (Met-S), and thyroid cancer. Conclusion  In women, BMI was positively, while blood glucose levels were inversely, associated with thyroid cancer.

  • 4.
    Andersson, Ulrika
    et al.
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Degerman, Sofie
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Dahlin, Anna M.
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Wibom, Carl
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Johansson, Gunnar
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Bondy, Melissa L.
    Melin, Beatrice S.
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    The association between longer relative leukocyte telomere length and risk of glioma is independent of the potentially confounding factors allergy, BMI, and smoking2019In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 30, no 2, p. 177-185Article in journal (Refereed)
    Abstract [en]

    Purpose: Previous studies have suggested an association between relative leukocyte telomere length (rLTL) and glioma risk. This association may be influenced by several factors, including allergies, BMI, and smoking. Previous studies have shown that individuals with asthma and allergy have shortened relative telomere length, and decreased risk of glioma. Though, the details and the interplay between rLTL, asthma and allergies, and glioma molecular phenotype is largely unknown. Methods: rLTL was measured by qPCR in a Swedish population-based glioma case–control cohort (421 cases and 671 controls). rLTL was related to glioma risk and health parameters associated with asthma and allergy, as well as molecular events in glioma including IDH1 mutation, 1p/19q co-deletion, and EGFR amplification. Results: Longer rLTL was associated with increased risk of glioma (OR = 1.16; 95% CI 1.02–1.31). Similar to previous reports, there was an inverse association between allergy and glioma risk. Specific, allergy symptoms including watery eyes was most strongly associated with glioma risk. High body mass index (BMI) a year prior diagnosis was significantly protective against glioma in our population. Adjusting for allergy, asthma, BMI, and smoking did not markedly change the association between longer rLTL and glioma risk. rLTL among cases was not associated with IDH1 mutation, 1p/19q co-deletion, or EGFR amplification, after adjusting for age at diagnosis and sex. Conclusions: In this Swedish glioma case–control cohort, we identified that long rLTL increases the risk of glioma, an association not confounded by allergy, BMI, or smoking. This highlights the complex interplay of the immune system, rLTL and cancer risk.

  • 5. Arthur, Rhonda
    et al.
    Møller, Henrik
    Garmo, Hans
    Häggström, Christel
    Umeå University, Faculty of Medicine, Department of Biobank Research. Department of Surgical Sciences, Uppsala University Hospital, Uppsala, Sweden.
    Holmberg, Lars
    Stattin, Pär
    Malmström, Håkan
    Lambe, Mats
    Hammar, Niklas
    Walldius, Göran
    Robinson, David
    Jungner, Ingmar
    Van Hemelrijck, Mieke
    Serum glucose, triglycerides, and cholesterol in relation to prostate cancer death in the Swedish AMORIS study2019In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 30, no 2, p. 195-206Article in journal (Refereed)
    Abstract [en]

    Purpose: Lifestyle-related conditions such as obesity are associated with prostate cancer progression, but the associations with hyperglycemia and dyslipidemia are unclear. This study, therefore, aims to examine the association of glucose, triglycerides, and total cholesterol with prostate cancer death. Methods: From the Swedish AMORIS cohort, we selected 14,150 men diagnosed with prostate cancer between 1996 and 2011 who had prediagnostic measurements of serum glucose, triglycerides, and total cholesterol. Multivariable Cox proportional hazards regressionmodels were used to determine the hazard ratios for death in relation to the aforementioned metabolic markers. Results: Using clinical cut-off points, a non-significant positive association was observed between glucose and prostate cancer death. When compared to those with glucose in the lowest quartile, those in the highest quartile had greater risk of prostate cancer death (HR 1.19; 95% CI 1.02-1.39). However, neither total cholesterol nor triglycerides were associated with prostate cancer death. Glucose and triglycerides were positively associated with overall, cardiovascular, and other deaths. Hypercholesterolemia was only associated with risk of CVD death. Conclusion: Our results suggest that glucose levels may influence prostate cancer survival, but further studies using repeated measurements are needed to further elucidate how glucose levels may influence prostate cancer progression.

  • 6.
    Arthur, Rhonda
    et al.
    Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, New York, NY 10461 USA;Kings Coll London, Translat Oncol & Urol Res, London, England;Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, 1300 Morris Pk, Bronx, NY 10461 USA.
    Møller, Henrik
    Kings Coll London, Translat Oncol & Urol Res, London, England.
    Garmo, Hans
    Kings Coll London, Translat Oncol & Urol Res, London, England;Uppsala Univ Hosp, Dept Surg Sci, Uppsala, Sweden.
    Häggström, Christel
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Endocrine Surgery. Umea Univ, Dept Biobank Res, Umea, Sweden.
    Holmberg, Lars
    Kings Coll London, Translat Oncol & Urol Res, London, England.
    Stattin, Pär
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Urology.
    Malmström, Håkan
    Karolinska Inst, Inst Environm Med, Unit Epidemiol, Stockholm, Sweden;Swedish Orphan Biovitrum Sobi, Biostat Data Management & Med Writing, Res & Dev, Stockholm, Sweden.
    Lambe, Mats
    Uppsala Univ Hosp, Reg Canc Ctr, Uppsala, Sweden.
    Hammar, Niklas
    AstraZeneca, Med Evidence & Observat Res, Global Med Dev, Molndal, Sweden.
    Walldius, Göran
    Karolinska Inst, Inst Environm Med, Unit Epidemiol, Stockholm, Sweden.
    Robinson, David
    Ryhov Hosp, Dept Urol, Jonkoping, Sweden.
    Jungner, Ingmar
    Karolinska Inst, Dept Clin Epidemiol, Stockholm, Sweden;CALAB Res, Stockholm, Sweden.
    Van Hemelrijck, Mieke
    Kings Coll London, Translat Oncol & Urol Res, London, England.
    Serum glucose, triglycerides, and cholesterol in relation to prostate cancer death in the Swedish AMORIS study2019In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 30, no 2, p. 195-206Article in journal (Refereed)
    Abstract [en]

    Purpose: Lifestyle-related conditions such as obesity are associated with prostate cancer progression, but the associations with hyperglycemia and dyslipidemia are unclear. This study, therefore, aims to examine the association of glucose, triglycerides, and total cholesterol with prostate cancer death

    Methods: From the Swedish AMORIS cohort, we selected 14,150 men diagnosed with prostate cancer between 1996 and 2011 who had prediagnostic measurements of serum glucose, triglycerides, and total cholesterol. Multivariable Cox proportional hazards regressionmodels were used to determine the hazard ratios for death in relation to the aforementioned metabolic markers.

    Results: Using clinical cut-off points, a non-significant positive association was observed between glucose and prostate cancer death. When compared to those with glucose in the lowest quartile, those in the highest quartile had greater risk of prostate cancer death (HR 1.19; 95% CI 1.02-1.39). However, neither total cholesterol nor triglycerides were associated with prostate cancer death. Glucose and triglycerides were positively associated with overall, cardiovascular, and other deaths. Hypercholesterolemia was only associated with risk of CVD death.

    Conclusion: Our results suggest that glucose levels may influence prostate cancer survival, but further studies using repeated measurements are needed to further elucidate how glucose levels may influence prostate cancer progression.

  • 7.
    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.

  • 8.
    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 1573-7225Article 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.

  • 9. Boeing, H
    et al.
    Dietrich, T
    Hoffmann, K
    Pischon, T
    Ferrari, P
    Lahmann, PH
    Boutron-Ruault, MC
    Clavel-Chapelon, F
    Allen, N
    Key, T
    Skeie, G
    Lund, E
    Olsen, A
    Tjonneland, A
    Overvad, K
    Jensen, MK
    Rohrmann, S
    Linseisen, J
    Trichopoulou, A
    Bamia, C
    Psalttopoulou, T
    Weinehall, L
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Epidemiology and Public Health Sciences.
    Johansson, Ingegerd
    Umeå University, Faculty of Medicine, Department of Odontology, Cariology.
    Sanchez, MJ
    Jakszyn, P
    Ardanaz, E
    Amiano, P
    Chirlaque, MD
    Quiros, JR
    Wirfalt, E
    Berglund, G
    Peeters, PH
    van Gils, CH
    Bueno-de-Mesquita, HB
    Buchner, FL
    Berrino, F
    Palli, D
    Sacerdote, C
    Tumino, R
    Panico, S
    Bingham, S
    Khaw, KT
    Slimani, N
    Norat, T
    Jenab, M
    Riboli, E
    Intake of fruits and vegetables and risk of cancer of the upper aero-digestive tract: the prospective EPIC-study.2006In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 17, no 7, p. 957-969Article in journal (Refereed)
    Abstract [en]

    Epidemiologic studies suggest that a high intake of fruits and vegetables is associated with decreased risk of cancers of the upper aero-digestive tract. We studied data from 345,904 subjects of the prospective European Investigation into Cancer and Nutrition (EPIC) recruited in seven European countries, who had completed a dietary questionnaire in 1992-1998. During 2,182,560 person years of observation 352 histologically verified incident squamous cell cancer (SCC) cases (255 males; 97 females) of the oral cavity, pharynx, larynx, and esophagus were identified. Linear and restricted cubic spline Cox regressions were fitted on variables of intake of fruits and vegetables and adjusted for potential confounders. We observed a significant inverse association with combined total fruits and vegetables intake (estimated relative risk (RR) = 0.91; 95% confidence interval (95% CI) 0.83-1.00 per 80 g/d of consumption), and nearly significant inverse associations in separate analyses with total fruits and total vegetables intake (RR: 0.97 (95% CI: 0.92-1.02) and RR = 0.89 (95% CI: 0.78-1.02) per 40 g/d of consumption). Overall, vegetable subgroups were not related to risk with the exception of intake of root vegetables in men. Restricted cubic spline regression did not improve the linear model fits except for total fruits and vegetables and total fruits with a significant decrease in risk at low intake levels (<120 g/d) for fruits. Dietary recommendations should consider the potential benefit of increasing fruits and vegetables consumption for reducing the risk of cancers of the upper aero-digestive tract, particularly at low intake.

  • 10.
    Bonn, Stephanie E.
    et al.
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Wiklund, Fredrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Sjolander, Arvid
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Szulkin, Robert
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Stattin, Par
    Umea Univ, Dept Surg & Perioperat Sci Urol & Androl, Umea, Sweden..
    Holmberg, Erik
    Univ Gothenburg, Dept Oncol, Inst Clin Sci, Sahlgrenska Acad, Gothenburg, Sweden..
    Gronberg, Henrik
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Bälter, Katarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden..
    Body mass index and weight change in men with prostate cancer: progression and mortality2014In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 25, no 8, p. 933-943Article in journal (Refereed)
    Abstract [en]

    Body mass index (BMI) is a modifiable lifestyle factor that has been associated with an increased risk of fatal prostate cancer and biochemical recurrence. The main purpose of the present study was to investigate the association between the exposure BMI at the time of a prostate cancer diagnosis and weight change after diagnosis, and the outcomes of prostate cancer progression and mortality in a large cohort study. Data from 4,376 men diagnosed with clinically localized prostate cancer between 1997 and 2002 were analyzed. BMI and weight change were self-reported in 2007. Hazard ratios (HRs) with 95 % confidence intervals (CIs) were estimated in complete-case analysis (n = 3,214) using Cox proportional hazards models. Progression was experienced among 639 (14.6 %) of the study participants, and in total, 450 (10.3 %) deaths of any cause and 134 (3.1 %) prostate cancer-specific deaths were recorded during follow-up. Obese men had a 47 % increased rate of overall mortality compared to normal weight men (HR 1.47, 95 % CI 1.03-2.10). No statistically significant associations were found for BMI and prostate cancer progression or prostate cancer-specific mortality. A weight loss > 5 % after diagnosis almost doubled the rate of overall mortality compared to maintaining a stable weight (HR 1.94, 95 % CI 1.41-2.66), while a weight gain > 5 % was associated with an almost doubled increased rate of prostate cancer-specific mortality (HR 1.93, 95 % CI 1.18-3.16). Being obese was associated with an increased rate of overall mortality, and gaining weight after a prostate cancer diagnosis was associated with an increased rate of prostate cancer-specific mortality.

  • 11. Bonn, Stephanie E.
    et al.
    Wiklund, Fredrik
    Sjölander, Arvid
    Szulkin, Robert
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Holmberg, Erik
    Grönberg, Henrik
    Bälter, Katarina
    Body mass index and weight change in men with prostate cancer: progression and mortality2014In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 25, no 8, p. 933-943Article in journal (Refereed)
    Abstract [en]

    Body mass index (BMI) is a modifiable lifestyle factor that has been associated with an increased risk of fatal prostate cancer and biochemical recurrence. The main purpose of the present study was to investigate the association between the exposure BMI at the time of a prostate cancer diagnosis and weight change after diagnosis, and the outcomes of prostate cancer progression and mortality in a large cohort study. Data from 4,376 men diagnosed with clinically localized prostate cancer between 1997 and 2002 were analyzed. BMI and weight change were self-reported in 2007. Hazard ratios (HRs) with 95 % confidence intervals (CIs) were estimated in complete-case analysis (n = 3,214) using Cox proportional hazards models. Progression was experienced among 639 (14.6 %) of the study participants, and in total, 450 (10.3 %) deaths of any cause and 134 (3.1 %) prostate cancer-specific deaths were recorded during follow-up. Obese men had a 47 % increased rate of overall mortality compared to normal weight men (HR 1.47, 95 % CI 1.03-2.10). No statistically significant associations were found for BMI and prostate cancer progression or prostate cancer-specific mortality. A weight loss > 5 % after diagnosis almost doubled the rate of overall mortality compared to maintaining a stable weight (HR 1.94, 95 % CI 1.41-2.66), while a weight gain > 5 % was associated with an almost doubled increased rate of prostate cancer-specific mortality (HR 1.93, 95 % CI 1.18-3.16). Being obese was associated with an increased rate of overall mortality, and gaining weight after a prostate cancer diagnosis was associated with an increased rate of prostate cancer-specific mortality.

  • 12. Bonn, Stephanie E
    et al.
    Wiklund, Fredrik
    Sjölander, Arvid
    Szulkin, Robert
    Stattin, Pär
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Urology.
    Holmberg, Erik
    Grönberg, Henrik
    Bälter, Katarina
    Body mass index and weight change in men with prostate cancer: progression and mortality.2014In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 25, no 8, p. 933-943Article in journal (Refereed)
    Abstract [en]

    PURPOSE: Body mass index (BMI) is a modifiable lifestyle factor that has been associated with an increased risk of fatal prostate cancer and biochemical recurrence. The main purpose of the present study was to investigate the association between the exposure BMI at the time of a prostate cancer diagnosis and weight change after diagnosis, and the outcomes of prostate cancer progression and mortality in a large cohort study.

    METHODS: Data from 4,376 men diagnosed with clinically localized prostate cancer between 1997 and 2002 were analyzed. BMI and weight change were self-reported in 2007. Hazard ratios (HRs) with 95 % confidence intervals (CIs) were estimated in complete-case analysis (n = 3,214) using Cox proportional hazards models.

    RESULTS: Progression was experienced among 639 (14.6 %) of the study participants, and in total, 450 (10.3 %) deaths of any cause and 134 (3.1 %) prostate cancer-specific deaths were recorded during follow-up. Obese men had a 47 % increased rate of overall mortality compared to normal weight men (HR 1.47, 95 % CI 1.03-2.10). No statistically significant associations were found for BMI and prostate cancer progression or prostate cancer-specific mortality. A weight loss >5 % after diagnosis almost doubled the rate of overall mortality compared to maintaining a stable weight (HR 1.94, 95 % CI 1.41-2.66), while a weight gain >5 % was associated with an almost doubled increased rate of prostate cancer-specific mortality (HR 1.93, 95 % CI 1.18-3.16).

    CONCLUSIONS: Being obese was associated with an increased rate of overall mortality, and gaining weight after a prostate cancer diagnosis was associated with an increased rate of prostate cancer-specific mortality.

  • 13. Borena, Wegene
    et al.
    Stocks, Tanja
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Jonsson, Håkan
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Strohmaier, Susanne
    Nagel, Gabriele
    Bjørge, Tone
    Manjer, Jonas
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Selmer, Randi
    Almquist, Martin
    Häggström, Christel
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Engeland, Anders
    Tretli, Steinar
    Concin, Hans
    Strasak, Alexander
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Ulmer, Hanno
    Serum triglycerides and cancer risk in the metabolic syndrome and cancer (Me-Can) collaborative study2011In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 22, no 2, p. 291-299Article in journal (Refereed)
    Abstract [en]

    Data from our study provided evidence for a possible role of serum triglycerides in cancer development.

  • 14. Bosette, C
    et al.
    Negri, E
    Kolonel, L
    Ron, E
    Franceschi, S
    preston-Martin, S
    McTiernan, A
    Dal Maso, L
    Mark, SD
    Mabuchi, K
    Land, C
    Jin, F
    Wingren, Gun
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Occupational and Environmental Medicine.
    Galanti, MR
    Hallquist, A
    Glattre, E
    Lund, E
    Levi, F
    Linos, D
    La Vecchia, C
    A pooled analysis of case-control studies of thyroid cancer. VII. Cruciferous and other vegetables (International)2002In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 13, no 8, p. 765-775Article in journal (Refereed)
    Abstract [en]

    Objective: To investigate the association between cruciferous and other vegetables and thyroid cancer risk we systematically reanalyzed the original data from 11 case-control studies conducted in the US, Asia, and Europe. Methods: A total of 2241 cases (1784 women, 457 men) and 3716 controls (2744 women, 972 men) were included. Odds ratios (OR) and the corresponding 95% confidence intervals (CI) were estimated for each study by logistic regression models, conditioned on age and sex, and adjusted for history of goiter, thyroid nodules or adenomas, and radiation. Summary ORs for all studies combined were computed as the weighted average of the estimates from each study. Results: A decreased risk for the highest level of cruciferous vegetable intake, as compared to the lowest, was observed in Los Angeles, Hawaii, Connecticut, southeastern Sweden, Troms°, and Switzerland, the OR were above unity in Japan and Uppsala, whereas no material association was found in northern Sweden, Italy, or Greece. The OR values for all studies combined were 0.87 (95% CI 0.75-1.01) for moderate and 0.94 (95% CI 0.80-1.10) for high cruciferous vegetables intake. The results were similar in studies from iodine-rich areas and endemic goiter areas, and were consistent when the analysis was restricted to papillary carcinomas and women. The summary OR values for vegetables other than cruciferous were 1.04 (0.88-1.22) for moderate and 0.82 (0.69-0.98) for high consumption. Conclusions: This combined analysis indicates that cruciferous vegetables are not positively related to thyroid cancer risk. Their effect does not seem to be substantially different from that of other vegetables, which appear to be protective on this cancer.

  • 15. Bosetti, C
    et al.
    Kolonel, L
    Negri, E
    Ron, E
    Franceschi, S
    Dal Maso, L
    Galanti, MR
    Mark, SD
    Preston-Martin, S
    McTiernan, A
    Land, C
    Jin, F
    Wingren, Gun
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Occupational and Environmental Medicine.
    Hallquist, A
    Glattre, E
    Lund, E
    Levi, F
    Linos, D
    La Vecchia, C
    A pooled analysis of case-control studies of thyroid cancer. VI. Fish and shellfish consumption2001In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 12, no 4, p. 375-382Article in journal (Refereed)
    Abstract [en]

    Objective: To better understand the role of fish and shellfish on thyroid cancer risk, we systematically re-analyzed the original data from 13 case-control studies conducted in the US, Japan, China, and Europe. Methods: A total of 2497 cases (2023 women, 474 men) and 4337 controls (3268 women, 1069 men) were considered. Odds ratio (OR) and corresponding 95% confidence interval (CI) were estimated for each study by logistic regression models, conditioned on age and sex, and adjusted for history of goiter, thyroid nodules or adenomas, and radiation. Combined ORs were computed as the weighted average of the estimates from each study. Results: The ORs for the highest level of total fish consumption (three or more times per week) as compared to the lowest one (less than once per week) was above unity in Hawaii, Connecticut, Japan, Norway, Troms°, and Vaud. Conversely, the ORs for the studies in Los Angeles, Shanghai, southeastern Sweden, Uppsala, northern Sweden, northern Italy, and Athens were below one. The pattern of risk for salt water fish and shellfish was not substantially different from that of total fish. Fish was not associated with thyroid cancer risk in all studies combined (OR = 0.99, 95% CI 0.85-1.2 for moderate, and OR=0.88, 95% CI 0.71-1.1 for high total fish consumption), but there was a suggestion of a protective effect in endemic goiter areas (OR = 0.65, 95% CI 0.48-0.88). Conclusion: This combined analysis indicates that relatively elevated fish consumption does not appreciably increase thyroid cancer risk, and may have a favorable influence in areas where iodine deficiency is, or was, common.

  • 16. Büchner, F L
    et al.
    Bueno-de-Mesquita, H B
    Linseisen, J
    Boshuizen, H C
    Kiemeney, L A L M
    Ros, M M
    Overvad, K
    Hansen, L
    Tjonneland, A
    Raaschou-Nielsen, O
    Clavel-Chapelon, F
    Boutron-Ruault, M-C
    Touillaud, M
    Kaaks, R
    Rohrmann, S
    Boeing, H
    Nöthlings, U
    Trichopoulou, A
    Zylis, D
    Dilis, V
    Palli, D
    Sieri, S
    Vineis, P
    Tumino, R
    Panico, S
    Peeters, P H M
    van Gils, C H
    Lund, E
    Gram, I T
    Braaten, T
    Martinez, C
    Agudo, A
    Arriola, L
    Ardanaz, E
    Navarro, C
    Rodríguez, L
    Manjer, J
    Wirfält, E
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Rasmuson, Torgny
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Key, T J
    Roddam, A W
    Bingham, S
    Khaw, K-T
    Slimani, N
    Bofetta, P
    Byrnes, G
    Norat, T
    Michaud, D
    Riboli, E
    Fruits and vegetables consumption and the risk of histological subtypes of lung cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC)2010In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 21, no 3, p. 357-371Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: To examine the association between fruit and vegetable consumption and risk of different histological subtypes of lung cancer among participants of the European Prospective Investigation into Cancer and Nutrition study. METHODS: Multivariable Cox proportional hazard models were used to analyze the data. A calibration study in a subsample was used to reduce dietary measurement errors. RESULTS: During a mean follow-up of 8.7 years, 1,830 incident cases of lung cancer (574 adenocarcinoma, 286 small cell, 137 large cell, 363 squamous cell, 470 other histologies) were identified. In line with our previous conclusions, we found that after calibration a 100 g/day increase in fruit and vegetables consumption was associated with a reduced lung cancer risk (HR 0.94; 95% CI 0.89-0.99). This was also seen among current smokers (HR 0.93; 95% CI 0.90-0.97). Risks of squamous cell carcinomas in current smokers were reduced for an increase of 100 g/day of fruit and vegetables combined (HR 0.85; 95% CI 0.76-0.94), while no clear effects were seen for the other histological subtypes. CONCLUSION: We observed inverse associations between the consumption of vegetables and fruits and risk of lung cancer without a clear effect on specific histological subtypes of lung cancer. In current smokers, consumption of vegetables and fruits may reduce lung cancer risk, in particular the risk of squamous cell carcinomas.

  • 17. Chang, E T
    et al.
    Hedelin, M
    Adami, H O
    Gronberg, H
    Bälter Augustsson, Katarina
    Alcohol drinking and risk of localized versus advanced and sporadic versus familial prostate cancer in Sweden2005In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 16, no 3, p. 275-284Article in journal (Refereed)
    Abstract [en]

    Background: It is unknown whether the association of alcohol consumption with prostate cancer risk varies between localized and advanced cases, or between sporadic and familial cases. Methods: We assessed recent alcohol drinking in a population-based case-control study of Swedish men, including 1499 cases and 1130 controls. Drinking status and average volume, frequency, and type of alcohol consumed were evaluated. Unconditional logistic regression was performed to estimate the odds ratios (ORs) and corresponding 95% confidence intervals (CIs) for associations between alcohol consumption and prostate cancer risk. Results: Prostate cancer cases were more likely than controls to be current or former, rather than never, drinkers. However, there was no association between recent total alcohol, beer, wine, and liquor consumption and risk of overall prostate cancer, nor advanced, sporadic, or familial prostate cancer. The OR for risk of overall disease among men who drank more than 135 g of total alcohol per week versus non-drinkers was 1.2 (95% CI: 0.9, 1.5), p(trend)=0.12. There was a marginal positive association between alcohol intake and risk of localized disease. Conclusions: We detected no association between recent alcohol consumption and risk of advanced, sporadic, or familial prostate cancer, and a borderline positive association with localized disease.

  • 18. Chang, Ellen T.
    et al.
    Ekström Smedby, Karin
    Zhang, Shumin M.
    Hjalgrim, Henrik
    Melbye, Mads
    Öst, Åke
    Wolk, Alicja
    Adami, Hans-Olov
    Glimelius, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology.
    Alcohol intake and risk of non-Hodgkin lymphoma in men and women2004In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 15, no 10, p. 1067-1076Article in journal (Other academic)
    Abstract [en]

    OBJECTIVE: The effect of alcohol intake on risk of NHL is unclear. We therefore conducted a population-based case-control study to examine the association between alcohol and NHL risk. METHODS: 613 NHL cases and 480 population controls in Sweden reported their average consumption of beer, wine, and liquor 2 years before the study. Unconditional logistic regression was used to estimate the odds ratios (OR) and corresponding 95% confidence intervals (CI) for associations between alcohol intake and NHL risk. RESULTS: Intake of total alcohol, beer, wine, or liquor was not associated with risk of overall NHL. There was no difference in risk of NHL among those who habitually consumed above 19.1 g of ethanol per day, compared to those who consumed on average 0-2.2 g of ethanol per day (OR = 1.2 (95% CI: 0.8, 1.7); Ptrend = 0.29). However, the association was significantly positive among males (OR = 1.8 (95% CI: 1.1, 2.9); Ptrend = 0.06). Total alcohol, beer, wine, or liquor intake was not associated with any major histopathologic subtype of NHL examined, apart from an association between high wine consumption and increased risk of chronic lymphocytic leukemia. CONCLUSIONS: Alcohol does not appear to be a major etiologic factor for overall NHL, nor its common subtypes.

  • 19. Chen, Tianhui
    et al.
    Lundin, Eva
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Grankvist, Kjell
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Clinical chemistry.
    Zeleniuch-Jacquotte, Anne
    Wulff, Marianne
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Obstetrics and Gynaecology.
    Afanasyeva, Yelena
    Schock, Helena
    Johansson, Robert
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Lenner, Per
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Wadell, Göran
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology, Virology.
    Toniolo, Paolo
    Lukanova, Annekatrin
    Maternal hormones during early pregnancy: a cross-sectional study2010In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 21, no 5, p. 719-727Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Little is known about correlates of first-trimester pregnancy hormones as in most studies maternal hormones have been measured later in gestation. We examined the associations of maternal characteristics and child sex with first-trimester maternal concentrations of four hormones implicated in breast cancer: human chorionic gonadotropin (hCG), alpha-fetoprotein (AFP), insulin-like growth factor (IGF)-I, and IGF-II. METHODS: About 338 serum samples donated to the Northern Sweden Maternity Cohort (NSMC), 1975-2001, during the first trimester of uncomplicated pregnancies, were analyzed for the hormones of interest as a part of a case-control study. The associations of maternal characteristics and child sex with hormone concentrations were investigated by correlation, general linear regression, and multivariate regression models. RESULTS: In the first trimester, greater maternal age was inversely correlated with IGF-I and IGF-II. In comparison with women carrying their first child, already parous women had higher IGF-I but lower hCG. Greater maternal weight and smoking were inversely correlated with hCG. No differences in hormone levels by child sex were observed. CONCLUSIONS: Our analyses indicated that potentially modifiable maternal characteristics (maternal weight and smoking) influence first-trimester pregnancy maternal hormone concentrations.

  • 20. Clendenen, Tess V.
    et al.
    Arslan, Alan A.
    Lokshin, Anna E.
    Liu, Mengling
    Lundin, Eva
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Koenig, Karen L.
    Berrino, Franco
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research. Umeå University, Faculty of Medicine, Department of Biobank Research.
    Idahl, Annika
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Obstetrics and Gynaecology.
    Krogh, Vittorio
    Lukanova, Annekatrin
    Marrangoni, Adele
    Muti, Paola
    Nolen, Brian M.
    Ohlson, Nina
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Shore, Roy E.
    Sieri, Sabina
    Zeleniuch-Jacquotte, Anne
    Circulating prolactin levels and risk of epithelial ovarian cancer2013In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 24, no 4, p. 741-748Article in journal (Refereed)
    Abstract [en]

    Indirect evidence from experimental and epidemiological studies suggests that prolactin may be involved in ovarian cancer development. However, the relationship between circulating prolactin levels and risk of ovarian cancer is unknown.

    We conducted a nested case-control study of 230 cases and 432 individually matched controls within three prospective cohorts to evaluate whether pre-diagnostic circulating prolactin is associated with subsequent risk of ovarian cancer. We also assessed whether lifestyle and reproductive factors are associated with circulating prolactin among controls.

    Prolactin levels were significantly lower among post- versus pre-menopausal women, parous versus nulliparous women, and past versus never users of oral contraceptives in our cross-sectional analysis of controls. In our nested case-control study, we observed a non-significant positive association between circulating prolactin and ovarian cancer risk (ORQ4vsQ1 1.56, 95 % CI 0.94, 2.63, p trend 0.15). Our findings were similar in multivariate-adjusted models and in the subgroup of women who donated blood a parts per thousand yen5 years prior to diagnosis. We observed a significant positive association between prolactin and risk for the subgroup of women with BMI a parts per thousand yen25 kg/m(2) (ORQ4vsQ1 3.10, 95 % CI 1.39, 6.90), but not for women with BMI < 25 kg/m(2) (ORQ4vsQ1 0.81, 95 % CI 0.40, 1.64).

    Our findings suggest that prolactin may be associated with increased risk of ovarian cancer, particularly in overweight/obese women. Factors associated with reduced risk of ovarian cancer, such as parity and use of oral contraceptives, were associated with lower prolactin levels, which suggests that modulation of prolactin may be a mechanism underlying their association with risk.

  • 21. Dal Maso, L
    et al.
    La Vecchia, C
    Franceschi, S
    Preston-Martin, S
    Ron, E
    Levi, F
    Mack, W
    Mark, SD
    McTiernan, A
    Kolonel, L
    Mabuchi, K
    Jin, F
    Wingren, Gun
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Occupational and Environmental Medicine.
    Galanti, MR
    Hallquist, A
    Glattre, E
    Lund, E
    Linos, D
    Negri, E
    A pooled analysis of thyroid cancer studies. V. Anthropometric factors2000In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 11, no 2, p. 137-144Article in journal (Refereed)
    Abstract [en]

    Objective: To assess the relation between anthropometric factors and thyroid cancer risk in a pooled analysis of individual data from 12 case-control studies conducted in the US, Japan, China and Europe. Methods: 2056 female and 417 male cases, 3358 female and 965 male controls were considered. Odds ratios (OR) were derived from logistic regression, conditioning on age, A-bomb exposure (Japan) and study, and adjusting for radiotherapy. Results: Compared to the lowest tertile of height, the pooled OR was 1.2 for females for the highest one, and 1.5 for males, and trends in risk were significant. With reference to weight at diagnosis, the OR for females was 1.2 for the highest tertile, and the trend in risk was significant, whereas no association was observed in males. Body mass index (BMI) at diagnosis was directly related to thyroid cancer risk in females (OR = 1.2 for the highest tertile), but not in males. No consistent pattern of risk emerged with BMI during the late teens. Most of the associations were observed both for papillary and follicular cancers, and in all age groups. However, significant heterogeneity was observed across studies. Conclusions: Height and weight at diagnosis are moderately related to thyroid cancer risk.

