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  • 1.
    Andrén, Ove
    et al.
    Örebro University, School of Medical Sciences. Department of Urology, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Widmark, A.
    Department of Radiation Sciences, Oncology, Umeå University, Umeå, Sweden.
    Fält, A.
    Ulvskog, E.
    Örebro University, School of Medical Sciences. Department of Oncology, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Davidsson, Sabina
    Örebro University, School of Medical Sciences. Department of Urology, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Karlsson, C. Thellenberg
    Department of Radiation Sciences, Oncology, Umeå University, Umeå, Sweden.
    Hjälm-Eriksson, M.
    Department of Oncology, Karolinska Institute, Stockholm, Sweden.
    Cabazitaxel followed by androgen deprivation therapy (ADT) significantly improves time to progression in patients with newly diagnosed metastatic hormone sensitive prostate cancer (mHSPC): A randomized, open label, phase III, multicenter trial2017In: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 28, no Suppl. 5, article id 811PArticle in journal (Other academic)
  • 2.
    Discacciati, A.
    et al.
    Unit of Nutritional Epidemiology, Division of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Orsini, N.
    Unit of Nutritional Epidemiology, Division of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Andersson, Swen-Olof
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Andrén, Ove
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Örebro University Hospital. Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Johansson, Jan-Erik
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Mantzoros, C. S.
    Division of Endocrinology, Diabetes and Metabolism, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, United States; Section of Endocrinology, Boston VA Healthcare System, Harvard Medical School, Boston, United States.
    Wolk, A.
    Unit of Nutritional Epidemiology, Division of Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Coffee consumption and risk of localized, advanced and fatal prostate cancer: a population-based prospective study2013In: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 24, no 7, p. 1912-1918Article in journal (Refereed)
    Abstract [en]

    Background: The epidemiological evidence on possible relationships between coffee consumption and prostate cancer (PCa) risk by subtype of the disease (localized, advanced) and fatal PCa risk is limited.

    Materials and methods: A population-based cohort of 44 613 Swedish men aged 45-79 years was followed up from January 1998 through December 2010 for incidence of localized (n = 2368), advanced (n = 918) and fatal (n = 515) PCa. We assessed the associations between coffee consumption and localized, advanced and fatal PCa risk using competing-risk regressions. We examined possible effect modification by body mass index (BMI).

    Results: For localized PCa, each one cup increase in daily coffee consumption was associated with a 3% reduced risk [sub-hazard ratio (SHR) = 0.97, 95% confidence interval (CI) = 0.95-0.99]. For advanced and fatal PCa, we found a non-significant inverse association; each one cup increase was associated with a 2% reduced risk of advanced [SHR (95% CI) = 0.98 (0.95-1.02)] and fatal PCa [SHR (95% CI) = 0.98 (0.93-1.03)]. We observed evidence of effect modification by BMI for localized PCa (P-interaction = 0.03); the inverse association was stronger among overweight and obese men (BMI >= 25 kg/m(2)) compared with normal-weight men (BMI < 25 kg/m(2)).

    Conclusions: We observed a clear inverse association between coffee consumption and risk of localized PCa, especially among overweight and obese men.

  • 3.
    Klintman, M.
    et al.
    Div Oncol, Dept Clin Sci, Lund University, Lund, Sweden; Dept Oncol, Skåne University Hospital, Lund, Sweden.
    Nilsson, F.
    Dept Clin Sci, Div Surg, Umeå University, Umeå, Sweden.
    Bendahl, P. -O
    Ferno, M.
    Div Oncol, Dept Clin Sci, Lund University, Lund, Sweden.
    Liljegren, Göran
    Örebro University Hospital. Div Surg, Dept Clin Sci, Örebro University Hospital, Örebro, Sweden; Ctr Assessment Med Technol (CAMTÖ), Örebro University Hospital, Örebro, Sweden.
    Emdin, S.
    Dept Clin Sci, Div Surg, Umeå University, Umeå, Sweden; Umeå University Hospital, Umeå, Sweden.
    Malmstrom, P.
    Div Oncol, Dept Clin Sci, Lund University, Lund, Sweden; Dept Oncol, Skåne University Hospital, Lund, Sweden.
    Grp, Swedish Breast Cancer
    A prospective, multicenter validation study of a prognostic index composed of S-phase fraction, progesterone receptor status, and tumour size predicts survival in node-negative breast cancer patients: NNBC, the node-negative breast cancer trial2013In: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 24, no 9, p. 2284-2291Article in journal (Refereed)
    Abstract [en]

    In a retrospective study on node-negative breast cancer, a prognostic index consisting of a proliferation factor, S-phase fraction (SPF), progesterone receptor status (PR), and tumour size identified one-third of patients as high risk, with a sixfold increased risk of breast cancer death. This prospective multicenter cohort study was set up to validate the index. In 576 T1-2N0 patients < 60 years, prospective analyses of PR and SPF were carried out. High risk was defined as >= 2 of the following: size > 20 mm, PR-negativity, and high SPF (in the absence of SPF, Bloom-Richardson grade 3). Median follow-up was 17.8 years. Thirty-one percent were high risk. In univariate analysis, the index was prognostic for breast cancer-specific survival after 5 years [hazard ratio (HR) = 4.7, 95% confidence interval (95% CI) 2.5-8.9], 10 years (HR = 2.2, 95% CI 1.5-3.3), and 15 years (HR = 1.7, 95% CI 1.2-2.5), and remained significant after adjustment for adjuvant medical treatment and age. In the 37% of patients with no risk factors, only one patient died of breast cancer the first 5 years. This prospective study validates a prognostic index consisting of a proliferation factor, PR-status, and tumour size. The index may be helpful for prognostic considerations and for selection of patients in need of adjuvant therapy.

  • 4.
    Lu, Donghao
    et al.
    Karolinska Institutet, Stockholm, