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  • 1.
    Akre [Fall], Katja
    et al.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm.
    Ekström, A. M.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm.
    Signorello, L B
    2International Epidemiology Institute, Rockville, USA.
    Hansson, L.-E.
    Mora Hospital, Mora.
    Nyrén, O.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm.
    Aspirin and risk for gastric cancer: a population-based case-control study in Sweden2001Ingår i: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 84, nr 7, s. 965-8Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    While aspirin and other non-steroid anti-inflammatory drugs (NSAIDs) are associated with gastric mucosal damage, they might reduce the risk for gastric cancer. In a population-based case-control study in 5 Swedish counties, we interviewed 567 incident cases of gastric cancer and 1165 controls about their use of pain relievers. The cases were uniformly classified to subsite (cardia/non-cardia) and histological type and information collected on other known risk factors for gastric cancer. Helicobacter pylori serology was tested in a subset of 542 individuals. Users of aspirin had a moderately reduced risk of gastric cancer compared to never users; odds ratio (OR) adjusted for age, gender and socioeconomic status was 0.7 (95% CI = 0.6-1.0). Gastric cancer risk fell with increasing frequency of aspirin use (P for trend = 0.02). The risk reduction was apparent for both cardia and non-cardia tumours but was uncertain for the diffuse histologic type. No clear association was observed between gastric cancer risk and non-aspirin NSAIDs or other studied pain relievers. Our finding lends support to the hypothesis that use of aspirin reduces the risk for gastric cancer.

  • 2.
    Akre [Fall], Katja
    et al.
    Department of Medical Epidemiology, Karolinska Institute, Stockholm.
    Signorello, Lisa B.
    Engstrand, Lars
    Bergström, Reinhold
    Larsson, Sune
    Eriksson, Bengt I.
    Nyrén, Olof
    Risk for gastric cancer after antibiotic prophylaxis in patients undergoing hip replacement2000Ingår i: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 60, nr 22, s. 6376-80Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Despite strong evidence of an association between Helicobacter pylori and gastric cancer, the benefit of eradicating H. pylori infection is unknown. Our aim was to test the hypothesis that exposure to high doses of antibiotics reduces risk for gastric cancer via possible eradication of H. pylori We conducted a nationwide case-control study nested in a cohort of 39,154 patients who underwent hip replacement surgery between 1965 and 1983. Such patients frequently receive prophylactic antibiotic treatment. During follow-up through 1989, we identified 189 incident cases of gastric cancer. For each case, three controls were selected from the cohort. Exposure data were abstracted from hospital records. Blood samples from a separate cohort undergoing hip replacement surgery were analyzed for anti-H. pylori IgG before and after surgery. Both long-term antibiotic treatment before surgery [odds ratio (OR), 0.3; 95% confidence interval (CI), 0.1-0.7] and prophylactic antibiotic treatment (OR, 0.7; 95% CI, 0.5-1.1) conferred a reduction in gastric cancer risk. The reduction appeared stronger after 5 years (OR, 0.6; 95% CI, 0.3-1.2) than during shorter follow-up after hip replacement (OR, 0.8; 95% CI, 0.4-1.7). There was an apparent decrease in risk with increasing body weight-adjusted doses of antibiotics (P = 0.13). However, the rate of H. pylori antibody disappearance was not strikingly higher in the cohort of patients undergoing hip replacement than in a control cohort. Our findings provide indirect support for the hypothesis that treatment with antibiotics at a relatively advanced age reduces the risk of gastric cancer.

  • 3. Andrén, Ove
    et al.
    Garmo, H.
    Mucci, L.
    Andersson, Swen-Olof
    Johansson, Jan-Erik
    Örebro universitet, Hälsoakademin.
    Fall, Katja
    Incidence and mortality of incidental prostate cancer: a Swedish register-based study2009Ingår i: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 100, nr 1, s. 170-173Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    In a national register-based study of incidence trends and mortality of incidental prostate cancer in Sweden, we found that a significant proportion (26.6%) of affected men diagnosed died of their disease, which challenges earlier descriptions of incidental prostate cancer as a non-lethal disease.

  • 4.
    Arora, Manish
    et al.
    Environmental and Occupational Medicine and Epidemiology Program, Harvard School of Public Health, Boston, USA; Cellular and Molecular Pathology Research Unit, Department of Oral Pathology and Oral Medicine, University of Sydney, Sydney, Australia; Population Oral Health, University of Sydney, Sydney, Australia.
    Weuve, Jennifer
    Environmental and Occupational Medicine and Epidemiology Program, Harvard School of Public Health, Boston, USA; Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Fall, Katja
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Pedersen, Nancy L.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Mucci, Lorelei A.
    Department of Epidemiology, Harvard School of Public Health, Boston, USA; Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, USA.
    An exploration of shared genetic risk factors between periodontal disease and cancers: a prospective co-twin study2010Ingår i: American Journal of Epidemiology, ISSN 0002-9262, E-ISSN 1476-6256, Vol. 171, nr 2, s. 253-9Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Biologic mechanisms underlying associations of periodontal disease with cancers remain unknown. The authors propose that both conditions share common genetic risk factors. They analyzed associations between baseline periodontal disease, measured by questionnaire-recorded tooth mobility, and incident cancers, identified by linkage with national registries, between 1963 and 2004 in 15,333 Swedish twins. The authors used co-twin analyses to control for familial factors and undertook analyses restricted to monozygotic twins to further control for confounding by genetic factors. They observed 4,361 cancer cases over 548,913 person-years. After adjustment for covariates, baseline periodontal disease was associated with increased risk of several cancers ranging from 15% for total cancer (proportional hazard ratio (HR) = 1.15, 95% confidence interval (CI): 1.01, 1.32) to 120% for corpus uterine cancer (HR = 2.20, 95% CI: 1.16, 4.18). Periodontal disease was also associated with increased risk of colorectal (HR = 1.62, 95% CI: 1.13, 2.33), pancreatic (HR = 2.06, 95% CI: 1.14, 3.75), and prostate (HR = 1.47, 95% CI: 1.04, 2.07) cancers. In co-twin analyses, dizygotic twins with baseline periodontal disease showed a 50% increase in total cancer risk (HR = 1.50, 95% CI: 1.04, 2.17), but in monozygotic twins this association was markedly attenuated (HR = 1.07, 95% CI: 0.63, 1.81). Similar patterns emerged for digestive tract cancers, suggesting that shared genetic risk factors may partially explain associations between periodontal disease and cancers.

  • 5.
    Bergh, Cecilia
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Udumyan, Ruzan
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Sjöqvist, Hugo
    Örebro universitet, Handelshögskolan vid Örebro Universitet.
    Fröbert, Ole
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Cardiology, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Montgomery, Scott
    Örebro universitet, Institutionen för medicinska vetenskaper. Clinical Epidemiology Unit, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology and Public Health, University College London, London, UK.
    Severe infections and subsequent delayed cardiovascular disease2017Ingår i: European Journal of Preventive Cardiology, ISSN 2047-4873, E-ISSN 2047-4881, Vol. 24, nr 18, s. 1958-1966Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Severe infections in adulthood are associated with subsequent short-term cardiovascular disease. Whether hospital admission for sepsis or pneumonia is associated with persistent increased risk (over a year after infection) is less well established.

    Design: The design of this study was as a register-based cohort study.

    Methods: Some 236,739 men born between 1952-1956 were followed from conscription assessments in adolescence to 2010. All-cause cardiovascular disease ( n = 46,754), including coronary heart disease ( n = 10,279) and stroke ( n = 3438), was identified through national registers 1970-2010 (at ages 18-58 years).

    Results: Sepsis or pneumonia in adulthood (resulting in hospital admission) are associated with increased risk of cardiovascular disease in the years following infection. The risk is highest during the first year after the infection, with an adjusted hazard ratio (and 95% confidence intervals) of 6.33 (5.65-7.09) and a notably increased risk persisted with hazard ratios of 2.47 (2.04-3.00) for the second and 2.12 (1.71-2.62) for the third year after infection. The risk attenuated with time, but remained raised for at least five years after infection; 1.87 (1.47-2.38). The results are adjusted for characteristics in childhood, cardiovascular risk factors and medical history in adolescence. Similar statistically significant associations were found for coronary heart disease and stroke.

    Conclusions: Raised risks of cardiovascular disease following hospital admission for sepsis or pneumonia were increased for more than five years after the infection, but with the highest magnitude during the first three years following infection, suggesting a period of vulnerability when health professionals and patients should be aware of the heightened risk for cardiovascular disease.

  • 6.
    Bergh, Cecilia
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Udumyan, Ruzan
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Sjöqvist, Hugo
    School of Medical Sciences, Örebro University, Örebro, sweden.
    Fröbert, Ole
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Cardiology.
    Montgomery, Scott
    Örebro universitet, Institutionen för medicinska vetenskaper. Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology and Public Health, University College London, UK .
    Severe infections and subsequent delayed cardiovascular disease: national cohort studyManuskript (preprint) (Övrigt vetenskapligt)
  • 7.
    Bergh, Cecilia
    et al.
    Örebro universitet, Institutionen för hälsovetenskaper.
    Hiyoshi, Ayako
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Public Health Sciences, Stockholm University, Stockholm, Sweden.
    Eriksson, Mats
    Örebro universitet, Institutionen för hälsovetenskaper.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Montgomery, Scott
    Örebro universitet, Institutionen för medicinska vetenskaper. Clinical Epidemiology Division, Department of Medicine, Karolinska University Hospital Solna, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology and Public Health, University College London, UK.
    Shared unmeasured characteristics among siblings confound the association of Apgar score with stress resilience in adolescence2019Ingår i: Acta Paediatrica, ISSN 0803-5253, E-ISSN 1651-2227Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    AIM: We investigated the association between low Apgar score, other perinatal characteristics and low stress resilience in adolescence. A within-siblings analysis was used to tackle unmeasured shared familial confounding.

    METHODS: We used a national cohort of 527,763 males born in Sweden between 1973 and 1992 who undertook military conscription assessments at mean age 18 years (17-20). Conscription examinations included a measure of stress resilience. Information on Apgar score and other perinatal characteristics was obtained through linkage with the Medical Birth Register. Analyses were conducted using ordinary least squares and fixed-effects linear regression models adjusted for potential confounding factors.

    RESULTS: Infants with a prolonged low Apgar score at five minutes had an increased risk of low stress resilience in adolescence compared to those with highest scores at one minute, with an adjusted coefficient and 95% confidence interval of -0.26 (-0.39, -0.13). The associations were no longer statistically significant when using within-siblings models. However, the associations with stress resilience and birthweight remained statistically significant in all analyses.

    CONCLUSION: The association with low Apgar score seems to be explained by confounding due to shared childhood circumstances among siblings from the same family, while low birthweight is independently associated with low stress resilience.

  • 8.
    Bergh, Cecilia
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Udumyan, Ruzan
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Appelros, Peter
    Department of Neurology, School of Medical Sciences, Örebro University, Örebro, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Montgomery, Scott
    Örebro universitet, Institutionen för medicinska vetenskaper. Clinical Epidemiology Unit, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology and Public Health, University College London, London, United Kingdom.
    Determinants in adolescence of stroke-related hospital stay duration in men: a national cohort study2016Ingår i: Stroke, ISSN 0039-2499, E-ISSN 1524-4628, Vol. 47, nr 9, s. 2416-2418Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background and purpose: Physical and psychological characteristics in adolescence are associated with subsequent stroke risk. Our aim is to investigate their relevance to length of hospital stay and risk of second stroke.

    Methods: Swedish men born between 1952 and 1956 (n=237 879) were followed from 1987 to 2010 using information from population-based national registers. Stress resilience, body mass index, cognitive function, physical fitness, and blood pressure were measured at compulsory military conscription examinations in late adolescence. Joint Cox proportional hazards models estimated the associations of these characteristics with long compared with short duration of stroke-related hospital stay and with second stroke compared with first.

    Results: Some 3000 men were diagnosed with nonfatal stroke between ages 31 and 58 years. Low stress resilience, underweight, and higher systolic blood pressure (per 1-mm Hg increase) during adolescence were associated with longer hospital stay (compared with shorter) in ischemic stroke, with adjusted relative hazard ratios (and 95% confidence intervals) of 1.46 (1.08-1.89), 1.41 (1.04-1.91), and 1.01 (1.00-1.02), respectively. Elevated systolic and diastolic blood pressures during adolescence were associated with longer hospital stay in men with intracerebral hemorrhage: 1.01 (1.00-1.03) and 1.02 (1.00-1.04), respectively. Among both stroke types, obesity in adolescence conferred an increased risk of second stroke: 2.06 (1.21-3.45).