  • 22. Elena, J. W.
    et al.
    Steplowski, E.
    Yu, K.
    Hartge, P.
    Tobias, G. S.
    Brotzman, M. J.
    Chanock, S. J.
    Stolzenberg-Solomon, R. Z.
    Arslan, A. A.
    Bueno-De-Mesquita, H. B.
    Helzlsouer, K.
    Jacobs, E. J.
    Lacroix, A.
    Petersen, G.
    Zheng, W.
    Albanes, D.
    Allen, N. E.
    Amundadottir, L.
    Bao, Y.
    Boeing, H.
    Boutron-Ruault, M. -C
    Buring, J. E.
    Gaziano, J. M.
    Giovannucci, E. L.
    Duell, E. J.
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research. Umeå University, Faculty of Medicine, Department of Biobank Research.
    Howard, B. V.
    Hunter, D. J.
    Hutchinson, A.
    Jacobs, K. B.
    Kooperberg, C.
    Kraft, P.
    Mendelsohn, J. B.
    Michaud, D. S.
    Palli, D.
    Phillips, L. S.
    Overvad, K.
    Patel, A. V.
    Sansbury, L.
    Shu, X. -O
    Simon, M. S.
    Slimani, N.
    Trichopoulos, D.
    Visvanathan, K.
    Virtamo, J.
    Wolpin, B. M.
    Zeleniuch-Jacquotte, A.
    Fuchs, C. S.
    Hoover, R. N.
    Gross, M.
    Diabetes and risk of pancreatic cancer: a pooled analysis from the pancreatic cancer cohort consortium2013In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 24, no 1, p. 13-25Article in journal (Refereed)
    Abstract [en]

    Purpose: Diabetes is a suspected risk factor for pancreatic cancer, but questions remain about whether it is a risk factor or a result of the disease. This study prospectively examined the association between diabetes and the risk of pancreatic adenocarcinoma in pooled data from the NCI pancreatic cancer cohort consortium (PanScan). Methods: The pooled data included 1,621 pancreatic adenocarcinoma cases and 1,719 matched controls from twelve cohorts using a nested case-control study design. Subjects who were diagnosed with diabetes near the time (<2 years) of pancreatic cancer diagnosis were excluded from all analyses. All analyses were adjusted for age, race, gender, study, alcohol use, smoking, BMI, and family history of pancreatic cancer. Results: Self-reported diabetes was associated with a forty percent increased risk of pancreatic cancer (OR = 1.40, 95 % CI: 1.07, 1.84). The association differed by duration of diabetes; risk was highest for those with a duration of 2-8 years (OR = 1.79, 95 % CI: 1.25, 2.55); there was no association for those with 9+ years of diabetes (OR = 1.02, 95 % CI: 0.68, 1.52). Conclusions: These findings provide support for a relationship between diabetes and pancreatic cancer risk. The absence of association in those with the longest duration of diabetes may reflect hypoinsulinemia and warrants further investigation.

  • 23. Eloranta, Sandra
    et al.
    Adolfsson, Jan
    Lambert, Paul C.
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Akre, Olof
    Andersson, Therese M-L.
    Dickman, Paul W.
    How can we make cancer survival statistics more useful for patients and clinicians: an illustration using localized prostate cancer in Sweden2013In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 24, no 3, p. 505-515Article in journal (Refereed)
    Abstract [en]

    Studies of cancer patient survival typically report relative survival or cause-specific survival using data from patients diagnosed many years in the past. From a risk-communication perspective, such measures are suboptimal for several reasons; their interpretation is not transparent for non-specialists, competing causes of death are ignored and the estimates are unsuitable to predict the outcome of newly diagnosed patients. In this paper, we discuss the relative merits of recently developed alternatives to traditionally reported measures of cancer patient survival. In a relative survival framework, using a period approach, we estimated probabilities of death in the presence of competing risks. To illustrate the methods, we present estimates of survival among 23,353 initially untreated, or hormonally treated men with intermediate- or high-risk localized prostate cancer using Swedish population-based data. Among all groups of newly diagnosed patients, the probability of dying from prostate cancer, accounting for competing risks, was lower compared to the corresponding estimates where competing risks were ignored. Accounting for competing deaths was particularly important for patients aged more than 70 years at diagnosis in order to avoid overestimating the risk of dying from prostate cancer. We argue that period estimates of survival, accounting for competing risks, provide the tools to communicate the actual risk that cancer patients, diagnosed today, face to die from their disease. Such measures should offer a more useful basis for risk communication between patients and clinicians and we advocate their use as means to answer prognostic questions.

  • 24.
    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.

  • 25.
    Essen, Anneli
    et al.
    Kings Coll London, Sch Canc & Pharmaceut Sci, Guys Hosp, Res Oncol Translat Oncol & Urol Res TOUR, 3rd Floor,Bermondsey Wing, London SE1 9RT, England.
    Santaolalla, Aida
    Kings Coll London, Sch Canc & Pharmaceut Sci, Guys Hosp, Res Oncol Translat Oncol & Urol Res TOUR, 3rd Floor,Bermondsey Wing, London SE1 9RT, England.
    Garmo, Hans
    Kings Coll London, Sch Canc & Pharmaceut Sci, Guys Hosp, Res Oncol Translat Oncol & Urol Res TOUR, 3rd Floor,Bermondsey Wing, London SE1 9RT, England;Reg Canc Ctr, Uppsala, Sweden.
    Hammar, Niklas
    Karolinska Inst, Inst Environm Med, Unit Epidemiol, Stockholm, Sweden;AstraZeneca, Global Med Affairs, Med Evidence & Observat Res, Molndal, Sweden.
    Walldius, Göran
    Karolinska Inst, Inst Environm Med, Dept Cardiovasc Epidemiol, Stockholm, Sweden.
    Jungner, Ingmar
    Karolinska Inst, Dept Clin Epidemiol, Stockholm, Sweden;CALAB Res, Stockholm, Sweden.
    Malmström, Håkan
    Karolinska Inst, Inst Environm Med, Unit Epidemiol, Stockholm, Sweden;Swedish Orphan Biovitrum AB, Biostat Res & Dev, Stockholm, Sweden.
    Holmberg, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Endocrine Surgery. Kings Coll London, Sch Canc & Pharmaceut Sci, Guys Hosp, Res Oncol Translat Oncol & Urol Res TOUR, 3rd Floor,Bermondsey Wing, London SE1 9RT, England.
    Van Hemelrijck, Mieke
    Kings Coll London, Sch Canc & Pharmaceut Sci, Guys Hosp, Res Oncol Translat Oncol & Urol Res TOUR, 3rd Floor,Bermondsey Wing, London SE1 9RT, England;Karolinska Inst, Inst Environm Med, Unit Epidemiol, Stockholm, Sweden.
    Baseline serum folate, vitamin B12 and the risk of prostate and breast cancer using data from the Swedish AMORIS cohort2019In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 30, no 6, p. 603-615Article in journal (Refereed)
    Abstract [en]

    Purpose: The roles of folate and vitamin B12 in prostate cancer (PCa) or breast cancer (BC) development are unclear. We investigated their roles using the prospective Swedish Apolipoprotein MOrtality RISk (AMORIS) study.

    Methods: 8,783 men and 19,775 women with vitamin B12 and folate serum measurements were included. Their associations with PCa and BC risk categories were evaluated using Cox proportional hazards regression.

    Results: During mean follow-up of 13years, 703 men developed PCa. There was an inverse association between folate>32nmol/L and high-risk PCa [hazard ratio (HR) 0.12, 95% confidence interval (CI) 0.02-0.90], and a positive association between folate<5nmol/L and metastatic PCa (HR 5.25, 95% CI 1.29-21.41), compared with folate 5-32nmol/L. No associations with vitamin B12 were found. 795 women developed BC during mean follow-up of 14years. When restricting to the fasting population, there was a positive association between folate>32nmol/L and BC (HR 1.47, 95% CI 1.06-2.04).

    Conclusion: High folate levels may protect against PCa and low folate levels may increase risk of metastatic PCa. High fasting folate levels may be associated with an increased BC risk. Vitamin B12 was not found to be linked with risk of PCa or BC. Longitudinal studies with serum and dietary information could help define new prevention targets and add information on the role of folate fortification.

  • 26. Franceschi, S
    et al.
    Preston-Martin, S
    Wingren, Gun
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Occupational and Environmental Medicine.
    A pooled analysis of case-control studies of thyroid cancer. IV. Benign thyroid diseases.1999In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 10, p. 583-595Article in journal (Refereed)
  • 27. Friedenreich, Christine
    et al.
    Cust, Anne
    Lahmann, Petra H
    Steindorf, Karen
    Boutron-Ruault, Marie-Christine
    Clavel-Chapelon, Françoise
    Mesrine, Sylvie
    Linseisen, Jakob
    Rohrmann, Sabine
    Boeing, Heiner
    Pischon, Tobias
    Tjønneland, Anne
    Halkjaer, Jytte
    Overvad, Kim
    Mendez, Michelle
    Redondo, M L
    Garcia, Carmen Martinez
    Larrañaga, Nerea
    Tormo, María-José
    Gurrea, Aurelio Barricarte
    Bingham, Sheila
    Khaw, Kay-Tee
    Allen, Naomi
    Key, Tim
    Trichopoulou, Antonia
    Vasilopoulou, Effie
    Trichopoulos, Dimitrios
    Pala, Valeria
    Palli, Domenico
    Tumino, Rosario
    Mattiello, Amalia
    Vineis, Paolo
    Bueno-de-Mesquita, H Bas
    Peeters, Petra H M
    Berglund, Göran
    Manjer, Jonas
    Lundin, Eva
    Umeå University, Faculty of Medicine, Medical Biosciences, Pathology.
    Lukanova, Annekatrin
    Slimani, Nadia
    Jenab, Mazda
    Kaaks, Rudolf
    Riboli, Elio
    Anthropometric factors and risk of endometrial cancer: the European prospective investigation into cancer and nutrition.2007In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 18, no 4, p. 399-413Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: To examine the association between anthropometry and endometrial cancer, particularly by menopausal status and exogenous hormone use subgroups. METHODS: Among 223,008 women in the European Prospective Investigation into Cancer and Nutrition (EPIC) study, there were 567 incident endometrial cancer cases during 6.4 years of follow-up. The analysis was performed with Cox proportional hazards modeling. RESULTS: Weight, body mass index (BMI), waist and hip circumferences and waist-hip ratio (WHR) were strongly associated with increased risk of endometrial cancer. The relative risk (RR) for obese (BMI 30- < 40 kg/m(2)) compared to normal weight (BMI < 25) women was 1.78, 95% CI = 1.41-2.26, and for morbidly obese women (BMI > or = 40) was 3.02, 95% CI = 1.66-5.52. The RR for women with a waist circumference of > or =88 cm vs. <80 cm was 1.76, 95% CI = 1.42-2.19. Adult weight gain of > or =20 kg compared with stable weight (+/-3 kg) increased risk independent of body weight at age 20 (RR = 1.75, 95% CI = 1.11-2.77). These associations were generally stronger for postmenopausal than premenopausal women, and oral contraceptives never-users than ever-users, and much stronger among never-users of hormone replacement therapy compared to ever-users. CONCLUSION: Obesity, abdominal adiposity, and adult weight gain were strongly associated with endometrial cancer risk. These associations were particularly evident among never-users of hormone replacement therapy.

