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  • 1.
    Chen, Jie
    et al.
    Stockholm University, Faculty of Science, Department of Physical Geography.
    Rodopoulou, Sophia
    Strak, Maciej
    de Hoogh, Kees
    Taj, Tahir
    Poulsen, Aslak Harbo
    Andersen, Zorana J.
    Bellander, Tom
    Brandt, Jørgen
    Zitt, Emanuel
    Fecht, Daniela
    Forastiere, Francesco
    Gulliver, John
    Hertel, Ole
    Hoffmann, Barbara
    Hvidtfeldt, Ulla Arthur
    Verschuren, W. M. Monique
    Jørgensen, Jeanette T.
    Katsouyanni, Klea
    Ketzel, Matthias
    Lager, Anton C. J.
    Stockholm University, Faculty of Social Sciences, The Swedish Institute for Social Research (SOFI). Stockholm University, Faculty of Social Sciences, Aging Research Center (ARC), (together with KI).
    Leander, Karin
    Liu, Shuo
    Ljungman, Petter
    Severi, Gianluca
    Boutron-Ruault, Marie-Christine
    Magnusson, Patrik K. E.
    Nagel, Gabriele
    Pershagen, Göran
    Peters, Annette
    Rizzuto, Debora
    Stockholm University, Faculty of Social Sciences, Aging Research Center (ARC), (together with KI). Karolinska Institutet, Sweden; Stockholm Gerontology Research Center, Sweden.
    van der Schouw, Yvonne T.
    Samoli, Evangelia
    Sørensen, Mette
    Stafoggia, Massimo
    Tjønneland, Anne
    Weinmayr, Gudrun
    Wolf, Kathrin
    Brunekreef, Bert
    Raaschou-Nielsen, Ole
    Hoek, Gerard
    Long-term exposure to ambient air pollution and bladder cancer incidence in a pooled European cohort: the ELAPSE project2022In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 126, no 10, p. 1499-1507Article in journal (Refereed)
    Abstract [en]

    Background: The evidence linking ambient air pollution to bladder cancer is limited and mixed.

    Methods: We assessed the associations of bladder cancer incidence with residential exposure to fine particles (PM2.5), nitrogen dioxide (NO2), black carbon (BC), warm season ozone (O3) and eight PM2.5 elemental components (copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc) in a pooled cohort (N = 302,493). Exposures were primarily assessed based on 2010 measurements and back-extrapolated to the baseline years. We applied Cox proportional hazard models adjusting for individual- and area-level potential confounders.

    Results: During an average of 18.2 years follow-up, 967 bladder cancer cases occurred. We observed a positive though statistically non-significant association between PM2.5 and bladder cancer incidence. Hazard Ratios (HR) were 1.09 (95% confidence interval (CI): 0.93–1.27) per 5 µg/m3 for 2010 exposure and 1.06 (95% CI: 0.99–1.14) for baseline exposure. Effect estimates for NO2, BC and O3 were close to unity. A positive association was observed with PM2.5 zinc (HR 1.08; 95% CI: 1.00–1.16 per 10 ng/m3).

    Conclusions: We found suggestive evidence of an association between long-term PM2.5 mass exposure and bladder cancer, strengthening the evidence from the few previous studies. The association with zinc in PM2.5 suggests the importance of industrial emissions.

  • 2. Dahlman, I
    et al.
    Mejhert, N
    Linder, K
    Agustsson, T
    Mutch, D M
    Kulyte, A
    Isaksson, B
    Permert, J
    Petrovic, Natasa
    Stockholm University, Faculty of Science, The Wenner-Gren Institute , Physiology.
    Nedergaard, Jan
    Stockholm University, Faculty of Science, The Wenner-Gren Institute , Physiology.
    Sjölin, E
    Brodin, D
    Clement, K
    Dahlman-Wright, K
    Rydén, M
    Arner, P
    Adipose tissue pathways involved in weight loss of cancer cachexia2010In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 102, no 10, p. 1541-8Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The regulatory gene pathways that accompany loss of adipose tissue in cancer cachexia are unknown and were explored using pangenomic transcriptome profiling. METHODS: Global gene expression profiles of abdominal subcutaneous adipose tissue were studied in gastrointestinal cancer patients with (n=13) or without (n=14) cachexia. RESULTS: Cachexia was accompanied by preferential loss of adipose tissue and decreased fat cell volume, but not number. Adipose tissue pathways regulating energy turnover were upregulated, whereas genes in pathways related to cell and tissue structure (cellular adhesion, extracellular matrix and actin cytoskeleton) were downregulated in cachectic patients. Transcriptional response elements for hepatic nuclear factor-4 (HNF4) were overrepresented in the promoters of extracellular matrix and adhesion molecule genes, and adipose HNF4 mRNA was downregulated in cachexia. CONCLUSIONS: Cancer cachexia is characterised by preferential loss of adipose tissue; muscle mass is less affected. Loss of adipose tissue is secondary to a decrease in adipocyte lipid content and associates with changes in the expression of genes that regulate energy turnover, cytoskeleton and extracellular matrix, which suggest high tissue remodelling. Changes in gene expression in cachexia are reciprocal to those observed in obesity, suggesting that regulation of fat mass at least partly corresponds to two sides of the same coin.