    Conclusions: Some characteristics relevant to length of stroke-related hospital stay and risk of second stroke are already present in adolescence. Early lifestyle influences are of importance not only to stroke risk by middle age but also to recurrence and use of healthcare resources among stroke survivors.

  • 9.
    Bergh, Cecilia
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Udumyan, Ruzan
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Fall, Katja
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Almroth, Henrik
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Montgomery, Scott
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Clinical Epidemiology Unit, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology and Public Health, University College London, London, United Kingdom .
    Stress resilience and physical fitness in adolescence and risk of coronary heart disease in middle age2015Ingår i: Heart, ISSN 1355-6037, E-ISSN 1468-201X, Vol. 101, nr 8, s. 623-629Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    OBJECTIVE: Psychosocial stress is a suggested risk for coronary heart disease (CHD). The relationship of stress resilience in adolescence with subsequent CHD risk is underinvestigated, so our objective was to assess this and investigate the possible mediating role of physical fitness.

    METHODS: In this register-based study, 237 980 men born between 1952 and 1956 were followed from 1987 to 2010 using information from Swedish registers. Stress resilience was measured at a compulsory military conscription examination using a semistructured interview with a psychologist. Some 10 581 diagnoses of CHD were identified. Cox regression estimated the association of stress resilience with CHD, with adjustment for established cardiovascular risk factors.

    RESULTS: Low-stress resilience was associated with increased CHD risk. The association remained after adjustment for physical fitness and other potential confounding and mediating factors, with adjusted HRs (and 95% CIs) of 1.17 (1.10 to 1.25), with some evidence of mediation by physical fitness. CHD incidence rates per 1000 person-years (and 95% CIs) for low-stress, medium-stress and high-stress resilience were 2.61 (2.52 to 2.70), 1.97 (1.92 to 2.03) and 1.59 (1.53 to 1.67) respectively. Higher physical fitness was inversely associated with CHD risk; however, this was attenuated by low-stress resilience, shown by interaction testing (p<0.001).

    CONCLUSIONS: Low-stress resilience in adolescence was associated with increased risk of CHD in middle age and may diminish the benefit of physical fitness. This represents new evidence of the role of stress resilience in determining risk of CHD and its interrelationship with physical fitness.

  • 10.
    Bergh, Cecilia
    et al.
    Region Örebro län. Örebro universitet, Institutionen för medicinska vetenskaper.
    Udumyan, Ruzan
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Montgomery, Scott
    Örebro universitet, Institutionen för medicinska vetenskaper. Clinical Epidemiology Unit, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology and Public Health, University College London, London, UK.
    Pre-stroke characteristics and stroke severity after first stroke in middle-aged men2015Ingår i: Nordic Stroke 2015: 18th Nordic Congress of Cerebrovascular Diseases, 2015Konferensbidrag (Refereegranskat)
  • 11.
    Bergh, Cecilia
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Department of Physiotherapy, Örebro University Hospital, Örebro, Sweden.
    Udumyan, Ruzan
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Fall, Katja
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Nilsagård, Ylva
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Region Örebro län. Centre for Health Care Sciences, Örebro University Hospital, Örebro, Sweden.
    Appelros, Peter
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Region Örebro län. Department of Neurology, Örebro University Hospital, Örebro, Sweden.
    Montgomery, Scott
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Region Örebro län. Departnment of Epidemiology and Public Health, University College London, London, UK; Cinical Epidemiology Unit, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Stress resilience in male adolescents and subsequent stroke risk: cohort study2014Ingår i: Journal of Neurology, Neurosurgery and Psychiatry, ISSN 0022-3050, E-ISSN 1468-330X, Vol. 85, nr 12, s. 1331-1336Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Objective Exposure to psychosocial stress has been identified as a possible stroke risk, but the role of stress resilience which may be relevant to chronic exposure is uncertain. We investigated the association of stress resilience in adolescence with subsequent stroke risk.

    Methods Register-based cohort study. Some 237 879 males born between 1952 and 1956 were followed from 1987 to 2010 using information from Swedish registers. Cox regression estimated the association of stress resilience with stroke, after adjustment for established stroke risk factors.

    Results Some 3411 diagnoses of first stroke were identified. Lowest stress resilience (21.8%) compared with the highest (23.7%) was associated with increased stroke risk, producing unadjusted HR (with 95% CIs) of 1.54 (1.40 to 1.70). The association attenuated slightly to 1.48 (1.34 to 1.63) after adjustment for markers of socioeconomic circumstances in childhood; and after further adjustment for markers of development and disease in adolescence (blood pressure, cognitive function and pre-existing cardiovascular disease) to 1.30 (1.18 to 1.45). The greatest reduction followed further adjustment for markers of physical fitness (BMI and physical working capacity) in adolescence to 1.16 (1.04 to 1.29). The results were consistent when stroke was subdivided into fatal, ischaemic and haemorrhagic, with higher magnitude associations for fatal rather than non-fatal, and for haemorrhagic rather than ischaemic stroke.

    Conclusions Stress susceptibility and, therefore, psychosocial stress may be implicated in the aetiology of stroke. This association may be explained, in part, by poorer physical fitness. Effective prevention might focus on behaviour/lifestyle and psychosocial stress.

  • 12.
    Blattner, Mirjam
    et al.
    Dept Pathol & Lab Med, Inst Precis Med, Weill Med Coll, Cornell Univ, New York, USA.
    Lee, Daniel J.
    Dept Pathol & Lab Med, Inst Precis Med, Weill Med Coll, Cornell Univ, New York, USA; Dept Urol, Weill Med Coll, Cornell Univ, New York, USA.
    O'Reilly, Catherine
    Dept Pathol & Lab Med, Inst Precis Med, Weill Med Coll, Cornell Univ, New York NY, USA.
    Park, Kyung
    Dept Pathol & Lab Med, Inst Precis Med, Weill Med Coll, Cornell Univ, New York NY, USA.
    MacDonald, Theresa Y.
    Dept Pathol & Lab Med, Inst Precis Med, Weill Med Coll, Cornell Univ, New York NY, USA.
    Khani, Francesca
    Dept Pathol & Lab Med, Inst Precis Med, Weill Med Coll, Cornell Univ, New York NY, USA.
    Turner, Kevin R.
    Dept Pathol & Lab Med, Inst Precis Med, Weill Med Coll, Cornell Univ, New York NY, USA.
    Chiu, Ya-Lin
    Dept Biostat & Epidemiol, Weill Med Coll, Cornell Univ, New York NY, USA.
    Wild, Peter J.
    Inst Surg Pathol, Univ Zurich Hosp, Zurich, Switzerland.
    Dolgalev, Igor
    Human Oncol & Pathogenesis Program, Mem Sloan Kettering Canc Ctr, New York NY, USA.
    Heguy, Adriana
    Human Oncol & Pathogenesis Program, Mem Sloan Kettering Canc Ctr, New York NY, USA.
    Sboner, Andrea
    Dept Pathol & Lab Med, Inst Precis Med, New York NY, USA; Weill Med Coll, Cornell Univ, Inst Computat Biomed, New York, NY, USA; Inst Precis Med, Weill Med Coll, Cornell Univ, New York NY, USA.
    Ramazangolu, Sinan
    Dept Pathol & Lab Med, Inst Precis Med, Weill Med Coll, Cornell Univ, New York NY, USA; Inst Computat Biomed, Weill Med Coll, Cornell Univ, New York NY, USA.
    Hieronymus, Haley
    Inst Computat Biomed, Weill Med Coll, Cornell Univ, New York NY, USA.
    Sawyers, Charles
    Mem Sloan Kettering Canc Ctr, Human Oncol & Pathogenesis Program, New York NY, USA.
    Tewari, Ashutosh K.
    Dept Urol, Weill Med Coll, Cornell Univ, New York NY, USA.
    Moch, Holger
    Inst Surg Pathol, Univ Zurich Hosp, Zurich, Switzerland.
    Yoon, Ghil Suk
    Sch Med, Dept Pathol, Kyungpook Natl Univ, Taegu, South Korea.
    Known, Yong Chul
    Sch Med, Dept Pathol, Catholic Univ Daegu, Taegu, South Korea.
    Andrén, Ove
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Region Örebro län. Dept Urol, Örebro University Hospital, Örebro, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Demichelis, Francecsa
    Inst Precis Med, Weill Med Coll, Cornell Univ, New York NY, USA; Ctr Integrat Biol, Univ Trento, Trento, Italy.
    Mosquera, Juan Miguel
    Dept Pathol & Lab Med, Inst Precis Med, Weill Med Coll, Cornell Univ, New York NY, USA.
    Robinson, Brian D.
    Dept Pathol & Lab Med, Inst Precis Med, Weill Med Coll, Cornell Univ, New York NY, USA; Dept Urol, Weill Med Coll, Cornell Univ, New York NY, USA .
    Barbieri, Christopher E.
    Dept Pathol & Lab Med, Inst Precis Med, Weill Med Coll, Cornell Univ, New York NY, USA; Dept Urol, Weill Med Coll, Cornell Univ, New York NY, USA .
    Rubin, Mark A.
    Dept Pathol & Lab Med, Inst Precis Med, Weill Med Coll, Cornell Univ, New York NY, USA; Dept Urol, Weill Med Coll, Cornell Univ, New York NY, USA; Inst Precis Med, Weill Med Coll, Cornell Univ, New York NY, USA .
    SPOP Mutations in Prostate Cancer across Demographically Diverse Patient Cohorts2014Ingår i: Neoplasia, ISSN 1522-8002, E-ISSN 1476-5586, Vol. 16, nr 1, s. 14-U34Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Recurrent mutations in the Speckle-Type POZ Protein (SPOP) gene occur in up to 15% of prostate cancers. However, the frequency and features of cancers with these mutations across different populations is unknown.

    OBJECTIVE: To investigate SPOP mutations across diverse cohorts and validate a series of assays employing high-resolution melting (HRM) analysis and Sanger sequencing for mutational analysis of formalin-fixed paraffin-embedded material.

    DESIGN, SETTING, AND PARTICIPANTS: 720 prostate cancer samples from six international cohorts spanning Caucasian, African American, and Asian patients, including both prostate-specific antigen-screened and unscreened populations, were screened for their SPOP mutation status. Status of SPOP was correlated to molecular features (ERG rearrangement, PTEN deletion, and CHD1 deletion) as well as clinical and pathologic features.

    RESULTS AND LIMITATIONS: Overall frequency of SPOP mutations was 8.1% (4.6% to 14.4%), SPOP mutation was inversely associated with ERG rearrangement (P < .01), and SPOP mutant (SPOPmut) cancers had higher rates of CHD1 deletions (P < .01). There were no significant differences in biochemical recurrence in SPOPmut cancers. Limitations of this study include missing mutational data due to sample quality and lack of power to identify a difference in clinical outcomes.

    CONCLUSION: SPOP is mutated in 4.6% to 14.4% of patients with prostate cancer across different ethnic and demographic backgrounds. There was no significant association between SPOP mutations with ethnicity, clinical, or pathologic parameters. Mutual exclusivity of SPOP mutation with ERG rearrangement as well as a high association with CHD1 deletion reinforces SPOP mutation as defining a distinct molecular subclass of prostate cancer.

  • 13.
    Blattner, Mirjam
    et al.
    Weill Cornell Med Coll, New York NY, USA.
    Lee, Daniel
    Weill Cornell Med Coll, New York NY, USA.
    O'Reilly, Catherine
    Weill Cornell Med Coll, New York NY, USA.
    Park, Kyung
    Weill Cornell Med Coll, New York NY, USA.
    MacDonald, Theresa Y.
    Weill Cornell Med Coll, New York NY, USA.
    Khani, Francesca
    Weill Cornell Med Coll, New York NY, USA.
    Turner, Kevin
    Weill Cornell Med Coll, New York NY, USA.
    Wild, Peter J.
    Univ Zurich Hosp, Zurich, Switzerland.
    Hieronymus, Haley
    Mem Sloan Kettering Canc Ctr, New York NY, USA.
    Sawyers, Charles L.
    Mem Sloan Kettering Canc Ctr, New York NY, USA.
    Tewari, Ashutosh K.
    Weill Cornell Med Coll, New York, USA.
    Moch, Holger
    Univ Zurich Hosp, Zurich, Switzerland.
    Yoon, Ghil Suk
    Sch Med, Kyungpook Natl Univ, Daegu, South Korea.
    Andrén, Ove
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Fall, Katja
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Mosquera, Juan Miguel
    Weill Cornell Med Coll, New York NY, USA.
    Robinson, Brian D.
    Weill Cornell Med Coll, New York NY, USA.
    Sboner, Andrea
    Weill Cornell Med Coll, New York NY, USA.
    Barbierie, Christopher E.
    Weill Cornell Med Coll, New York NY, USA.
    Rubin, Mark A.
    Weill Cornell Med Coll, New York NY, USA.
    SPOP mutations in prostate cancer across demographically diverse patient cohorts2014Ingår i: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 74, nr 19, artikel-id 2244Artikel i tidskrift (Övrigt vetenskapligt)
  • 14.
    Bond, Emily
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Lu, Donghao
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Herweijer, Eva
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Sundström, Karin
    Department of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden; Division of Pathology, Karolinska Universitetssjukhuset Huddinge, Stockholm, Sweden.
    Valdimarsdottir, Unnur
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Center of Public Health Sciences, Faculty of Medicine, University of Iceland, Reykjavik, Iceland; Department of Epidemiology, Harvard School of Public Health, Boston MA, USA .
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Arnheim-Dahlstrom, Lisen
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Sparén, Par
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fang, Fang
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Sexually transmitted infections after bereavement - a population-based cohort study2016Ingår i: BMC Infectious Diseases, ISSN 1471-2334, E-ISSN 1471-2334, Vol. 16, artikel-id 419Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Loss of a loved one has consistently been associated with various health risks. Little is however known about its relation to sexually transmitted infections (STIs).

    Methods: We conducted a population-based cohort study during 1987-2012 using the Swedish Multi-Generation Register, including 3,002,209 women aged 10-44 years. Bereavement was defined as death of a child, parent, sibling or spouse (N = 979,579, 33 %). STIs were defined as hospital visits with an STI as main or secondary diagnosis. Poisson regression and negative binomial regression were used to estimate incidence rate ratios (IRRs) and 95 % confidence intervals (CIs) of STIs, comparing incidence rates of women who had experienced loss to those who had not.

    Results: Bereaved women were at significantly higher risk of nearly all STIs studied. The relative risk of any STI was highest during the first year after loss (IRR: 1.45, 95 % CI: 1.27-1.65) and predominantly among women with subsequent onset of psychiatric disorders after bereavement (IRR: 2.61, 95 % CI: 2.00-3.34). Notably, a consistent excess risk, persisting for over five years, was observed for acute salpingitis (IRR: 1.28, 95 % CI: 1.13-1.44), a severe complication of bacterial STIs.

    Conclusion: These data suggest that women who have experienced bereavement are at increased risk of STIs.

  • 15. Carlsson, Sigrid
    et al.
    Sandin, Fredrik
    Fall, Katja
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Lambe, Mats
    Adolfsson, Jan
    Stattin, Par
    Bill-Axelson, Anna
    Risk of suicide in men with low-risk prostate cancer2013Ingår i: European Journal of Cancer, ISSN 0959-8049, E-ISSN 1879-0852, Vol. 49, nr 7, s. 1588-1599Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Purpose:

    Risk of suicide is increased among men with prostate cancer. We investigated this association among men with low-risk cancer, usually detected by prostate specific antigen (PSA)-testing.

    Patients and Methods:

    Relative risk (RR) of suicide was calculated by use of Poisson regression analysis within the Prostate Cancer data Base Sweden (PCBaSe) 2.0, a nation-wide, population-based database, comparing 105,736 men diagnosed with prostate cancer between 1997-2009 to 528,658 matched prostate cancer-free men.

    Results:

    During the first 6 months after diagnosis, there were 38 suicides among men with prostate cancer; incidence rate 0.73 per 1000 person-years (PY) and 30 suicides in the comparison cohort; 0.11 per 1000 PY, corresponding to a RR of suicide of 6.5 (95% confidence interval (CI) 4.0-10). Risk was highest among men with distant metastases, incidence rate 1.25 per 1000 PY, RR 10 (95% CI 5.1-21) but risk was also increased for men with low-risk tumours, incidence rate difference 0.45 per 1000 PY and RR 5.2 (95% CI 2.3-12) and across categories of socioeconomic status and comorbidity. Eighteen months after diagnosis, risk of suicide had decreased to 0.27 per 1000 PY, RR 1.0 (95% CI 0.68-1.5) for low-risk prostate cancer but remained increased among men with metastases, 0.57 per 1000 PY, RR 1.8 (95% CI 1.1-2.9).

    Conclusion:

    Although the increase in absolute risk of suicide was modest, our findings reflect the severe psychological stress that prostate cancer patients may experience after diagnosis. The increased risk of suicide observed in men with prostate cancer, including low-risk, calls for increased awareness.

  • 16.
    Chen, Ruoqing
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; School of Medical Sciences, Örebro University, Örebro, Sweden.
    Czene, Kamila
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Kennedy, Beatrice
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Valdimarsdottir, Unnur
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Centre of Public Health Sciences, Faculty of Medicine, University of Iceland, Reykjavík, Iceland; Department of Epidemiology, Harvard TH Chan School of Public Health, Boston MA, USA.
    Fang, Fang
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Impact of parental cancer on IQ, stress resilience, and physical fitness in young men2018Ingår i: Clinical Epidemiology, ISSN 1179-1349, E-ISSN 1179-1349, Vol. 10, s. 593-602Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: A parental cancer diagnosis is a stressful life event, potentially leading to increased risks of mental and physical problems among children. This study aimed to investigate the associations of parental cancer with IQ, stress resilience, and physical fitness of the affected men during early adulthood.

    Materials and methods: In this Swedish population-based study, we included 465,249 men born during 1973-1983 who underwent the military conscription examination around the age of 18 years. We identified cancer diagnoses among the parents of these men from the Cancer Register. IQ, stress resilience, and physical fitness of the men were assessed at the time of conscription and categorized into three levels: low, moderate, and high (reference category). We used multinomial logistic regression to assess the studied associations. Results: Overall, parental cancer was associated with higher risks of low stress resilience (relative risk ratio [RRR]: 1.09 [95% confidence interval (CI) 1.04-1.15]) and low physical fitness (RRR: 1.12 [95% CI 1.05-1.19]). Stronger associations were observed for parental cancer with a poor expected prognosis (low stress resilience: RRR: 1.59 [95% CI 1.31-1.94]; low physical fitness: RRR: 1.45 [95% CI 1.14-1.85]) and for parental death after cancer diagnosis (low stress resilience: RRR: 1.29 [95% CI 1.16-1.43]; low physical fitness: RRR: 1.40 [95% CI 1.23-1.59]). Although there was no overall association between parental cancer and IQ, parental death after cancer diagnosis was associated with a higher risk of low IQ (RRR: 1.11 [95% CI 1.01-1.24]).

    Conclusion: Parental cancer, particularly severe and fatal type, is associated with higher risks of low stress resilience and low physical fitness among men during early adulthood. Men who experienced parental death after cancer diagnosis also have a higher risk of low IQ.

  • 17.
    Chen, Ruoqing
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Regodón Wallin, Amanda
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Sjölander, Arvid
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Valdimarsdóttir, Unnur
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Center of Public Health Sciences, Faculty of Medicine, University of Iceland, Reykjavik, Iceland.
    Ye, Weimin
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Tiemeier, Henning
    Department of Epidemiology, Erasmus MC University Medical Center, Rotterdam, The Netherlands; Department of Child and Adolescent Psychiatry, Erasmus MC University Medical Center, Rotterdam, The Netherlands.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Almqvist, Catarina
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Lung and Allergy Unit, Astrid Lindgren Children’s Hospital, Karolinska University Hospital, Stockholm, Sweden.
    Czene, Kamila
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fang, Fang
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Childhood injury after a parental cancer diagnosis2015Ingår i: eLIFE, E-ISSN 2050-084X, Vol. 4, artikel-id e08500Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    A parental cancer diagnosis is psychologically straining for the whole family. We investigated whether a parental cancer diagnosis is associated with a higher-than-expected risk of injury among children by using a Swedish nationwide register-based cohort study. Compared to children without parental cancer, children with parental cancer had a higher rate of hospital contact for injury during the first year after parental cancer diagnosis (hazard ratio [HR]=1.27, 95% confidence interval [CI]=1.22-1.33), especially when the parent had a comorbid psychiatric disorder after cancer diagnosis (HR=1.41, 95% CI=1.08-1.85). The rate increment declined during the second and third year after parental cancer diagnosis (HR=1.10, 95% CI=1.07-1.14) and became null afterwards (HR=1.01, 95% CI=0.99-1.03). Children with parental cancer also had a higher rate of repeated injuries than the other children (HR=1.13, 95% CI= 1.12-1.15). Given the high rate of injury among children in the general population, our findings may have important public health implications.

  • 18.
    Chen, Ruoqing
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Sjölander, Arvid
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Valdimarsdottir, Unnur
    Center of Public Health Sciences, Faculty of Medicine, University of Iceland, Reykjavik, Iceland.
    Varnum, Catherine
    University of Maryland School of Medicine, Baltimore MD, USA.
    Almqvist, Catarina
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Lung and Allergy Unit, Astrid Lindgren Children’s Hospital, Karolinska University Hospital, Stockholm, Sweden.
    Ye, Weimin
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Örebro Univ Hosp, Örebro, Sweden.
    Czene, Kamila
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fang, Fang
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Parental cancer diagnosis and child mortality: a population-based cohort study in Sweden2015Ingår i: Cancer Epidemiology, ISSN 1877-7821, E-ISSN 1877-783X, Vol. 39, nr 1, s. 79-85Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Objective: Cancer diagnosis is known to induce severe psychological stress for the diagnosed patients; however, how it affects the next-of-kin is less well documented. This study aimed to assess the impact of parental cancer on the risk of childhood death.

    Methods: A population-based cohort study was conducted using the Swedish national registries, including 2,871,242 children followed during the period of 1991-2009. Parental cancer diagnosis was defined as a time-varying exposure. We used Cox proportional hazards regression to calculate the hazard ratio (HR) and its corresponding 95% confidence interval (CI) as an estimate of the association between parental cancer and childhood mortality. We adjusted for attained age, sex, gestational age, mode of delivery and birth weight of the child, maternal age at child's birth, as well as educational level and socioeconomic classification of the parents in the analyses.

    Results: Among 113,555 children with parental cancer, 127 deaths occurred during 561,198 person-years of follow-up. A parental cancer diagnosis was associated with an increased rate of death among children at the age of 1-18 (HR for all-cause death: 1.39; 95% CI: 1.16-1.66). For young children (aged 112), an increased rate was only noted for death due to cancer (HR: 2.06; 95% CI: 1.13-3.75) after parental cancer diagnosis. Among adolescents (aged 13-18), an increased rate was noted for all-cause death (HR: 1.52; 95% CI: 1.25-1.86), and for both non-cancer-related (HR: 1.43; 95% CI: 1.14-1.79) and cancer-related (HR: 2.07; 95% CI: 1.33-3.24) death in the exposed children.

    Conclusion: Children have an increased rate of death if they have a parent diagnosed with cancer as compared to children without such experience; this association appears to be slightly stronger among adolescents. (C) 2014 Elsevier Ltd. All rights reserved.

  • 19.
    Chen, Ruoqing
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Wallin, Amanda Regodón
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Selinus, Eva Norén
    Centre for Psychiatry Research & Education, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Sjölander, Arvid
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Clinical Epidemiology and Biostatistics, School of Medical Sciences, Örebro University, Örebro, Sweden.
    Valdimarsdóttir, Unnur
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Centre of Public Health Sciences, Faculty of Medicine, University of Iceland, Reykjavík, Iceland; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA.
    Czene, Kamila
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fang, Fang
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Psychiatric disorders among children of parents with cancer: a Swedish register-based matched cohort study2018Ingår i: Psycho-Oncology, ISSN 1057-9249, E-ISSN 1099-1611, Vol. 27, nr 7, s. 1854-1860Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    OBJECTIVE: To investigate the risk of psychiatric disorders among children of parents with cancer in a nationwide population-based setting.

    METHODS: Based on Swedish national registers, the study included 101,339 children with parental cancer diagnosed either during pregnancy (N=1,047) or after birth (N=100,292) that were born during 1983-2000. For each exposed child, we randomly selected 10 unexposed children from the general population after individual matching by year of birth and sex. The matched cohort was followed during 2001-2010. Clinical diagnoses of psychiatric disorders and use of prescribed psychiatric medications were identified for all children. Cox regression and logistic regression were used to evaluate the associations of parental cancer with psychiatric disorder diagnosis and psychiatric medication use respectively.