  • 28. Galanti, M. Rosaria
    et al.
    Hansson, Lisbeth
    Uppsala University, Disciplinary Domain of Humanities and Social Sciences, Faculty of Social Sciences, Department of Statistics.
    Bergström, Reinhold
    Uppsala University, Disciplinary Domain of Humanities and Social Sciences, Faculty of Social Sciences, Department of Statistics.
    Wolk, Alicja
    Hjartåker, Anette
    Lund, Eiliv
    Grimelius, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology.
    Ekbom, Anders
    Diet and the risk of papillary and follicular thyroid carcinoma: A population-based case-control study in Sweden and Norway1997In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 8, no 2, p. 205-214Article in journal (Refereed)
    Abstract [en]

    A population-based case-control study was conducted in two regions of Sweden and Norway to investigate the association between dietary habits and the risk of thyroid cancer. The consumption of selected foods was reported in a self-completed food-frequency questionnaire by 246 cases with histologically confirmed papillary (n = 209) and follicular (n = 37) thyroid carcinoma, and 440 age- and gender-matched controls. Odds ratios (OR) and their 95 percent confidence interval (CI) were calculated as estimates of the relative risk using conditional logistic regression. High consumption of butter (OR = 1.6, CI = 1.1-2.5) and cheese (OR = 1.5, CI = 1.0-2.4) was associated with increased risks. Residence in areas of endemic goiter in Sweden was associated with an elevated risk, especially among women (OR = 2.5, CI = 1.3-4.9). High consumption of cruciferous vegetables was associated with increased risk only in persons who ever lived in such areas. A decreased risk was associated with consumption of iodized salt in northern Norway, and with use of iodized salt during adolescence among women (OR = 0.6, CI = 0.6-1.0). The results of this study suggest a role of diet and environment in the risk of thyroid cancer.

  • 29. Gaur, Anjali
    et al.
    Collins, Helen
    Wulaningsih, Wahyu
    Holmberg, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Garmo, Hans
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Hammar, Niklas
    Walldius, Goran
    Jungner, Ingmar
    Van Hemelrijck, Mieke
    Iron metabolism and risk of cancer in the Swedish AMORIS study2013In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 24, no 7, p. 1393-1402Article in journal (Refereed)
    Abstract [en]

    Pre-clinical studies have shown that iron can be carcinogenic, but few population-based studies investigated the association between markers of the iron metabolism and risk of cancer while taking into account inflammation. We assessed the link between serum iron (SI), total-iron binding capacity (TIBC), and risk of cancer by levels of C-reactive protein (CRP) in a large population-based study (n = 220,642). From the Swedish Apolipoprotein Mortality Risk (AMORIS) study, we selected all participants (> 20 years old) with baseline measurements of serum SI, TIBC, and CRP. Multivariate Cox proportional hazards regression was carried out for standardized and quartile values of SI and TIBC. Similar analyses were performed for specific cancers (pancreatic, colon, liver, respiratory, kidney, prostate, stomach, and breast cancer). To avoid reverse causation, we excluded those with follow-up < 3 years. We found a positive association between standardized TIBC and overall cancer [HR 1.03 (95 % CI 1.01-1.05)]. No statistically significant association was found between SI and cancer risk except for postmenopausal breast cancer [HR for standardized SI 1.09 (95 % CI 1.02-1.15)]. The association between TIBC and specific cancer was only statistically significant for colon cancer [i.e., HR for standardized TIBC: 1.17 (95 % CI 1.08-1.28)]. A borderline interaction between SI and levels of CRP was observed only in stomach cancer. As opposed to pre-clinical findings for serum iron and cancer, this population-based epidemiological study showed an inverse relation between iron metabolism and cancer risk. Minimal role of inflammatory markers observed warrants further study focusing on developments of specific cancers.

  • 30. Gustafsson, Leif
    et al.
    Pontén, Jan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology.
    Zack, Matthew
    Adami, Hans-Olov
    International incidence rates of invasive cervical cancer after introduction of cytological screening1997In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 8, no 5, p. 755-763Article in journal (Refereed)
    Abstract [en]

    Because Pap-smear screening can detect pre-invasive cervical cancer, such screening can markedly reduce the occurrence of invasive cancer. However, its impact in different populations is uncertain. This study compares the changes in cervical cancer incidence at different ages after the introduction of screening in different populations, and addresses the impact of organized and opportunistic smear taking. We identified 17 cancer registries large enough and existing long enough to analyze screening effects. For each registry, we calculated the relative reduction in age-specific incidence rates and in incidence rates age-standardized to the world population after the introduction of cytologic screening. In 11 of the 17 populations, age-standardized incidence rates declined markedly from 27 percent in Norway and to 77 percent in Finland. Age-specific declines were confined to women aged 30 to 70 years old with a nadir around ages 40 to 55. In six other populations, age-standardized incidence rates declined less than 25 percent, an amount too small to provide unambiguous evidence of a screening effect. In several populations, cytologic screening had a more pronounced effect than is generally recognized. Because age-specific declines in cervical cancer incidence rates were strikingly similar in populations with widely different screening practices, organized screening may not be markedly superior to opportunistic screening. The reduction in reported cancer incidence because of screening is smaller in younger and older women.

  • 31. Guénel, Pascal
    et al.
    Cyr, Diane
    Sabroe, Svend
    Lynge, Elsebeth
    Merletti, Franco
    Ahrens, Wolfgang
    Baumgardt-Elms, Cornelia
    Ménégoz, Francois
    Olsson, Håkan
    Paulsen, Stein
    Simonato, Lorenzo
    Wingren, Gun
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Occupational and Environmental Medicine.
    Alcohol drinking may increase risk of breast cancer in men: A European population-based case-control study2004In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 15, no 6, p. 571-580Article in journal (Refereed)
    Abstract [en]

    Objective: It has been estimated that alcohol drinking increases the risk of breast cancer in women by approximately 7% for each increment of 10 g alcohol per day. However, the few studies conducted on breast cancer among men have failed to detect an association with quantitative measures of alcohol drinking, even if the alcohol intake is generally higher in men than in women. On the other hand, increased risks of male breast cancer were inconsistently reported in alcoholics or patients with liver cirrhosis. We have investigated the role of alcohol drinking in male breast cancer using data collected in a population-based case-control study on seven rare cancers, conducted in Denmark, France, Germany, Italy, and Sweden. Methods: The cases were 74 histologically verified male breast cancer patients aged 35-70 years. The controls (n = 1432) were selected from population registers, and frequency-matched to the cases by age group and geographic area. To check for consistency, a separate analysis was conducted using as controls the patients with a rare cancer other than male breast recruited simultaneously in the European study (n = 519 men). Results: Based on population controls, the risk of developing breast cancer in men increased by 16% (95% CI: 7-26%) per 10 g alcohol /day (p < 0.001). An odds ratio of 5.89 (95% CI: 2.21-15.69) was observed for alcohol intake greater than 90 g per day, as compared with light consumers ( < 15 g per day). Similar associations were observed when other rare cancers patients were used as controls. Conclusion: We found that the relative risk of breast cancer in men is comparable to that in women for alcohol intakes below 60 g per day. It continues to increase at high consumption levels not usually studied in women.

  • 32. Göhler, Stella
    et al.
    Da Silva Filho, Miguel Inacio
    Johansson, Robert
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Enquist-Olsson, Kerstin
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Henriksson, Roger
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology. Cancer Center Stockholm Gotland, 10239 Stockholm, Sweden.
    Hemminki, Kari
    Lenner, Per
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Försti, Asta
    Functional germline variants in driver genes of breast cancer2017In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 28, no 4, p. 259-271Article in journal (Refereed)
    Abstract [en]

    Purpose Germline mutations in tumour suppressor genes cause various cancers. These genes are also somatically mutated in sporadic tumours. We hypothesized that there may also be cancer-related germline variants in the genes commonly mutated in sporadic breast tumours. Methods After excluding the well-characterized breast cancer (BC) genes, we screened 15 novel genes consistently classified as BC driver genes in next-generation sequencing approaches for single nucleotide polymorphisms (SNPs). Altogether 40 SNPs located in the core promoter, 5'- and 3'-UTR or which were nonsynonymous SNPs were genotyped in 782 Swedish incident BC cases and 1,559 matched controls. After statistical analyses, further evaluations related to functional prediction and signatures of selection were performed. Results TBX3 was associated with BC risk (rs2242442: OR = 0.76, 95% CI 0.64-0.92, dominant model) and with less aggressive tumour characteristics. An association with BC survival and aggressive tumour characteristics was detected for the genes ATR (rs2227928: HR = 1.63; 95% CI 1.00-2.64, dominant model), RUNX1 (rs17227210: HR = 3.50, 95% CI 1.42-8.61, recessive model) and TTN (rs2303838: HR = 2.36; 95% CI 1.04-5.39; rs2042996: HR = 2.28; 95% CI 1.19-4.37, recessive model). According to the experimental ENCODE data all these SNPs themselves or SNPs in high linkage disequilibrium with them (r (2) ae<yen> 0.80) were located in regulatory regions. RUNX1 and TTN showed also several signatures of positive selection. Conclusion The study gave evidence that germline variants in BC driver genes may have impact on BC risk and/or survival. Future studies could discover further germline variants in known or so far unknown driver genes which contribute to cancer development.