  • 3. Heikkila, Katriina
    et al.
    Nyberg, Solja T.
    Madsen, Ida E. H.
    de Vroome, Ernest
    Alfredsson, Lars
    Bjorner, Jacob J.
    Borritz, Marianne
    Burr, Hermann
    Erbel, Raimund
    Ferrie, Jane E.
    Fransson, Eleonor I.
    Geuskens, Goedele A.
    Hooftman, Wendela E.
    Houtman, Irene L.
    Jöckel, Karl-Heinz
    Knutsson, Anders
    Koskenvuo, Markku
    Lunau, Thorsten
    Nielsen, Martin L.
    Nordin, Maria
    Oksanen, Tuula
    Pejtersen, Jan H.
    Pentti, Jaana
    Shipley, Martin J.
    Steptoe, Andrew
    Suominen, Sakari B.
    Theorell, Töres
    Stockholm University, Faculty of Social Sciences, Stress Research Institute.
    Vahtera, Jussi
    Westerholm, Peter J. M.
    Westerlund, Hugo
    Stockholm University, Faculty of Social Sciences, Stress Research Institute.
    Dragano, Nico
    Rugulies, Reiner
    Kawachi, Ichiro
    Batty, G. David
    Singh-Manoux, Archana
    Virtanen, Marianna
    Kivimäki, Mika
    Long working hours and cancer risk: a multi-cohort study2016In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 114, p. 813-818Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Working longer than the maximum recommended hours is associated with an increased risk of cardiovascular disease, but the relationship of excess working hours with incident cancer is unclear.

    METHODS: This multi-cohort study examined the association between working hours and cancer risk in 116 462 men and women who were free of cancer at baseline. Incident cancers were ascertained from national cancer, hospitalisation and death registers; weekly working hours were self-reported.

    RESULTS: During median follow-up of 10.8 years, 4371 participants developed cancer (n colorectal cancer: 393; n lung cancer: 247; n breast cancer: 833; and n prostate cancer: 534). We found no clear evidence for an association between working hours and the overall cancer risk. Working hours were also unrelated the risk of incident colorectal, lung or prostate cancers. Working ⩾55 h per week was associated with 1.60-fold (95% confidence interval 1.12-2.29) increase in female breast cancer risk independently of age, socioeconomic position, shift- and night-time work and lifestyle factors, but this observation may have been influenced by residual confounding from parity.

    CONCLUSIONS: Our findings suggest that working long hours is unrelated to the overall cancer risk or the risk of lung, colorectal or prostate cancers. The observed association with breast cancer would warrant further research.

  • 4. Mogensen, Hanna
    et al.
    Tettamanti, Giorgio
    Elmerdahl Frederiksen, Line
    Talbäck, Mats
    Härkönen, Juho
    Stockholm University, Faculty of Social Sciences, Department of Sociology. European University Institute, Italy.
    Modig, Karin
    Pedersen, Camilla
    Krøyer, Anja
    Hirvonen, Elli
    Kyrönlahti, Anniina
    Heyman, Mats
    Sällfors Holmqvist, Anna
    Hasle, Henrik
    Madanat-Harjuoja, Laura
    Malila, Nea
    Falck Winther, Jeanette
    Erdmann, Friederike
    Feychting, Maria
    Educational attainment in survivors of childhood cancer in Denmark, Finland, and Sweden2024In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 130, no 2, p. 260-268Article in journal (Refereed)
    Abstract [en]

    Background: Survivors of childhood cancer may face difficulties at school. We investigated whether childhood cancer affects attainment of upper secondary education, in a register-based cohort study from Denmark, Finland, and Sweden, where we limit bias from selection and participation.

    Methods: From the national cancer registers, we identified all long-term survivors of childhood cancer diagnosed aged 0–14 years in 1971–2005 (n = 7629), compared them to matched population comparisons (n = 35,411) and siblings (n = 6114), using odds ratios (OR) and 95% confidence intervals (CI).

    Results: Overall, 6127 survivors (80%) had attained upper secondary education by age 25, compared to 84% among comparison groups. Elevated OR for not attaining this level were mainly confined to survivors of central nervous system (CNS) tumours (ORSurv_PopComp2.05, 95%CI: 1.83–2.29). Other risk groups were survivors who had spent more time in hospital around cancer diagnosis and those who had hospital contacts in early adulthood, particularly psychiatric. Survivors of all cancer types were less likely to have attained upper secondary education without delay.

    Conclusions: Although survivors of childhood cancer experienced delays in their education, many had caught up by age 25. Except for survivors of CNS tumours, survivors attained upper secondary education to almost the same extent as their peers.

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