    RESULTS: Parental cancer during pregnancy was not associated with the risk of psychiatric disorders overall, although paternal cancer during pregnancy was associated with a higher risk of psychiatric medication use among females. Parental cancer after birth was associated with higher risks of psychiatric disorder diagnoses, particularly stress reaction and adjustment disorders (males:hazard ratio[HR]:1.24, 95% confidence interval[CI]:1.08-1.43; females:HR:1.27, 95%CI:1.14-1.41), and use of psychiatric medication (males:odds ratio[OR]:1.09, 95%CI:1.04-1.13;females:OR:1.14, 95%CI:1.10-1.18). The positive associations were stronger for parental cancer with poor expected survival and for parental death after cancer diagnosis.

    CONCLUSIONS: Parental cancer, primarily the life-threatening cancer, might confer a higher risk of psychiatric disorders among children. These findings have potential implications for healthcare professionals in providing targeted support to children living with a parent with cancer.

  • 20.
    Davidsson, Sabina
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Fiorentino, Michelangelo
    Mol Pathol Lab, Addarii Inst Oncol, Dept Hematol Oncol, Univ Bologna, Bologna, Italy; Sch Med, Dana Farber Canc Inst, Dept Pathol, Brigham & Womens Hosp & Adult Oncol, Harvard Univ, Boston MA, USA.
    Andrén, Ove
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Fang, Fang
    Sch Med, Channing Lab, Dept Med, Brigham & Womens Hosp, Harvard Univ, Boston MA, USA; Dept Med Epidemiol & Biostat, Karolinska Inst, Stockholm, Sweden.
    Mucci, Lorelei A.
    Sch Publ Hlth, Dept Epidemiol, Harvard Univ, Boston MA, USA; Sch Med, Channing Lab, Dept Med, Brigham & Womens Hosp, Harvard Univ, Boston MA, USA.
    Varenhorst, Eberhard
    Dept Urol, Linköping Univ Hosp, Linköping, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Rider, Jennifer R.
    Dept Urol, Örebro Univ Hosp, Örebro, Sweden; Sch Med, Dana Farber Canc Inst, Dept Pathol, Brigham & Womens Hosp & Adult Oncol, Harvard Univ, Boston MA, USA.
    Inflammation, focal atrophic lesions, and prostatic intraepithelial neoplasia with respect to risk of lethal prostate cancer2011Ingår i: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 20, nr 10, s. 2280-2287Artikel i tidskrift (Refereegranskat)
    Abstract [en]

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

  • 21.
    Davidsson, Sabina
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Region Örebro län.
    Ohlson, Anna-Lena
    Dept Urology, Örebro University Hospital, Örebro, Sweden.
    Andersson, Swen-Olof
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Region Örebro län.
    Fall, Katja
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Meisner, Allison
    School of Public Health, Dept Epidemiology, Harvard University, Boston MA, USA.
    Fiorentino, Michelangelo
    School of Public Health, Dept Epidemiology, Harvard University, Boston MA, USA; Molecular Pathology Lab, Dept Hematological Oncology, Addarii Institute of Oncology, University of Bologna, Bologna, Italy.
    Andrén, Ove
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Region Örebro län.
    Rider, Jennifer R
    School of Public Health, Dept Epidemiology and School of Medicine, Harvard Univ, Boston MA, USA; Dept Med, Channing Lab, Brigham & Womens Hosp, Boston MA, USA.
    CD4 helper T cells, CD8 cytotoxic T cells, and FOXP3(+) regulatory T cells with respect to lethal prostate cancer2013Ingår i: Modern Pathology, ISSN 0893-3952, E-ISSN 1530-0285, Vol. 26, nr 3, s. 448-455Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Prostate cancer represents a major contributor to cancer mortality, but the majority of men with prostate cancer will die of other causes. Thus, a challenge is identifying potentially lethal disease at diagnosis. Conflicting results have been reported when investigating the relationship between infiltration of lymphocytes and survival in prostate cancer. One of the mechanisms suggested is the recruitment of regulatory T cells (T(regs)), a subpopulation of T cells that have a role in promoting tumor growth. T(regs) counteract tumor rejection through suppressive functions on the anti-immune response but their prognostic significance is still unknown. We report here the results of a conducted case-control study nested in a cohort of men treated with transurethral resection of the prostate and diagnosed incidentally with prostate cancer. Cases are men who died of prostate cancer (n=261) and controls are men who survived >10 years after their diagnosis (n=474). Infiltration of both T(helper) and T(cytotoxic) cells was frequently observed and the majority of the T(regs) were CD4(+). T(helper) or T(cytotoxic) cells were not associated with lethal prostate cancer. However, we found a nearly twofold increased risk of lethal prostate cancer when comparing the highest with the lowest quartile of CD4(+) T(reg) cells (95% confidence interval: 1.3-2.9). Our conclusion is that men with greater numbers of CD4(+) T(regs) in their prostate tumor environment have an increased risk of dying of prostate cancer. Identification of CD4(+) T(regs) in tumor tissue may predict clinically relevant disease at time of diagnosis independently of other clinical factors.Modern Pathology advance online publication, 5 October 2012; doi:10.1038/modpathol.2012.164.

  • 22.
    Dickerman, Barbra A.
    et al.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, USA.
    Torfadottir, Johanna E.
    Centre for Public Health Sciences, University of Iceland, Reykjavik, Iceland.
    Valdimarsdottir, Unnur A.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, USA; Centre for Public Health Sciences, University of Iceland, Reykjavik, Iceland; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Wilson, Kathryn M.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, USA; Centre for Public Health Sciences, University of Iceland, Reykjavik, Iceland; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Steingrimsdottir, Laufey
    Unit for Nutrition Research, University Hospital, Reykjavik, Iceland; Faculty of Food Science and Nutrition, University of Iceland, Reykjavik, Iceland.
    Aspelund, Thor
    Centre for Public Health Sciences, University of Iceland, Reykjavik, Iceland; The Icelandic Heart Association, Kopavogur, Iceland.
    Batista, Julie L.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, USA; .
    Fall, Katja
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, USA.
    Giovannucci, Edward
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, USA; Channing Division of Network Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston MA, USA; Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston MA, USA.
    Sigurdardottir, Lara G.
    Centre for Public Health Sciences, University of Iceland, Reykjavik, Iceland; Faculty of Medicine, University of Iceland, Reykjavik, Iceland; Department of Education and Prevention, The Icelandic Cancer Society, Reykjavik, Iceland.
    Tryggvadottir, Laufey
    The Icelandic Cancer Registry, Reykjavik, Iceland.
    Gudnason, Vilmundur
    The Icelandic Heart Association, Kopavogur, Iceland; Faculty of Medicine, University of Iceland, Reykjavik, Iceland.
    Markt, Sarah C.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, USA.
    Mucci, Lorelei A.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, USA; Channing Division of Network Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston MA, USA.
    Midlife metabolic factors and prostate cancer risk in later life2018Ingår i: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 142, nr 6, s. 1166-1173Artikel i tidskrift (Refereegranskat)
    Abstract [en]

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

  • 23.
    Downer, Mary K.
    et al.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, United States; Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston MA, United States; Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston MA, United States.
    Batista, Julie L.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, United States; Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston MA, United States.
    Mucci, Lorelei A.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, United States; Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston MA, United States.
    Stampfer, Meir J.
    Epstein, Mara Meyer
    Department of Medicine and the Meyers Primary Care Institute, University of Massachusetts Medical School, Worcester MA, United States.
    Håkansson, Niclas
    The National Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Wolk, Alicja
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Johansson, Jan-Erik
    Region Örebro län. Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Andrén, Ove
    Region Örebro län. Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, United States; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Andersson, Swen-Olof
    Region Örebro län. Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Dairy intake in relation to prostate cancer survival2017Ingår i: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 140, nr 9, s. 2060-2069Artikel i tidskrift (Refereegranskat)
    Abstract [en]

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

  • 24.
    Emilsson, Louise
    et al.
    Institute of Health and Society, University of Oslo, Oslo, Norway; Vårdcentralen Värmlands Nysäter and Centre for Clinical Research, County Council of Värmland, Värmland, Sweden; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, USA.
    Løberg, Magnus
    Institute of Health and Society, University of Oslo, Oslo, Norway; Department of Transplantation Medicine and K. G. Jebsen Center for Colorectal Cancer Research, Oslo University Hospital, Oslo, Norway.
    Bretthauer, Michael
    Institute of Health and Society, University of Oslo, Oslo, Norway; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA, Department of Transplantation Medicine and K. G. Jebsen Center for Colorectal Cancer Research, Oslo University Hospital, Oslo, Norway.
    Holme, Øyvind
    Institute of Health and Society, University of Oslo, Oslo, Norway; Department of Medicine, Sørlandet Hospital, Kristiansand, Norway.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, USA; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Jodal, Henriette C.
    Institute of Health and Society, University of Oslo, Oslo, Norway.
    Adami, Hans-Olov
    Institute of Health and Society, University of Oslo, Oslo, Norway; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, USA; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Kalager, Mette
    Institute of Health and Society, University of Oslo, Oslo, Norway; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, USA.
    Colorectal cancer death after adenoma removal in Scandinavia2017Ingår i: Scandinavian Journal of Gastroenterology, ISSN 0036-5521, E-ISSN 1502-7708, Vol. 52, nr 12, s. 1377-1384Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    OBJECTIVES: Improved understanding of the subsequent risk death from colorectal cancer (CRC) among individuals who had adenomas removed is needed. We aimed to quantify this risk using prospectively collected data from population-based cohorts.

    MATERIALS AND METHODS: Using Norwegian and Swedish registries, a cohort of 90,864 individuals with colorectal adenomas removed between 1980 and 2013 was identified. Surveillance was only recommended for high-risk adenomas. The validity of the registry data did not allow classification into low- and high-risk adenomas. Virtually complete follow-up was achieved through linkage to nationwide registers. We calculated incidence-based standardised mortality ratios (SMRs) with 95% confidence intervals (CI).

    RESULTS: The median follow-up was 7.2 years; 48,058 individuals were followed for more than 10 years. We observed 819 deaths (0.9%) from CRC and expected 731 CRC deaths (0.8%), corresponding to an absolute excess risk of 88 cases (0.1%) and a relative risk of 12% (SMR 1.12; 95%CI 1.05-1.20). The relative risk of CRC death following adenoma removal was slightly higher in Sweden (SMR 1.22; 95%CI 1.11-1.34) than in Norway (SMR 1.03; 95%CI 0.93-1.14), and higher in women (SMR 1.24; 95%CI 1.12-1.36) than in men (SMR 1.02; 95%CI 0.93-1.13). Among individuals with more than 10 years of follow-up, the estimates were similar to the overall cohort, absolute excess risk 0.1% (SMR 1.15; 95%CI 1.06-1.24).

    CONCLUSION: The excess risk of CRC death following adenoma removal is small. Optimal surveillance recommendations should be tested in randomised trials.

  • 25.
    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 universitet, Institutionen för hälsovetenskap och medicin. 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 tissue2012Ingår i: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 23, nr 8, s. 1359-1366Artikel i tidskrift (Refereegranskat)
    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.

  • 26.
    Epstein, Mara M.
    et al.
    Channing Lab, Dept Medicine, Brigham & Womens Hosp, Harvard University, Boston MA, USA; School of Public Health, Dept. of Epidemiology, Harvard University, Boston MA, USA.
    Kasperzyk, Julie L.
    Channing Lab, Dept Medicine, Brigham & Womens Hosp, Harvard University, Boston MA, USA; School of Public Health, Dept. of Epidemiology, Harvard University, Boston MA, USA.
    Andrén, Ove
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Giovannucci, Edward L.
    Channing Lab, Dept Medicine, Brigham & Womens Hosp, Harvard University, Boston MA, USA; School of Public Health, Dept. of Epidemiology and Dept. of Nutrition, Harvard University, Boston MA, USA.
    Wolk, Alicja
    Inst. Environmental Medicine, Karolinska Institute, Stockholm, Sweden.
    Håkansson, Niclas
    Inst. Environmental Medicine, Karolinska Institute, Stockholm, Sweden.
    Andersson, Swen-Olof
    Örebro County Council, Örebro, Sweden.
    Johansson, Jan-Erik
    Örebro County Council, Örebro, Sweden.
    Fall, Katja
    School of Public Health, Dept. Epidemiology, Harvard University, Boston MA, USA; Dept. Genetics & Pathology, Uppsala University Hospital, Uppsala, Sweden; Center for Public Health Services, University of Iceland, Reykjavik, Iceland.
    Mucci, Lorelei A.
    Channing Lab, Dept. of Medicine, School of Medicine, Brigham & Womens Hospital, Harvard University, Boston MA, USA; School of Public Health, Dept. Epidemiology, Harvard University, Boston MA, USA; Center for Public Health Services, Univ Iceland, Reykjavik, Iceland.
    Dietary zinc and prostate cancer survival in a Swedish cohort2011Ingår i: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 93, nr 3, s. 586-593Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Zinc is involved in many essential cellular functions, including DNA repair and immune system maintenance. Although experimental evidence supports a role for zinc in prostate carcinogenesis, epidemiologic data are inconsistent; no data on cancer-specific survival have been reported.