  • 33. Hedelin, M
    et al.
    Klint, A
    Chang, E T
    Bellocco, R
    Johansson, J E
    Andersson, S O
    Heinonen, S M
    Adlercreutz, H
    Adami, H O
    Gronberg, H
    Bälter Augustsson, Katarina
    Karolinska institutet, Sweden.
    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]

    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. 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. 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). Our results support the hypothesis that certain foods high in phytoestrogens are associated with a lower risk of prostate cancer.

  • 34. 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.

  • 35.
    Holgersson, Magdalena Bentmar
    et al.
    Lund Univ, Dept Translat Med, Jan Waldenstroms Gata 35,Bldg 91,Plan 10, S-20502 Malmo, Sweden..
    Ruhayel, Yasir
    Skane Univ Hosp, Dept Urol, Malmo, Sweden..
    Karlsson, Magnus
    Lund Univ, Dept Orthoped & Clin Sci, Malmo, Sweden..
    Giwercman, Aleksander
    Lund Univ, Dept Translat Med, Jan Waldenstroms Gata 35,Bldg 91,Plan 10, S-20502 Malmo, Sweden..
    Bjartell, Anders
    Lund Univ, Dept Translat Med, Jan Waldenstroms Gata 35,Bldg 91,Plan 10, S-20502 Malmo, Sweden.;Skane Univ Hosp, Dept Urol, Malmo, Sweden..
    Ohlsson, Claes
    Gothenburg Univ, Sahlgrenska Acad, Ctr Bone & Arthrit Res, Dept Internal Med & Clin Nutr, Gothenburg, Sweden.;Gothenburg Univ, Sahlgrenska Acad, Ctr Bone & Arthrit Res, Dept Geriatr, Gothenburg, Sweden..
    Mellstrom, Dan
    Gothenburg Univ, Sahlgrenska Acad, Ctr Bone & Arthrit Res, Dept Internal Med & Clin Nutr, Gothenburg, Sweden.;Gothenburg Univ, Sahlgrenska Acad, Ctr Bone & Arthrit Res, Dept Geriatr, Gothenburg, Sweden..
    Ljunggren, Östen
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Endocrinology and mineral metabolism.
    Haghsheno, Mohammad-Ali
    Univ Gothenburg, Sahlgrenska Acad, Inst Clin Sci, Dept Urol,Sahlgrenska Canc Ctr, Gothenburg, Sweden..
    Damber, Jan-Erik
    Univ Gothenburg, Sahlgrenska Acad, Inst Clin Sci, Dept Urol,Sahlgrenska Canc Ctr, Gothenburg, Sweden..
    Giwercman, Yvonne Lundberg
    Lund Univ, Dept Translat Med, Jan Waldenstroms Gata 35,Bldg 91,Plan 10, S-20502 Malmo, Sweden..
    Lower prostate cancer risk in Swedish men with the androgen receptor E213 A-allele2017In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 28, no 3, p. 227-233Article in journal (Refereed)
    Abstract [en]

    In a previous population-based study on 3369 European men with self-reported prostate cancer (PCa), it was shown that androgen receptor (AR) haplotype designated H2 was associated with high levels of serum PSA (prostate-specific antigen) concentration, and, at the same time, with low risk for PCa. The aim of this study was to replicate this finding in other cohorts, with registry-based cancer diagnosis. Using data from two population-based cohorts; the Malmo Diet and Cancer Study (MDCS, n = 12,121) and the Swedish Osteoporotic fractures in men study (MrOS, n = 1,120), 628 men with PCa and 1,374 controls were identified and genotyped. PCa data were collected from the Swedish national cancer registry. PCa odds ratios (ORs) and 95% confidence intervals (CIs) were calculated for carriers of the particular AR haplotype, tagged by the rs6624304 T-allele. The 15% of men who were carriers of the AR haplotype H2 had approximately one-third lower risk for PCa diagnosis compared to those with the most common H1 variant (OR 0.65; 95% CI 0.45-0.94; p = 0.021). The same trend, although not statistically significant (OR 0.75; 95% CI 0.47-1.24; p = 0.275), was observed in MrOS Sweden. When both cohorts were merged, an even more significant result was observed (OR 0.68; 95% CI 0.51-0.90; p = 0.008). Swedish men with the variant AR haplotype H2, tagged by rs6624304, have significantly lower risk of PCa compared to those with the more common variant.

  • 36.
    Holmberg, Lars
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Endocrine Surgery.
    Adolfsson, Jan
    Mucci, Lorelei
    Garmo, Hans
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences.
    Adami, Hans-Olov
    Möller, Henrik
    Johansson, Jan-Erik
    Stampfer, Meir
    Season of diagnosis and prognosis in breast and prostate cancer2009In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 20, no 5, p. 633-670Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Patients with breast or prostate cancer diagnosed during the summer season have been observed to have better survival. The extent to which this is due to biological and/or health care system related factors is unclear. METHODS: Using the Swedish Cancer Register and clinical databases, we analyzed overall survival by month of diagnosis among the incident cases of breast (n = 89,630) cancer and prostate (n = 72,375) cancer diagnosed from 1960 to 2004. We retrieved data on tumor stage from 1976 for breast cancer and 1997 for prostate cancer. Cox proportional hazards models were used to calculate relative risk of survival by the season of diagnosis. RESULTS: There was a higher hazard ratio of death in men and women diagnosed with cancer in the summer with a relative hazard of 1.20 (95% confidence interval 1.15-1.25) for July for prostate cancer and 1.14 (95% confidence interval 1.09-1.19) for August for breast cancer when compared to being diagnosed in January. This difference coincided with a lower mean number of cases diagnosed per day, and a higher proportion of advanced cases diagnosed in the summer. This pattern of presentation was stronger in the later years. CONCLUSION: The difference in stage distribution explains the seasonal variation in prognosis seen in this study. The variation may be because of structure of the health care system and a strong tradition of vacationing from mid June to mid August. Thus, the health care infrastructure and the late presentation of symptomatic disease may influence cancer survival studied by season of diagnosis substantially.

  • 37. Huerta, José María
    et al.
    Navarro, Carmen
    Chirlaque, María-Dolores
    Tormo, María-José
    Steindorf, Karen
    Buckland, Genevieve
    Carneiro, Fátima
    Johnsen, Nina Føns
    Overvad, Kim
    Stegger, Jakob
    Tjønneland, Anne
    Boutron-Ruault, Marie-Christine
    Clavel-Chapelon, Françoise
    Morois, Sophie
    Boeing, Heiner
    Kaaks, Rudolf
    Rohrmann, Sabine
    Vigl, Matthäus
    Lagiou, Pagona
    Trichopoulos, Dimitrios
    Trichopoulou, Antonia
    Bas Bueno-de-Mesquita, H
    Monninkhof, Evelyn M
    Numans, Mattijs E
    Peeters, Petra H
    Mattiello, Amalia
    Pala, Valeria
    Palli, Domenico
    Tumino, Rosario
    Vineis, Paolo
    Agudo, Antonio
    Ardanaz, Eva
    Arriola, Larraitz
    Molina-Montes, Esther
    Rodríguez, Laudina
    Lindkvist, Björn
    Manjer, Jonas
    Stenling, Roger
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Lund, Eiliv
    Crowe, Francesca L
    Key, Timothy J
    Khaw, Kay-Tee
    Wareham, Nicholas J
    Jenab, Mazda
    Norat, Teresa
    Romaguera, Dora
    Riboli, Elio
    González, Carlos A
    Prospective study of physical activity and risk of primary adenocarcinomas of the oesophagus and stomach in the EPIC (European Prospective Investigation into Cancer and nutrition) cohort.2010In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 21, no 5, p. 657-669Article in journal (Refereed)
    Abstract [en]

    Overall and distal (non-cardia) gastric tumours were inversely associated with time spent on cycling and sports and a total PA index. No association was found for any type of PA and risk of cardia cancers of the stomach.

  • 38. Jayasekara, Harindra
    et al.
    English, Dallas R.
    Hodge, Allison M.
    Room, Robin
    Stockholm University, Faculty of Social Sciences, Centre for Social Research on Alcohol and Drugs (SoRAD). La Trobe University, Australia; The University of Melbourne, Australia.
    Hopper, John L.
    Milne, Roger L.
    Giles, Graham G.
    MacInnis, Robert J.
    Lifetime alcohol intake and pancreatic cancer incidence and survival: findings from the Melbourne Collaborative Cohort Study2019In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 30, no 4, p. 323-331Article in journal (Refereed)
    Abstract [en]

    Purpose Pancreatic cancer has one of the worst prognoses with 5-year survival below 10%. There is some evidence that alcohol consumption might increase the risk of pancreatic cancer. We examined associations of pre-diagnostic alcohol intake with (i) incidence of pancreatic cancer, and (ii) overall survival following pancreatic cancer. Methods Usual alcohol intake was estimated at recruitment in 1990-1994 for 38,472 participants in the Melbourne Collaborative Cohort Study using recalled frequency and quantity of beverage-specific intake for 10-year periods from age 20. Pancreatic cancer incidence (C25 according to International Classification of Diseases for Oncology) and vital status were ascertained through to 30 September 2015. Cox regression was performed to estimate multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for associations with lifetime, age 20-29, and baseline alcohol intakes. Results By the end of follow-up (average 20.2 years), 239 incident cases of pancreatic cancer were diagnosed, of which 228 had died. No evidence of an association was observed between alcohol intake and risk of pancreatic cancer. Higher lifetime alcohol intake was associated with lower overall survival following a diagnosis of pancreatic cancer (mortality HR 1.09 per 10 g/day increment, 95% CI 1.00-1.19; p value=0.04). A similar finding was observed for age 20-29 intake (HR 1.09 per 10 g/day increment, 95% CI 1.02-1.18; p value=0.01) but not with baseline intake. Conclusions We observed an association between lower alcohol use from an early age and improved survival following pancreatic cancer, but this finding needs to be confirmed by other studies.