    Objective: Our objective was to determine whether dietary zinc assessed near the time of prostate cancer diagnosis is associated with improved disease-specific survival.

    Design: This population-based cohort consists of 525 men aged < 80 y from Orebro County, Sweden, with a diagnosis of prostate cancer made between 1989 and 1994. Study participants completed self-administered food-frequency questionnaires, and zinc intake was derived from nutrient databases. Cox proportional hazards regression was used to estimate multivariate hazard ratios (HRs) and 95% CIs for time to death from prostate cancer as well as death from all causes through February 2009 by quartile (Q) of dietary zinc intake. Models were also stratified by disease stage at diagnosis (localized or advanced).

    Results: With a median follow-up of 6.4 y, 218 (42%) men died of prostate cancer and 257 (49%) died of other causes. High dietary zinc intake was associated with a reduced risk of prostate cancer-specific mortality (HR(Q4 vs Q1): 0.64; 95% CI: 0.44, 0.94; P for trend = 0.05) in the study population. The association was stronger in men with localized tumors (HR: 0.24; 95% CI: 0.09, 0.66; P for trend = 0.005). Zinc intake was not associated with mortality from other causes.

    Conclusion: These results suggest that high dietary intake of zinc is associated with lower prostate cancer-specific mortality after diagnosis, particularly in men with localized disease. Am J Clin Nutr 2011;93:586-93.

  • 27. Epstein, Mara M
    et al.
    Kasperzyk, Julie L
    Mucci, Lorelei A
    Giovannucci, Edward
    Price, Alkes
    Wolk, Alicja
    Håkansson, Niclas
    Fall, Katja
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Andersson, Swen-Olof
    Andrén, Ove
    Dietary fatty acid intake and prostate cancer survival in Örebro county, Sweden2012Ingår i: American Journal of Epidemiology, ISSN 0002-9262, E-ISSN 1476-6256, Vol. 176, nr 3, s. 240-252Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Although dietary fat has been associated with prostate cancer risk, the association between specific fatty acids and prostate cancer survival remains unclear. Dietary intake of 14 fatty acids was analyzed in a population-based cohort of 525 Swedish men with prostate cancer in Örebro County (1989-1994). Multivariable hazard ratios and 95% confidence intervals for time to prostate cancer death by quartile and per standard deviation increase in intake were estimated by Cox proportional hazards regression. Additional models examined the association by stage at diagnosis (localized: T0-T2/M0; advanced: T0-T4/M1, T3-T4/M0). Among all men, those with the highest omega-3 docosahexaenoic acid and total marine fatty acid intakes were 40% less likely to die from prostate cancer (P(trend) = 0.05 and 0.04, respectively). Among men with localized prostate cancer, hazard ratios of 2.07 (95% confidence interval: 0.93, 4.59; P(trend) = 0.03) for elevated total fat, 2.39 (95% confidence interval: 1.06, 5.38) for saturated myristic acid, and 2.88 (95% confidence interval: 1.24, 6.67) for shorter chain (C4-C10) fatty acid intakes demonstrated increased risk for disease-specific mortality for the highest quartile compared with the lowest quartile. This study suggests that high intake of total fat and certain saturated fatty acids may worsen prostate cancer survival, particularly among men with localized disease. In contrast, high marine omega-3 fatty acid intake may improve disease-specific survival for all men.

  • 28.
    Etzioni, Ruth
    et al.
    Program in Biostatistics, Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle WA, United States.
    Mucci, Lorelei
    Department of Epidemiology, Harvard School of Public Health, Harvard Medical School, Boston MA, United States; Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston MA, United States.
    Chen, Shu
    Program in Epidemiology, Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle WA, United States.
    Johansson, Jan-Erik
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Adami, Hans-Olov
    Department of Epidemiology, Harvard School of Public Health, Harvard Medical School, Boston MA, United States; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Increasing use of radical prostatectomy for nonlethal prostate cancer in Sweden2012Ingår i: Clinical Cancer Research, ISSN 1078-0432, E-ISSN 1557-3265, Vol. 18, nr 24, s. 6742-6747Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    PURPOSE: The number of patients in Sweden treated with radical prostatectomy for localized prostate cancer has increased exponentially. The extent to which this increase reflects treatment of nonlethal disease detected through prostate-specific antigen (PSA) screening is unknown.

    EXPERIMENTAL DESIGN: We undertook a nationwide study of all 18,837 patients with prostate cancer treated with radical prostatectomy in Sweden from 1988 to 2008 with complete follow-up through 2009. We compared cumulative incidence curves, fit Cox regression and cure models, and conducted a simulation study to determine changes in treatment of nonlethal cancer, in cancer-specific survival over time, and effect of lead-time due to PSA screening.

    RESULTS: The annual number of radical prostatectomies increased 25-fold during the study period. The 5-year cancer-specific mortality rate decreased from 3.9% [95% confidence interval (CI), 2.5-5.3] among patients diagnosed between 1988 and 1992 to 0.7% (95% CI, 0.4-1.1) among those diagnosed between 1998 and 2002 (P(trend) < 0.001). According to the cure model, the risk of not being cured declined by 13% (95% CI, 12%-14%) with each calendar year. The simulation study indicated that only about half of the improvement in disease-specific survival could be accounted for by lead-time.

    CONCLUSION: Patients overdiagnosed with nonlethal prostate cancer appear to account for a substantial and growing part of the dramatic increase in radical prostatectomies in Sweden, but increasing survival rates are likely also due to true reductions in the risk of disease-specific death over time. Because the magnitude of harm and costs due to overtreatment can be considerable, identification of men who likely benefit from radical prostatectomy is urgently needed.

  • 29.
    Fadl, Shalan
    et al.
    Department of Paediatrics, Örebro University Hospital, Örebro, Sweden.
    Wåhlander, Håkan
    The Queen Silvia Children`s Hospital, Institution of Clinical Sciences, Sahlgrenska University Hospital, Gothenburg University, Gothenburg, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Cao, Yang
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. Unit of Biostatistics, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Sunnegårdh, Jan
    The Queen Silvia Children`s Hospital, Institution of Clinical Sciences, Sahlgrenska University Hospital, Gothenburg University, Gothenburg, Sweden.
    The highest mortality rates in childhood dilated cardiomyopathy occur during the first year after diagnosis2018Ingår i: Acta Paediatrica, ISSN 0803-5253, E-ISSN 1651-2227, Vol. 107, nr 4, s. 672-677Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    AIM: The aim of the study was to assess the incidence, mortality and morbidity of dilated cardiomyopathy (DCM) and non-compaction of the left ventricle (LVNC) in Swedish children.

    METHODS: We reviewed hospital records of all children with dilated cardiomyopathy (DCM) or left ventricular non-compaction cardiomyopathy (LVNC) up to the age of 18 in the healthcare region of western Sweden from 1991 to 2015.

    RESULTS: In total, 69 cases (61% males) were identified. The combined incidence of DCM and LVNC was 0.77 (95% CI 0.59-0.96) per 100,000 person years. Children were divided into six groups and their outcomes were analysed depending on their aetiology. Idiopathic DCM was reported in 43% and familial dilated and left ventricular non-compaction aetiology was present in 32%. DCM due to various diseases occurred in 8%. DCM associated with neuromuscular diseases was present in 16%. The overall risk of death or receiving transplants in children with idiopathic and familial DCM was 30% over the study period and 21% died in the first year after diagnosis.

    CONCLUSION: The combined incidence of DCM and LVNC was similar to previous reports. Most children with idiopathic DCM presented during infancy and mortality was highest during the first year after diagnosis.

  • 30.
    Fall, Katja
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, United States of America.
    Fang, Fang
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Mucci, Lorelei A.
    Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, United States of America; Channing Laboratory, Department of Medicine, Harvard Medical School, Boston, Massachusetts, United States of America.
    Ye, Weimin
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Andrén, Ove
    Örebro University Hospital, Örebro, Sweden.
    Johansson, Jan-Erik
    Örebro universitet, Hälsoakademin. Örebro University Hospital, Örebro, Sweden.
    Andersson, Swen-Olof
    Örebro University Hospital, Örebro, Sweden.
    Sparén, Pär
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Klein, Georg
    The Microbiology Tumor Biology Center, Karolinska Institutet, Stockholm, Sweden.
    Stampfer, Meir
    Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, United States of America; Channing Laboratory, Department of Medicine, Harvard Medical School, Boston, Massachusetts, United States of America.
    Adami, Hans-Olov
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, United States of America.
    Valdimarsdóttir, Unnur
    Centre of Public Health Sciences, University of Iceland, Reykjavík, Iceland.
    Immediate risk for cardiovascular events and suicide following a prostate cancer diagnosis: prospective cohort study2009Ingår i: PLoS Medicine, ISSN 1549-1277, E-ISSN 1549-1676, Vol. 6, nr 12, s. e1000197-Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Stressful life events have been shown to be associated with altered risk of various health consequences. The aim of the present study was to investigate whether the emotional stress evoked by a prostate cancer diagnosis increases the immediate risks of cardiovascular events and suicide.

    METHODS AND FINDINGS: We conducted a prospective cohort study by following all men in Sweden who were 30 y or older (n = 4,305,358) for a diagnosis of prostate cancer (n = 168,584) and their subsequent occurrence of cardiovascular events and suicide between January 1, 1961 and December 31, 2004. We used Poisson regression models to calculate relative risks (RRs) and 95% confidence intervals (CIs) of cardiovascular events and suicide among men who had prostate cancer diagnosed within 1 y to men without any cancer diagnosis. The risks of cardiovascular events and suicide were elevated during the first year after prostate cancer diagnosis, particularly during the first week. Before 1987, the RR of fatal cardiovascular events was 11.2 (95% CI 10.4-12.1) during the first week and 1.9 (95% CI 1.9-2.0) during the first year after diagnosis. From 1987, the RR for cardiovascular events, nonfatal and fatal combined, was 2.8 (95% CI 2.5-3.2) during the first week and 1.3 (95% CI 1.3-1.3) during the first year after diagnosis. While the RR of cardiovascular events declined, the RR of suicide was stable over the entire study period: 8.4 (95% CI 1.9-22.7) during the first week and 2.6 (95% CI 2.1-3.0) during the first year after diagnosis. Men 54 y or younger at cancer diagnosis demonstrated the highest RRs of both cardiovascular events and suicide. A limitation of the present study is the lack of tumor stage data, which precluded possibilities of investigating the potential impact of the disease severity on the relationship between a recent diagnosis of prostate cancer and the risks of cardiovascular events and suicide. In addition, we cannot exclude residual confounding as a possible explanation.

    CONCLUSIONS: Men newly diagnosed with prostate cancer are at increased risks for cardiovascular events and suicide. Future studies with detailed disease characteristic data are warranted.