  • 39. Jayasekara, Harindra
    et al.
    MacInnis, Robert J.
    Hodge, Allison M.
    Hopper, John L.
    Giles, Graham G.
    Room, Robin
    Stockholm University, Faculty of Social Sciences, Centre for Social Research on Alcohol and Drugs (SoRAD). University of Melbourne, Australia; Turning Point Alcohol and Drug Centre, Australia.
    English, Dallas R.
    Lifetime alcohol consumption and upper aero-digestive tract cancer risk in the Melbourne Collaborative Cohort Study2015In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 26, no 2, p. 297-301Article in journal (Refereed)
    Abstract [en]

    Cohort studies have rarely examined the association between upper aero-digestive tract (UADT) cancer risk and lifetime alcohol intake. We examined the associations between incident squamous cell carcinoma of the UADT (oral cavity, pharynx, larynx, and esophagus) and alcohol intake for different periods in life using data from the Melbourne Collaborative Cohort Study. Usual alcohol intake for 10-year periods from age 20 was calculated using recalled frequency and quantity of beverage-specific consumption. Cox regression with age as the time axis was performed to estimate hazard ratios (HR) and 95 % confidence intervals (CI) for the associations of UADT cancer with alcohol intake for different periods in life compared with abstention. During a mean follow-up of 16.2 person-years, 98 incident cases of UADT cancer were identified. We observed a dose-dependent association between lifetime alcohol intake and the risk of UADT cancer (multivariable-adjusted HR 2.67, 95 % CI 1.27-5.60 for an intake of a parts per thousand yen40 g/day and multivariable-adjusted HR 1.16, 95 % CI 1.06-1.28 for a 10 g/day increment in intake). A positive association with baseline alcohol intake (multivariable-adjusted HR 1.12, 95 % CI 1.02-1.24 for a 10 g/day increment in intake) was found to be a slightly weaker predictor of risk than lifetime intake. Limiting alcohol intake from early adulthood may reduce UADT cancer risk.

  • 40. Jayasekara, Harindra
    et al.
    MacInnis, Robert J.
    Hodge, Allison M.
    Room, Robin
    Stockholm University, Faculty of Social Sciences, Centre for Social Research on Alcohol and Drugs (SoRAD). La Trobe University, Australia; The University of Melbourne, Australia.
    Milne, Roger L.
    Hopper, John L.
    Giles, Graham G.
    English, Dallas R.
    Is breast cancer risk associated with alcohol intake before first full-term pregnancy?2016In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 27, no 9, p. 1167-1174Article in journal (Refereed)
    Abstract [en]

    Purpose

    It is plausible that breast tissue is particularly susceptible to carcinogens, including ethanol, between menarche and the first full-term pregnancy (first pregnancy). There is some epidemiological evidence that intake before the first pregnancy is more closely associated with risk of breast cancer than is intake thereafter. We examined this association using lifetime alcohol consumption data from a prospective cohort study.

    Methods

    We calculated usual alcohol intake for age periods 15-19 years and for 10-year period from age 20 to current age (in grams per day) using recalled frequency and quantity of beverage-specific consumption for 13,630 parous women who had their first pregnancy at age 20 years or later, had no cancer history and were aged 40-69 years at enrollment. Cox regression was performed to estimate hazard ratios (HRs) and their 95 % confidence intervals (CIs).

    Results

    A total of 651 incident invasive adenocarcinomas of the breast were diagnosed during a mean follow-up of 16.1 years. Alcohol consumption was low overall with only a few drinking >= 40 g/day. Intake before the first pregnancy was markedly lower (mean intake: 2.5 g/day; abstention: 58.8 %) than intake thereafter (mean intake: 6.0 g/day; abstention: 33.6 %). Any alcohol intake before the first pregnancy was associated with an increased risk of breast cancer (HR 1.35, 95 % CI 1.10-1.66 for drinking compared with abstention), whereas any intake after the first pregnancy was not (HR 0.89, 95 % CI 0.72-1.09).

    Conclusions

    Limiting alcohol intake before the first pregnancy might reduce women's risk of breast cancer.

  • 41. Johansson, Mattias
    et al.
    Van Guelpen, Bethany
    Hultdin, Johan
    Wiklund, Fredrik
    Adami, Hans-Olov
    Bälter, Katarina
    Karolinska institutet, Sweden.
    Gronberg, Henrik
    Stattin, Par
    The MTHFR 677C -> T polymorphism and risk of prostate cancer: results from the CAPS study2007In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 18, no 10, p. 1169-1174Article in journal (Refereed)
    Abstract [en]

    The methylenetetrahydrafolate reductase (MTHFR) enzyme may influence cancer development by affecting DNA methylation, synthesis and repair. The MTHFR 677C -> T single nucleotide polymorphism (SNP) has been associated with decreased enzyme activity and has therefore been implicated in cancer development. We analyzed the MTHFR 677C -> T SNP in 2,777 incident prostate cancer cases and 1,639 population controls from the CAncer Prostate in Sweden study (CAPS). No significant association was found overall between prostate cancer risk and the 677C -> T SNP (p = 0.27) with heterozygote (CT) and homozygote (TT) allele carriers showing ORs of 1.12 (95% CI: 0.98-1.27) and 1.02 (95% CI: 0.80-1.30), respectively. In the subgroup of low risk prostate cancer, heterozygote-but not homozygote-allele carriers displayed a slight over-risk with an OR of 1.21 (95% CI: 1.03-1.41). Among men under 65 years of age, the 677C -> T SNP was associated with prostate cancer risk (p = 0.007), with odds ratios of 1.33 (95% CI: 1.09-1.63) for heterozygote allele carriers and 0.86 (95% CI: 0.6-1.24) for homozygote allele carriers. However, this association was attributed to a shift in the genotype distribution in the young controls. In conclusion, our results do not provide strong support for the hypothesis that the MTHFR 677C -> T polymorphism is related to prostate cancer risk.

  • 42.
    Johansson, Mattias
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Van Guelpen, Bethany
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Hultdin, Johan
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Clinical chemistry.
    Wiklund, Fredrik
    Adami, Hans-Olov
    Bälter, Katarina
    Grönberg, Henrik
    Stattin, Pär
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    The MTHFR 677C --> T polymorphism and risk of prostate cancer: results from the CAPS study2007In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 18, no 10, p. 1169-1174Article in journal (Refereed)
    Abstract [en]

    The methylenetetrahydrafolate reductase (MTHFR) enzyme may influence cancer development by affecting DNA methylation, synthesis and repair. The MTHFR 677C→T single nucleotide polymorphism (SNP) has been associated with decreased enzyme activity and has therefore been implicated in cancer development. We analyzed the MTHFR 677C→T SNP in 2,777 incident prostate cancer cases and 1,639 population controls from the CAncer Prostate in Sweden study (CAPS). No significant association was found overall between prostate cancer risk and the 677C→T SNP (p = 0.27) with heterozygote (CT) and homozygote (TT) allele carriers showing ORs of 1.12 (95% CI: 0.98–1.27) and 1.02 (95% CI: 0.80–1.30), respectively. In the subgroup of low risk prostate cancer, heterozygote—but not homozygote—allele carriers displayed a slight over-risk with an OR of 1.21 (95% CI: 1.03–1.41). Among men under 65 years of age, the 677C→T SNP was associated with prostate cancer risk (p = 0.007), with odds ratios of 1.33 (95% CI: 1.09–1.63) for heterozygote allele carriers and 0.86 (95% CI: 0.6–1.24) for homozygote allele carriers. However, this association was attributed to a shift in the genotype distribution in the young controls. In conclusion, our results do not provide strong support for the hypothesis that the MTHFR 677C→T polymorphism is related to prostate cancer risk.

  • 43.
    Jokinen, Jussi
    et al.
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Psychiatry. Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Mattsson, Fredrik
    Lagergren, Katarina
    Lagergren, Jesper
    Ljung, Rickard
    Suicide attempt and future risk of cancer: a nationwide cohort study in Sweden2015In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 26, no 3, p. 501-509Article in journal (Refereed)
    Abstract [en]

    Purpose: Little is known about cancer incidence among patients with a history of suicide attempt. Suicide attempters have lower levels of oxytocin, a hormone related to lactation, stress, social functioning, and well-being, and recent research indicates influence on carcinogenesis. We hypothesized that the low oxytocin levels among suicide attempters results in an increased risk of cancer in general and in organs with oxytocin receptors in particular.

    Methods: A nationwide cohort study of patients aged 15 years or older with hospitalization for self-inflicted injury or attempted suicide was identified from the Swedish patient register in 1968–2011. The cancer outcomes were identified from the Swedish cancer register. Cancer risk in suicide attempters was compared with the risk in the background population of the corresponding age, sex, and calendar period by calculating standardized incidence ratios (SIRs) with 95 % confidence intervals (95 % CI).

    Results: The 186,627 patients (83,637 men and 102,990 women) hospitalized for self-inflicted injury or attempted suicide contributed with 2.6 million person-years at risk. The SIR for all cancer was 1.3 (95 % CI 1.27–1.33) in men and 1.25 (1.22–1.28) in women. For cancers in organs rich in oxytocin receptors (uterus, breast, and brain), the corresponding SIRs were 1.02 (0.87–1.19) and 1.13 (1.09–1.17), respectively. There was a particularly increased risk of cancers related to alcohol and tobacco in both sexes.

    Conclusion: Patients attempting suicide have an increased risk of cancer. However, this increase does not seem to be associated with low oxytocin levels, but rather to exposures like tobacco smoking and alcohol consumption.

  • 44. Kaaks, Rudolf
    et al.
    Lundin, Eva
    Rinaldi, Sabina
    Manjer, Jonas
    Biessy, Carine
    Söderberg, Stefan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Lenner, Per
    Janzon, Lars
    Riboli, Elio
    Berglund, Göran
    Hallmans, Göran
    Prospective study of IGF-I, IGF-binding proteins, and breast cancer risk, in northern and southern Sweden.2002In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 13, no 4, p. 307-316Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: To examine the possible relationships of breast cancer risk to prediagnostic plasma levels of insulin; insulin-like growth factor-I (IGF-I); and IGF-binding proteins -1, -2, and -3.

    METHODS: Within two prospective cohorts in Umeå and Malmö we measured plasma concentrations of insulin, IGF-I, and IGFBPs for a total of 513 incident breast cancer cases and 987 matched controls.

    RESULTS: Globally, risk was unassociated with levels of IGF-I, IGFBP-3, or IGF-I adjusted for IGFBP-3. When breaking down the analysis by subgroups of age at blood donation, an increase in risk was observed for increasing levels of IGF-I in women aged 55 or older, in the Umeå cohort only (odds ratios of 1.00, 1.73, 1.76, 1.90; Ptrend = 0.05). This effect weakened, however, when the analysis was restricted to subjects who did not use exogenous hormones for the treatment of menopausal symptoms. Levels of IGF-I and IGFBP-3 were not related to risk in younger women, recruited before age 50, contrary to observations from previous studies. In a subcohort where blood samples had been collected after at least four hours of fasting, breast cancer risk showed no clear associations with levels of insulin, IGFBP-1, or IGFBP-2.

    CONCLUSIONS: Our results do not confirm earlier findings of an association of plasma IGF-I levels with breast cancer risk especially in young women, but suggest a possible association with postmenopausal breast cancer risk, possibly among ERT/HRT users only. Our results do not support the hypothesis that elevated plasma insulin levels, and reduced levels of IGFBP-I and IGFBP-2, are associated with increased breast cancer risk.

  • 45.
    Karalexi, M. A.
    et al.
    University of Athens.
    Dessypris, N.
    University of Athens.
    Skalkidou, Alkistis
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, Research group (Dept. of women´s and children´s health), Obstetric research.
    Biniaris-Georgallis, S. -I
    University of Athens.
    Kalogirou, E. I.
    University of Athens.
    Thomopoulos, T. P.
    University of Athens.
    Herlenius, E.
    Karolinska Institute .
    Spector, L. G.
    University of Minnesota.
    Loutradis, D.
    University of Athens.
    Chrousos, G. P.
    University of Athens.
    Petridou, E. Th.
    University of Athens.
    Maternal fetal loss history and increased acute leukemia subtype risk in subsequent offspring: a systematic review and meta-analysis2017In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 28, no 6, p. 599-624Article, review/survey (Refereed)
    Abstract [en]

    Purpose History of fetal loss including miscarriage and stillbirth has been inconsistently associated with childhood (0-14 years) leukemia in subsequent offspring. A quantitative synthesis of the inconclusive literature by leukemia subtype was therefore conducted. Methods Eligible studies (N = 32) were identified through the screening of over 3500 publications. Random-effects meta-analyses were conducted on the association of miscarriage/stillbirth history with overall (AL; 18,868 cases/35,685 controls), acute lymphoblastic (ALL; 16,150 cases/38,655 controls), and myeloid (AML; 3042 cases/32,997 controls) leukemia. Sensitivity and subgroup analyses by age and ALL subtype, as well as meta-regression were undertaken. Results Fetal loss history was associated with increased AL risk [Odds Ratio (OR) 1.10, 95% Confidence Intervals (CI) 1.04-1.18]. The positive association was seen for ALL (OR 1.12, 95%CI 1.05-1.19) and for AML (OR 1.13, 95%CI 0.91-1.41); for the latter the OR increased in sensitivity analyses. Notably, stillbirth history was significantly linked to ALL risk (OR 1.33, 95%CI 1.02-1.74), but not AML. By contrast, the association of ALL and AML with previous miscarriage reached marginal significance. The association of miscarriage history was strongest in infant ALL (OR 2.34, 95%CI 1.19-4.60). Conclusions In this meta-analysis involving > 50,000 children, we found noteworthy associations by indices of fetal loss, age at diagnosis, and leukemia type; namely, of stillbirth with ALL and miscarriage history with infant ALL. Elucidation of plausible underlying mechanisms may provide insight into leukemia pathogenesis and indicate monitoring interventions prior to and during pregnancy.

  • 46. Kelly, Rachel S.
    et al.
    Roulland, Sandrine
    Morgado, Ester
    Sungalee, Stephanie
    Jouve, Nathalie
    Tumino, Rosario
    Krogh, Vittorio
    Panico, Salvatore
    Polidoro, Silvia
    Masala, Giovanna
    Sanchez, Maria-Jose
    Chirlaque, Maria-Dolores
    Sala, Nuria
    Barricarte Gurrea, Aurelio
    Dorronsoro, Miren
    Travis, Ruth C.
    Riboli, Elio
    Gunter, Marc
    Murphy, Neil
    Vermeulen, Roel
    Bueno-de-Mesquita, H. B.
    Peeters, Petra H.
    Trichopoulou, Antonia
    Trichopoulos, Dimitrios
    Lagiou, Pagona
    Nieters, Alexandra
    Canzian, Federico
    Kaaks, Rudolf
    Boeing, Heiner
    Weiderpass, Elisabete
    Stocks, Tanja
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences. Department of Clinical Sciences in Malmö, Lund University, Lund, Sweden.
    Melin, Beatrice
    Umeå University, Faculty of Medicine, Department of Radiation Sciences.
    Overvad, Kim
    Tjonneland, Anne
    Olsen, Anja
    Brennan, Paul
    Johansson, Mattias
    Nadel, Bertrand
    Vineis, Paolo
    Determinants of the t(14;18) translocation and their role in t(14;18)-positive follicular lymphoma2015In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 26, no 12, p. 1845-1855Article in journal (Refereed)
    Abstract [en]

    Purpose: The strong association between t(14;18) translocation and follicular lymphoma (FL) is well known. However, the determinants of this chromosomal aberration and their role in t(14;18) associated FL remain to be established.

    Methods: t(14;18) frequency within the B cell lymphoma 2 major breakpoint region was determined for 135 incident FL cases and 251 healthy controls as part of a nested case–control study within the European Prospective Investigation into Cancer cohort. Quantitative real-time PCR was performed in DNA extracted from blood samples taken at recruitment. The relationship between prevalence and frequency of the translocation with baseline anthropometric, lifestyle, and dietary factors in cases and controls was determined. Unconditional logistic regression was used to explore whether the risk of FL associated with these factors differed in t(14;18)+ as compared to t(14;18) cases.

    Results: Among incident FL cases, educational level (χ 2 p = 0.021) and height (χ 2 p = 0.025) were positively associated with t(14;18) prevalence, and cases with high frequencies [t(14;18)HF] were significantly taller (t test p value = 0.006). These findings were not replicated in the control population, although there were a number of significant associations with dietary variables. Further analyses revealed that height was a significant risk factor for t(14;18)+ FL [OR 6.31 (95 % CI 2.11, 18.9) in the tallest versus the shortest quartile], but not t(14;18) cases.

    Conclusions: These findings suggest a potential role for lifestyle factors in the prevalence and frequency of the t(14;18) translocation. The observation that the etiology of FL may differ by t(14;18) status, particularly with regard to height, supports the subdivision of FL by translocation status.

  • 47.
    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.

  • 48. Kyro, Cecilie
    et al.
    Skeie, Guri
    Loft, Steffen
    Landberg, Rikard
    Christensen, Jane
    Lund, Eiliv
    Nilsson, Lena M.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research. Umeå University, Faculty of Medicine, Department of Biobank Research.
    Palmqvist, Richard
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Tjonneland, Anne
    Olsen, Anja
    Intake of whole grains from different cereal and food sources and incidence of colorectal cancer in the Scandinavian HELGA cohort2013In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 24, no 7, p. 1363-1374Article in journal (Refereed)
    Abstract [en]

    A high intake of whole grains has been associated with a lower incidence of colorectal cancer, but few studies are available on the association with whole grains from different cereals, for example, wheat, rye and oats, and none has addressed these separately. The objective of this study was to investigate the association between whole-grain intake and colorectal cancer. We used data from the large population-based Scandinavian cohort HELGA consisting of 108,000 Danish, Swedish, and Norwegian persons, of whom 1,123 developed colorectal cancer during a median of 11 years of follow-up. Detailed information on daily intake of whole-grain products, including whole-grain bread, crispbread, and breakfast cereals, was available, and intakes of total whole grains and specific whole-grain species (wheat, rye, and oats) were estimated. Associations between these whole-grain variables and the incidence of colorectal cancer were investigated using Cox proportional hazards models. Intake of whole-grain products was associated with a lower incidence of colorectal cancer per 50-g increment (incidence rate ratio [IRR], 0.94; 95 % confidence interval [CI], 0.89, 0.99), and the same tendency was found for total whole-grain intake (IRR pr. 25-g increment, 0.94; 95 % CI, 0.88, 1.01). Intake of whole-grain wheat was associated with a lower incidence of colorectal cancer (IRR for highest versus lowest quartile of intake, 0.66; 95 % CI, 0.51, 0.85), but no statistical significant linear trend was observed (p for trend: 0.18). No significant association was found for whole-grain rye or oats. Whole-grain intake was associated with a lower incidence of colorectal cancer.

  • 49. La Vecchia, C
    et al.
    Ron, E
    Franceschi, S
    Dal Maso, L
    Mark, SD
    Chatenoud, L
    Braga, C
    Preston-Martin, S
    McTiernan, A
    Kolonel, L
    Mabuchi, K
    Jin, F
    Wingren, Gun
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Occupational and Environmental Medicine.
    Galanti, MR
    Hallquist, A
    Lund, E
    Levi, F
    Linos, D
    Negri, E
    A pooled analysis of case-control studies of thyroid cancer. III. Oral contraceptives, menopausal replacement therapy and other female hormones.  1999In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 10, p. 157-166Article in journal (Refereed)
  • 50.
    Lambe, Mats
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm; Regional Oncologic Centre, Uppsala, Sweden .
    Wigertz, Annette
    Regional Oncologic Centre, Uppsala, Sweden .
    Garmo, Hans
    Regional Oncologic Centre, Uppsala, Sweden .
    Walldius, Göran
    Department of Medicine, and Unit of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden .
    Jungner, Ingmar
    Department of Medicine, Clinical Epidemiology Unit, Karolinska Institutet and CALAB Research, Stockholm, Sweden.
    Hammar, Niklas
    Unit of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden; AstraZeneca R&D, Södertälje, Sweden .
    Impaired glucose metabolism and diabetes and the risk of breast, endometrial, and ovarian cancer2011In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 22, no 8, p. 1163-1171Article in journal (Refereed)
    Abstract [en]

    Background

    Epidemiological evidence indicates that individuals with type 2 diabetes are at an increased risk of cancer. Elevated glucose levels, below the diagnostic threshold for diabetes, have also been suggested to be associated with increased cancer risks.

    Methods

    We investigated possible associations between glucose levels and the risk of breast, endometrial, and ovarian cancer in a cohort of more than 230,000 women, for which information on outcome and potential confounders was obtained by record linkage to population-based registers.

    Results

    Diabetes was associated with an increased risk of postmenopausal breast cancer (HR = 1.22, 95% CI 1.04–1.43). An indication of a slightly elevated breast cancer risk was also found in postmenopausal women with impaired glucose metabolism (HR = 1.11, 95% CI 0.96–1.28). Diabetes (HR = 1.46, 95% CI 1.09–1.96) and impaired glucose metabolism (HR = 1.41, 95% CI 1.08–1.85) were associated with an increased risk of endometrial cancer. No associations were found between glucose levels and ovarian cancer risk. Following adjustment for BMI, estimates were attenuated for endometrial cancer, while point estimates for breast and ovarian cancer remained essentially unchanged.

    Conclusions

    Our results indicate that glucose levels below the diagnostic threshold for diabetes modify the risk not only of endometrial cancer but possibly also of postmenopausal breast cancer.

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