  • 31.
    Fall, Katja
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Örebro University Hospital, Örebro, Sweden; Harvard School of Public Health, Boston MA,USA.
    Garmo, Hans
    Regional Oncology Center, Syracuse NY, USA.
    Gudbjörnsdottir, Soffia
    Sahlgrenska University Hospital, Gothenburgh University, Göteborg, Sweden.
    Stattin, Pär
    Memorial Sloan-Kettering Cancer Center, New York City NY, USA.
    Zethelius, Björn
    Department of Public Health and Caring Sciences/Geriatrics, Uppsala University, Uppsala, Sweden; Medical Products Agency, Uppsala, Sweden.
    Diabetes Mellitus and Prostate Cancer Risk: A Nationwide Case-Control Study within PCBaSe Sweden2013Ingår i: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 22, nr 6, s. 1102-1109Artikel i tidskrift (Refereegranskat)
  • 32.
    Fall, Katja
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Örebro University hospital, Örebro, Sweden.
    Holmberg, L
    Sundström, J.
    Good prognosis studies can provide better clinical decisions. Validated risk-/prognosis factors helps the physician2013Ingår i: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 110, nr 6, s. 279-283Artikel i tidskrift (Refereegranskat)
  • 33.
    Fall, Katja
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Enheten för klinisk epidemiologi och biostatistik, Örebro Universitetssjukhus, Örebro, Sweden.
    Holmberg, Lars
    Regionalt cancercentrum, Uppsala-Örebro, Uppsala Universitet, Uppsala, Sweden; King´s College, London, UK.
    Sundström, Johan
    Institutionen för medicinska vetenskaper, Uppsala Clinical Research Center, Uppsala Universitet, Uppsala, Sweden; Akademiska sjukhuset, Uppsala, Sweden; George Institute for Global Health, Sydney, Australien.
    Bra prognosstudier kan ge bättre kliniska beslut [Good prognosis studies can provide better clinical decisions]: Validerade risk-/prognosfaktorer hjälper läkaren [Validated risk-/prognosis factors helps the physician].2013Ingår i: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 110, nr 6, s. 279-83Artikel i tidskrift (Refereegranskat)
  • 34.
    Fall, Katja
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm; Department of Epidemiology, Harvard School of Public Health, Boston, USA; Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, USA.
    Stark, J. R.
    Department of Epidemiology, Harvard School of Public Health, Boston, USA; Channing Laboratory, Department of Medicine, Brigham Women’s Hospital and Harvard Medical School, Boston, USA.
    Mucci, L. A.
    Department of Epidemiology, Harvard School of Public Health, Boston, USA; Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, USA.
    Chan, J.
    Departments of Epidemiology & Biostatistics and Urology, University of California, San Francisco, USA.
    Stampfer, M. J.
    Department of Epidemiology, Harvard School of Public Health, Boston, USA; Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, USA.
    Kurth, T.
    Department of Epidemiology, Harvard School of Public Health, Boston, USA; Division of Preventive Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, USA.
    Febbo, P. G.
    Duke University School of Medicine, Durham, USA.
    Kantoff, P.
    Division of Solid Tumor Oncology, Dana-Farber Cancer Institute, Boston, USA.
    Ma, J.
    Department of Epidemiology, Harvard School of Public Health, Boston, USA; Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, USA.
    No association between a polymorphic variant of the IRS-1 gene and prostate cancer risk2008Ingår i: The Prostate, ISSN 0270-4137, E-ISSN 1097-0045, Vol. 68, nr 13, s. 1416-20Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Objective: Insulin receptor substrate-1 (IRS-1) acts as a docking protein between the insulin-like growth factor-1 (IGF-1) receptor and intracellular signaling molecules in the IGF-1 signaling pathway. Accumulating data support a role of IGF-1 in prostate carcinogenesis. We assessed the influence of the most common IRS-1 gene polymorphism (Gly972Arg) on prostate cancer risk, alone and in combination with IGF-1 and other components in the IGF-1 signaling pathway.

    Materials and methods: In a nested case-control study within the Physicians' Health Study, the IRS-1 polymorphism was assayed from prospectively collected samples from 564 incident prostate cancer cases and 758 controls matched on age and smoking. We calculated relative risks (RR) and 95% confidence intervals (CI) using conditional logistic regression.

    Results: Among the controls, 0.8% were homozygous (AA) and 12% were heterozygous (GA) for the polymorphic allele. There was no association between carriage of the A allele and total prostate cancer risk (RR = 1.1 95% CI = 0.8-1.5), advanced disease (stage C or D or lethal prostate cancer, RR = 1.3 95% CI = 0.8-2.3), or plasma IGF-1 levels. We explored possible interactions with body mass index and components in the IGF-1 pathway including IGFBP3, PI3k, and PTEN but none of these factors influenced the relation between IRS-1 genotype and prostate cancer risk.

    Conclusions: Our data do not support an association between carriage of the variant IRS-1 gene and prostate cancer risk.

  • 35. Fall, Katja
    et al.
    Strömberg, Fredrik
    Rosell, Johan
    Andrén, Ove
    Örebro universitet, Hälsoakademin.
    Varenhorst, Eberhard
    Reliability of death certificates in prostate cancer patients2008Ingår i: Scandinavian Journal of Urology and Nephrology, ISSN 0036-5599, E-ISSN 1651-2065, Vol. 42, nr 4, s. 352-357Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    OBJECTIVE: To evaluate the reliability of cause-of-death diagnoses among prostate cancer patients. MATERIAL AND METHODS: Information from death certificates obtained from the Swedish Death Register was compared with systematically reviewed medical records from the population-based Swedish Regional Prostate Cancer Register, South-East Region. In total, 5675 patients were included who had been diagnosed with prostate cancer between 1987 and 1999 and who had died before 1 January 2003. RESULTS: The proportion of prostate cancer cases classified as having died from prostate cancer was 3% higher in the official death certificates than in the reviewed records [0.03, 95% confidence interval (CI) 0.02 to 0.04]. Overall agreement between the official cause of death and the reviewed data was 86% (95% CI 85 to 87%). A higher accuracy was observed among men with localized disease (88%, 95% CI 87 to 89%), aged 60 years or younger at death (96%, 95% CI 93 to 100%), or who had undergone curative treatment (91%, 95% CI 88 to 95%). This study indicates a relatively high reliability of official cause-of-death statistics of prostate cancer patients in Sweden. CONCLUSION: Mortality data obtained from death certificates may be useful in the evaluation of large-scale prostate cancer intervention programmes, especially among younger patients with localized disease.

  • 36.
    Fall, Katja
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm.
    Ye, W.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm.
    Nyrén, O.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, stockholm.
    Antibiotic treatment and risk of gastric cancer2006Ingår i: Gut, ISSN 0017-5749, E-ISSN 1468-3288, Vol. 55, nr 6, s. 793-6Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background/aims: Helicobacter pylori infection is undoubtedly an important risk factor for gastric cancer. It remains unclear however whether antibiotic treatment may prevent gastric cancer development. Our aim was to assess long term gastric cancer risks in historic cohorts of patients presumed to have been heavily exposed to antibiotics.

    Subjects: Using the Swedish Inpatient Register, we identified 501 757 individuals discharged with any one of 10 selected infectious disease diagnoses between 1970 and 2003.

    Methods: We counted person time and non-cardia gastric cancer occurrences through linkage to virtually complete population and health care registers. Standardised incidence ratios (SIRs) were calculated for comparisons with cancer incidence rates of the general population in Sweden.

    Results: No reduction in gastric cancer risk was observed in the infectious disease cohort in total (SIR 1.08 (95% confidence intervals 1.00-1.17) or for any of the presumed antibiotic regimens. There were no clear trends towards decreasing risk with time of follow up, but the risk tended to fall with increasing age at first hospitalisation for the infection (p<0.04).

    Conclusions: Our results do not confirm earlier observational findings of a reduced risk of gastric cancer following exposure to heavy antibiotic treatment among hip replacement patients. Suboptimal drug regimens, inadequate timing of H pylori eradication, or insufficient follow up time may possibly explain the lack of association in this setting. Although our findings do not rule out the cancer preventive potential of H pylori eradication, they emphasise that detection of such an effect, if any, may require considerable efforts.

  • 37.
    Fall, Katja
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm.
    Ye, Weimin
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm.
    Nyrén, Olof
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm.
    Risk for gastric cancer after cholecystectomy2007Ingår i: American Journal of Gastroenterology, ISSN 0002-9270, E-ISSN 1572-0241, Vol. 102, nr 6, s. 1180-4Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: It is becoming increasingly evident that chronic inflammation may predispose cancer development. In the stomach, inflammation caused by Helicobacter pylori infection is linked to gastric cancer. Cholecystectomy is regularly followed by duodenogastric bile reflux and reactive gastritis. To test whether a noninfectious long-standing inflammation impels gastric carcinogenesis as well, we assessed the risk of gastric cancer in a large, population-based cohort of cholecystectomized patients.

    Methods: We identified 251,672 individuals, in the Swedish National Inpatient Register, who had undergone cholecystectomy between 1970 and 1997. All incident cases of gastric cancer were identified through linkage to the Swedish Cancer Registry. Standardized incidence ratios (SIRs) were calculated for comparisons with cancer rates of the general population in Sweden.

    Results: We found an 11% greater overall risk of distal gastric cancer (SIR=1.11, 95% CI 1.04-1.19). The risk increase was only observed among men (SIR=1.21, 95% CI 1.10-1.32), whereas no excess risk was evident for women. For men, the risk was elevated for up to 10 yr after surgery, but this elevation disappeared with longer follow-up time. There was no clear association between cholecystectomy and cardia cancer (SIR=0.95, 95% CI 0.76-1.16).

    Conclusions: Inconsistency over gender strata, implausibly short induction and latency time, and disappearance of the effect over time makes a causal relationship between cholecystectomy and distal gastric cancer less likely. The findings set aside concerns of harmful long-term consequences of cholecystectomy.

  • 38.
    Fall, Tove
    et al.
    Department of Medical Sciences, Molecular Epidemiology and Science for Life Laboratory, Uppsala University, Uppsala, Sweden.
    Lundholm, Cecilia
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Örtqvist, Anne K.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Orebro Univ Hosp, Orebro, Sweden.
    Fang, Fang
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Hedhammar, Åke
    Department of Clinical Sciences, Swedish University of Agricultural Sciences, Uppsala, Sweden .
    Kämpe, Olle
    Centre for Molecular Medicine, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden .
    Ingelsson, Erik
    Department of Medical Sciences, Molecular Epidemiology and Science for Life Laboratory, Uppsala University, Uppsala, Sweden.
    Almqvist, Catarina
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Astrid Lindgren Children’s Hospital, Lung and Allergy Unit, Karolinska University Hospital, Stockholm, Sweden.
    Early Exposure to Dogs and Farm Animals and the Risk of Childhood Asthma2015Ingår i: JAMA pediatrics, ISSN 2168-6203, E-ISSN 2168-6211, Vol. 169, nr 11, artikel-id e153219Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    IMPORTANCE: The association between early exposure to animals and childhood asthma is not clear, and previous studies have yielded contradictory results.

    OBJECTIVE: To determine whether exposure to dogs and farm animals confers a risk of asthma.

    DESIGN, SETTING AND PARTICIPANTS: In a nationwide cohort study, the association between early exposure to dogs and farm animals and the risk of asthma was evaluated and included all children born in Sweden from January 1, 2001, to December 31, 2010 (N = 1 011 051), using registry data on dog and farm registration, asthma medication, diagnosis, and confounders for parents and their children. The association was assessed as the odds ratio (OR) for a current diagnosis of asthma at age 6 years for school-aged children and as the hazard ratio (HR) for incident asthma at ages 1 to 5 years for preschool-aged children. Data were analyzed from January 1, 2007, to September 30, 2012.

    EXPOSURES: Living with a dog or farm animal.

    MAIN OUTCOMES AND MEASURES: Childhood asthma diagnosis and medication used.

    RESULTS: Of the 1 011 051 children born during the study period, 376 638 preschool-aged (53 460 [14.2%] exposed to dogs and 1729 [0.5%] exposed to farm animals) and 276 298 school-aged children (22 629 [8.2%] exposed to dogs and 958 [0.3%] exposed to farm animals) were included in the analyses. Of these, 18 799 children (5.0%) in the preschool-aged children's cohort experienced an asthmatic event before baseline, and 28 511 cases of asthma and 906 071 years at risk were recorded during follow-up (incidence rate, 3.1 cases per 1000 years at risk). In the school-aged children's cohort, 11 585 children (4.2%) experienced an asthmatic event during the seventh year of life. Dog exposure during the first year of life was associated with a decreased risk of asthma in school-aged children (OR, 0.87; 95% CI, 0.81-0.93) and in preschool-aged children 3 years or older (HR, 0.90; 95% CI, 0.83-0.99) but not in children younger than 3 years (HR, 1.03; 95% CI, 1.00-1.07). Results were comparable when analyzing only first-born children. Farm animal exposure was associated with a reduced risk of asthma in both school-aged children and preschool-aged children (OR, 0.48; 95% CI, 0.31-0.76, and HR, 0.69; 95% CI, 0.56-0.84), respectively.

    CONCLUSIONS AND RELEVANCE: In this study, the data support the hypothesis that exposure to dogs and farm animals during the first year of life reduces the risk of asthma in children at age 6 years. This information might be helpful in decision making for families and physicians on the appropriateness and timing of early animal exposure.

  • 39.
    Fang, Fang
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Clinical Epidemiology and Biostatistics Unit, Örebro University Hospital, Örebro, Sweden; Department of Epidemiology, Harvard School of Public Health, Boston, USA; Center of Public Health Sciences, University of Iceland, Reykjavík, Iceland.
    Mittleman, M.A.
    Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, USA; Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Sparen, P.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Ye, W.M.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Adami, H. O.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Valdimarsdottir, Unnur
    Department of Epidemiology, Harvard School of Public Health, Boston, USA; Center of Public Health Sciences, University of Iceland, Reykjavík, Iceland .
    Suicide and cardiovascular death after a cancer diagnosis2012Ingår i: New England Journal of Medicine, ISSN 0028-4793, E-ISSN 1533-4406, Vol. 366, nr 14, s. 1310-1318Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Receiving a diagnosis of cancer is a traumatic experience that may trigger immediate adverse health consequences beyond the effects of the disease or treatment.

    Methods: Using Poisson and negative binomial regression models, we conducted a historical cohort study involving 6,073,240 Swedes to examine the associations between a cancer diagnosis and the immediate risk of suicide or death from cardiovascular causes from 1991 through 2006. To adjust for unmeasured confounders, we also performed a nested, self-matched case-crossover analysis among all patients with cancer who died from suicide or cardiovascular diseases in the cohort.

    Results: As compared with cancer-free persons, the relative risk of suicide among patients receiving a cancer diagnosis was 12.6 (95% confidence interval [CI], 8.6 to 17.8) during the first week (29 patients; incidence rate, 2.50 per 1000 person-years) and 3.1 (95% CI, 2.7 to 3.5) during the first year (260 patients; incidence rate, 0.60 per 1000 person-years). The relative risk of cardiovascular death after diagnosis was 5.6 (95% CI, 5.2 to 5.9) during the first week (1318 patients; incidence rate, 116.80 per 1000 person-years) and 3.3 (95% CI, 3.1 to 3.4) during the first 4 weeks (2641 patients; incidence rate, 65.81 per 1000 person-years). The risk elevations decreased rapidly during the first year after diagnosis. Increased risk was particularly prominent for cancers with a poor prognosis. The case-crossover analysis largely confirmed results from the main analysis.

    Conclusions: In this large cohort study, patients who had recently received a cancer diagnosis had increased risks of both suicide and death from cardiovascular causes, as compared with cancer-free persons. (Funded by the Swedish Council for Working Life and Social Research and others.).

  • 40.
    Fang, Fang
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fall, Katja
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology, Harvard School of Public Health, Boston, USA; Centre of Public Health Sciences, School of Health Sciences, University of Iceland, Reykjavík, Iceland.
    Sparén, Pär
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Adami, Hans-Olov
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Valdimarsdóttir, Heiddis B.
    Department of Psychology, University of Iceland, Reykjavík, Iceland; Department of Oncological Sciences, Mount Sinai School of Medicine, New York, USA.
    Lambe, Mats
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Regional Oncologic Center, Uppsala, Sweden.
    Valdimarsdóttir, Unnur
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology, Harvard School of Public Health, Boston, USA; Centre of Public Health Sciences, School of Health Sciences, University of Iceland, Reykjavík, Iceland.
    Risk of infection-related cancers after the loss of a child: a follow-up study in Sweden2011Ingår i: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 71, nr 1, s. 116-22Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    It is unknown whether severe emotional stress due to loss of a child influences the risk of cancers susceptible to immune modulation such as infection-related cancers. We conducted a historic cohort study in 1990 to 2004 on the basis of the Swedish Multi-Generation Register including 4,687,073 parents. Death of a child was identified through the Causes of Death Register. Poisson regression was used to derive the relative risks (RR) and 95% confidence intervals (CI) of infection-related cancers, comparing the incidence rates of parents who lost a child with those who never lost a child. A total of 101,306 parents (2%) had lost a child during follow-up, among whom 1,608 subsequently developed infection-related cancers. After adjustment for age, sex, calendar year, educational level, and civil status, the overall RR of 14 cancers studied was 1.07 (95% CI: 1.02-1.12). Parents who lost a child were particularly at a higher risk for cancers potentially associated with human papilloma virus (HPV) infection such as cervical cancer (RR: 1.46; 95% CI: 1.17-1.80). Higher RRs for most cancers were obtained within 5 years after child loss and excess risk for liver and stomach cancers was confined to that period. No association was observed for lymphoma and nonmelanoma skin cancer at any time point after child loss. Although potential confounding by unmeasured factors cannot be ruled out, our findings lend support to the hypothesis that severe life stressors, such as child loss, may raise the risk for several, chiefly HPV-related, cancers.

  • 41.
    Fang, Fang
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Valdimarsdottir, Unnur
    Centre of Public Health Sciences, Faculty of Medicine, School of Health Sciences, University of Iceland, Reykjavik, Iceland; Department of Epidemiology, Harvard TH Chan School of Public Health, Boston MA, USA.
    Stress and cancer: Nordic pieces to the complex puzzle2015Ingår i: European Journal of Epidemiology, ISSN 0393-2990, E-ISSN 1573-7284, Vol. 30, nr 7, s. 525-527Artikel i tidskrift (Övrigt vetenskapligt)
  • 42.
    Fang, Fang
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Valdimarsdottir, Unnur
    Center of Public Health Sciences, University of Iceland, Reykjavík, Iceland.
    Suicide and Cardiovascular Death after a Cancer Diagnosis REPLY2012Ingår i: New England Journal of Medicine, ISSN 0028-4793, E-ISSN 1533-4406, Vol. 367, nr 3, s. 277-277Artikel i tidskrift (Refereegranskat)
  • 43.
    Fang, Fang
    et al.
    Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, USA; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Kasperzyk, Julie L.
    Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, USA; Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Shui, Irene
    Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Hendrickson, Whitney
    Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, USA; Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Hollis, Bruce W.
    Department of Pediatrics, Medical University of South Carolina, Charleston, USA.
    Fall, Katja
    Department of Epidemiology, Harvard School of Public Health, Boston, USA; Clinical Epidemiology and Biostatistics Unit, Örebro University Hospital, Örebro, Sweden.
    Ma, Jing
    Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, USA.
    Gaziano, J. Michael
    Divisions of Preventive Medicine and Aging, Department of Medicine, Brigham and Women's Hospital, Boston, USA; Massachusetts Veteran's Epidemiology, Research and Information Center, Geriatric Research Education and Clinical Center, VA Boston Healthcare System, Boston, USA.
    Stampfer, Meir J.
    Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, USA; Department of Epidemiology, Harvard School of Public Health, Boston, USA; Department of Nutrition, Harvard School of Public Health, Boston, USA.
    Mucci, Lorelei A.
    Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, USA; Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Giovannucci, Edward
    Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, USA; Department of Epidemiology, Harvard School of Public Health, Boston, USA; Department of Nutrition, Harvard School of Public Health, Boston, USA.
    Prediagnostic plasma vitamin D metabolites and mortality among patients with prostate cancer2011Ingår i: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 6, nr 4, artikel-id e18625Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Laboratory evidence suggests that vitamin D might influence prostate cancer prognosis.

    Methodology/principal findings: We examined the associations between prediagnostic plasma levels of 25(OH)vitamin D [25(OH)D] and 1,25(OH)(2) vitamin D [1,25(OH)(2)D] and mortality among 1822 participants of the Health Professionals Follow-up Study and Physicians' Health Study who were diagnosed with prostate cancer. Cox proportional hazards models were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) of total mortality (n = 595) and lethal prostate cancer (death from prostate cancer or development of bone metastases; n = 202). In models adjusted for age at diagnosis, BMI, physical activity, and smoking, we observed a HR of 1.22 (95% CI: 0.97, 1.54) for total mortality, comparing men in the lowest to the highest quartile of 25(OH)D. There was no association between 1,25(OH)(2)D and total mortality. Men with the lowest 25(OH)D quartile were more likely to die of their cancer (HR: 1.59; 95% CI: 1.06, 2.39) compared to those in the highest quartile (P(trend) = 0.006). This association was largely explained by the association between low 25(OH)D levels and advanced cancer stage and higher Gleason score, suggesting that these variables may mediate the influence of 25(OH)D on prognosis. The association also tended to be stronger among patients with samples collected within five years of cancer diagnosis. 1,25(OH)(2)D levels were not associated with lethal prostate cancer.

    Conclusions/significance: Although potential bias of less advanced disease due to more screening activity among men with high 25(OH)D levels cannot be ruled out, higher prediagnostic plasma 25(OH)D might be associated with improved prostate cancer prognosis.

  • 44.
    Fang, Fang
    et al.
    Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, USA; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Keating, Nancy L.
    Department of Health Care Policy, Harvard Medical School, Boston, USA; Division of General Internal Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, USA.
    Mucci, Lorelei A.
    Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, USA; Department of Epidemiology, Harvard School of Public Health, Boston, USA; Centre of Public Health Sciences, Faculty of Medicine, University of Iceland, Reykjavík, Iceland; Department of Nutrition, Harvard School of Public Health, Boston, USA.
    Adami, Hans-Olov
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology, Harvard School of Public Health, Boston, USA; Centre of Public Health Sciences, Faculty of Medicine, University of Iceland, Reykjavík, Iceland .
    Stampfer, Meir J.
    Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, USA; Department of Epidemiology, Harvard School of Public Health, Boston, USA; Centre of Public Health Sciences, Faculty of Medicine, University of Iceland, Reykjavík, Iceland .
    Valdimarsdóttir, Unnur
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Nutrition, Harvard School of Public Health, Boston, USA.
    Fall, Katja
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology, Harvard School of Public Health, Boston, USA; Centre of Public Health Sciences, Faculty of Medicine, University of Iceland, Reykjavík, Iceland; Department of Nutrition, Harvard School of Public Health, Boston, USA.
    Immediate risk of suicide and cardiovascular death after a prostate cancer diagnosis: cohort study in the United States2010Ingår i: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 102, nr 5, s. 307-14Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Receiving a cancer diagnosis is a stressful event that may increase risks of suicide and cardiovascular death, especially soon after diagnosis.

    Methods: We conducted a cohort study of 342,497 patients diagnosed with prostate cancer from January 1, 1979, through December 31, 2004, in the Surveillance, Epidemiology, and End Results Program. Follow-up started from the date of prostate cancer diagnosis to the end of first 12 calendar months after diagnosis. The relative risks of suicide and cardiovascular death were calculated as standardized mortality ratios (SMRs) comparing corresponding incidences among prostate cancer patients with those of the general US male population, with adjustment for age, calendar period, and state of residence. We compared risks in the first year and months after a prostate cancer diagnosis. The analyses were further stratified by calendar period at diagnosis, tumor characteristics, and other variables.

    Results: During follow-up, 148 men died of suicide (mortality rate = 0.5 per 1000 person-years) and 6845 died of cardiovascular diseases (mortality rate = 21.8 per 1000 person-years). Patients with prostate cancer were at increased risk of suicide during the first year (SMR = 1.4, 95% confidence interval [CI] = 1.2 to 1.6), especially during the first 3 months (SMR = 1.9, 95% CI = 1.4 to 2.6), after diagnosis. The elevated risk was apparent in pre-prostate-specific antigen (PSA) (1979-1986) and peri-PSA (1987-1992) eras but not since PSA testing has been widespread (1993-2004). The risk of cardiovascular death was slightly elevated during the first year (SMR = 1.09, 95% CI = 1.06 to 1.12), with the highest risk in the first month (SMR = 2.05, 95% CI = 1.89 to 2.22), after diagnosis. The first-month risk was statistically significantly elevated during the entire study period, and the risk was higher for patients with metastatic tumors (SMR = 3.22, 95% CI = 2.68 to 3.84) than for those with local or regional tumors (SMR = 1.57, 95% CI = 1.42 to 1.74).

    Conclusion: A diagnosis of prostate cancer may increase the immediate risks of suicide and cardiovascular death.

  • 45.
    Fang, Fang
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm.
    Valdimarsdóttir, Unnur
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm; Centre for Public Health Sciences, University of Iceland, Reykjavik, Iceland.
    Bellocco, Rino
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm; Department of Statistics, University of Milano-Bicocca, Milan, Italy.
    Ronnevi, Lars-Olof
    Department of Neurology, Karolinska Hospital Stockholm.
    Sparén, Pär
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm.
    Fall, Katja
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm; Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Ye, Weimin
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm.
    Amyotrophic lateral sclerosis in Sweden, 1991-20052009Ingår i: Archives of Neurology, ISSN 0003-9942, E-ISSN 1538-3687, Vol. 66, nr 4, s. 515-9Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Objectives: To investigate the temporal trend of amyotrophic lateral sclerosis (ALS) incidence in Sweden between January 1, 1991, and December 31, 2005, and to explore incidence variations according to major demographic factors.

    Design: Population-based study.

    Setting: Academic research.

    Participants: All incident cases of ALS identified through the Swedish Inpatient Register between January 1, 1991, and December 31, 2005.

    Main outcome measure: Age-standardized incidence rates were calculated by applying the observed age-specific incidence rates to the age distribution of the Swedish population in 1991. A linear regression model was used to assess the potential trend of the incidence during calendar years. We also followed up the entire population registered in the 1990 Population and Housing Census for incidence of ALS. Relative risk and 95% confidence interval of ALS associated with demographic variables were estimated using Poisson regression models.

    Results: The age-standardized incidence rates increased from 2.32 per 100,000 person-years in 1991-1993 to 2.98 per 100,000 person-years in 2003-2005, representing an annual increase of approximately 2% during the 15 years (P value for trend, .002). The age-specific incidence rates increased in all age groups except those younger than 50 years. The observed increase remained significant when restricting the analysis to individuals born in Sweden (P value for trend, <.001). Compared with individuals born from April through June, those born from October through December were at 11% increased risk of ALS (95% confidence interval, 1.01-1.23).

    Conclusions: The incidence of ALS has been increasing during the last 15 years in Sweden. Further studies are warranted to explore the underlying reasons for this observed trend.

  • 46.
    Fang, Fang
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm.
    Valdimarsdóttir, Unnur
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm; Centre of Public Health Sciences,University of Iceland, Reykjavik, Iceland.
    Fürst, Carl Johan
    Stockholms Sjukhem, Palliative Care Unit, Stockholm.
    Hultman, Christina
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm; Department of Neuroscience, Psychiatry, Ulleråker,Uppsala University,Uppsala.
    Fall, Katja
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm.
    Sparén, Pär
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm.
    Ye, Weimin
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm.
    Suicide among patients with amyotrophic lateral sclerosis2008Ingår i: Brain, ISSN 0006-8950, E-ISSN 1460-2156, Vol. 131, nr 10, s. 2729-33Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Studies on the suicide risk among patients with amyotrophic lateral sclerosis (ALS) in countries without legalized euthanasia or assisted suicide are important additions to data on the wish to die of these patients. We conducted a population-based cohort study in Sweden between 1965 and 2004, which comprised of 6,642 patients with incident ALS identified from the Swedish Inpatient Register. We calculated the standardized mortality ratios (SMRs) of suicide among the patients using the suicide rates of the general Swedish population as a reference. In total, 21 patients committed suicide during follow-up, compared to the predicted 3.6 suicides. Thus, we noted an almost 6-fold increased risk for suicide among ALS patients [SMR 5.8, 95% confidence interval (CI) 3.6-8.8]. Patients who committed suicide were, on average, around 7 years younger at the time of their first period of hospitalization than patients who did not commit suicide. The highest relative risk for suicide was observed within the first year after the patient's first period of hospitalization (SMR 11.2, 95% CI 5.8-19.6). After that, the relative risks decreased with time after hospitalization (P-value for trend = 0.006), but remained elevated 3 years later. The relative risks of suicide among ALS patients did not show a clear trend over time in contrast to the decreasing trend of relative risks for suicide among patients with cancer during the same period. Patients with ALS are at excess risk of suicide in Sweden and the relative risk is higher during the earlier stage of the disease.

  • 47.
    Fang, Fang
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Valdimarsdóttir, Unnur
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Centre for Public Health Sciences, University of Iceland, Reykjavik, Iceland.
    Mucci, Lorelei
    Centre for Public Health Sciences, University of Iceland, Reykjavik, Iceland; Department of Epidemiology, Harvard School of Public Health, Boston, USA; Channing Laboratory, Brigham and Women’s Hospital, Harvard Medical School, Boston, USA.
    Sparén, Pär
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Ye, Weimin
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fall, Katja
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Centre for Public Health Sciences, University of Iceland, Reykjavik, Iceland; Department of Genetics and Pathology, Uppsala University, Uppsala, Sweden.
    Hospitalization for osteoarthritis and prostate cancer specific mortality among Swedish men with prostate cancer2010Ingår i: Cancer Epidemiology, ISSN 1877-7821, E-ISSN 1877-783X, Vol. 34, nr 5, s. 644-7Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Purpose: To examine the potential role of nonsteroidal anti-inflammatory drugs (NSAIDs) use on prostate cancer (PCa) specific mortality.

    Methods: We studied the association between hospitalization for osteoarthritis prior to PCa diagnosis, as a surrogate for heavy use of NSAIDs, and PCa specific mortality in a large population of PCa patients in Sweden in 1980-2004.

    Results: Hospitalization for osteoarthritis before PCa diagnosis was associated to a lower PCa specific mortality (hazard ratio [HR], 0.92; 95% confidence interval [CI], 0.88-0.96), but not to the risk of death from other causes (HR, 1.03; 95% CI, 0.99-1.08). The association was stronger among younger patients and patients diagnosed in earlier calendar years.

    Conclusions: Our data demonstrate a modestly decreased PCa specific mortality among PCa patients with hospitalization for osteoarthritis prior to PCa diagnosis, compared to those without such experience. This finding lends support to the hypothesis that NSAIDs use may influence PCa progression.

  • 48.
    Fang, Fang
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm.
    Ye, Weimin
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm.
    Fall, Katja
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm.
    Lekander, Mats
    Department of Clinical Neuroscience and Osher Center for Integrative Medicine, Karolinska Institutet, Stockholm.
    Wigzell, Hans
    Microbiology and Tumor Biology Center, Karolinska Institutet, Stockholm.
    Sparén, Pär
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm.
    Adami, Hans-Olov
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm; Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Valdimarsdóttir, Unnur
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm; Centre for Public Health Sciences, Faculty of Medicine, University of Iceland, Reykjavik, Iceland.
    Loss of a child and the risk of amyotrophic lateral sclerosis2008Ingår i: American Journal of Epidemiology, ISSN 0002-9262, E-ISSN 1476-6256, Vol. 167, nr 2, s. 203-10Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Between 1987 and 2005, the authors conducted a case-control study nested within the entire Swedish population to investigate whether loss of a child due to death is associated with the risk of amyotrophic lateral sclerosis (ALS). The study comprised 2,694 incident ALS cases and five controls per case individually matched by year of birth, gender, and parity. Odds ratios and their corresponding 95% confidence intervals for ALS were estimated by using conditional logistic regression models. Compared with that for parents who never lost a child, the overall odds ratio of ALS for bereaved parents was 0.7 (95% confidence interval (CI): 0.6, 0.8) and decreased to 0.4 (95% CI: 0.2, 0.8) 11-15 years after the loss. The risk reduction was also modified by parental age at the time of loss, with the lowest odds ratio of 0.4 (95% CI: 0.2, 0.9) for parents older than age 75 years. Loss of a child due to malignancy appeared to confer a lower risk of ALS (odds ratio = 0.5, 95% CI: 0.3, 0.8) than loss due to other causes. These data indicate that the risk of developing ALS decreases following the severe stress of parental bereavement. Further studies are needed to explore potential underlying mechanisms.

  • 49.
    Fang, Xin
    et al.
    Unit of Biostatistics, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Liang, Chun
    Department of Cardiology, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai, China.
    Li, Mei
    Department of Cardiology, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai, China.
    Montgomery, Scott
    Örebro universitet, Institutionen för medicinska vetenskaper. Clinical Epidemiology Unit, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology and Public Health, University College London, London, UK.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper. Clinical Epidemiology Unit, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Aaseth, Jan
    Faculty of Public Health, Hedmark University College, Elverum, Norway; Kongsvinger Hospital Division, Innlandet Hospital Trust, Kongsvinger, Norway.
    Cao, Yang
    Örebro universitet, Institutionen för medicinska vetenskaper. Unit of Biostatistics, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Dose-response relationship between dietary magnesium intake and cardiovascular mortality: A systematic review and dose-based meta-regression analysis of prospective studies2016Ingår i: Journal of Trace Elements in Medicine and Biology, ISSN 0946-672X, E-ISSN 1878-3252, Vol. 38, s. 64-73Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Although epidemiology studies have reported the relationship, including a dose-response relationship, between dietary magnesium intake and risk of cardiovascular disease (CVD), the risk for CVD mortality is inconclusive and the evidence for a dose-response relationship has not been summarized.

    Objective: We conducted a systematic review and meta-analysis of prospective studies to summarize the evidence regarding the association of dietary magnesium intake with risk of CVD mortality and describe their dose-response relationship.

    Design: We identified relevant studies by searching major scientific literature databases and grey literature resources from their inception to August 2015, and reviewed references lists of retrieved articles. We included population-based studies that reported mortality risks, i.e. relative risks (RRs), odds ratios (ORs) or hazard ratios (HRs) of CVD mortality or cause-specific CVD death. Linear dose-response relationships were assessed using random-effects meta-regression. Potential nonlinear associations were evaluated using restricted cubic splines.

    Results: Out of 3002 articles, 9 articles from 8 independent studies met the eligibility criteria. These studies comprised 449,748 individuals and 10,313 CVD deaths. Compared with the lowest dietary magnesium consumption group in the population, the risk of CVD mortality was reduced by 16% in women and 8% in men. No significant linear dose-response relationship was found between increment in dietary magnesium intake and CVD mortality across all the studies. After adjusting for age and BMI, the risk of CVD mortality was reduced by 24-25% per 100 mg/d increment in dietary magnesium intake in women of all the participants and in all the US participants.

    Conclusion: Although the combined data confirm the role of dietary magnesium intake in reducing CVD mortality, the dose-response relationship was only found among women and in US population.

  • 50.
    Fiore, Christopher
    et al.
    Center for Molecular Oncologic Pathology, Dana Farber Cancer Institute, Boston MA, USA; Brigham and Women’s Hospital, Harvard Medical School, Boston MA, USA.
    Bailey, Dyane
    Center for Molecular Oncologic Pathology, Dana Farber Cancer Institute, Boston MA, USA; Brigham and Women’s Hospital, Harvard Medical School, Boston MA, USA.
    Conlon, Niamh
    Department of Pathology, Trinity College, Dublin, Ireland.
    Wu, Xiaoqiu
    Center for Molecular Oncologic Pathology, Dana Farber Cancer Institute, Boston MA, USA; Brigham and Women’s Hospital, Harvard Medical School, Boston MA, USA.
    Martin, Neil
    Department of Radiation Oncology, Harvard Radiation Oncology Program, Boston MA, USA.
    Fiorentino, Michelangelo
    Center for Molecular Oncologic Pathology, Dana Farber Cancer Institute, Boston MA, USA; Brigham and Women’s Hospital, Harvard Medical School, Boston MA, USA; Pathology Unit, Addarii Institute, S Orsola-Malpighi Hospital, Bologna, Italy.
    Finn, Stephen
    Center for Molecular Oncologic Pathology, Dana Farber Cancer Institute, Boston MA, USA; Brigham and Women’s Hospital, Harvard Medical School, Boston MA, USA; Department of Pathology, Trinity College, Dublin, Ireland.
    Fall, Katja
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Harvard School of Public Health, Boston MA, USA.
    Andersson, Swen-Olof
    Harvard School of Public Health, Boston MA, USA.
    Andren, Ove
    Harvard School of Public Health, Boston MA, USA.
    Loda, Massimo
    Center for Molecular Oncologic Pathology, Dana Farber Cancer Institute, Boston MA, USA; Brigham and Women’s Hospital, Harvard Medical School, Boston MA, USA.
    Flavin, Richard
    Center for Molecular Oncologic Pathology, Dana Farber Cancer Institute, Boston MA, USA; Brigham and Women’s Hospital, Harvard Medical School, Boston MA, USA; Department of Pathology, Trinity College, Dublin, Ireland.
    Utility of multispectral imaging in automated quantitative scoring of immunohistochemistry2012Ingår i: Journal of Clinical Pathology, ISSN 0021-9746, E-ISSN 1472-4146, Vol. 65, nr 6, s. 496-502Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Automated scanning devices and image analysis software provide a means to overcome the limitations of manual semiquantitative scoring of immunohistochemistry. Common drawbacks to automated imaging systems include an inability to classify tissue type and an inability to segregate cytoplasmic and nuclear staining.

    Methods: Immunohistochemistry for the membranous marker a-catenin, the cytoplasmic marker stathmin and the nuclear marker Ki-67 was performed on tissue microarrays (TMA) of archival formalin-fixed paraffin-embedded tissue comprising 471 (alpha-catenin and stathmin) and 511 (Ki-67) cases of prostate adenocarcinoma. These TMA were quantitatively analysed using two commercially available automated image analysers, the Ariol SL-50 system and the Nuance system from CRi. Both systems use brightfield microscopy for automated, unbiased and standardised quantification of immunohistochemistry, while the Nuance system has spectral deconvolution capabilities. Results Overall concordance between scores from both systems was excellent (r=0.90; 0.83-0.95). The software associated with the multispectral imager allowed accurate automated classification of tissue type into epithelial glandular structures and stroma, and a single-step segmentation of staining into cytoplasmic or nuclear compartments allowing independent evaluation of these areas. The Nuance system, however, was not able to distinguish reliably between tumour and non-tumour tissue. In addition, variance in the labour and time required for analysis between the two systems was also noted.

    Conclusion: Despite limitations, this study suggests some beneficial role for the use of a multispectral imaging system in automated analysis of immunohistochemistry.

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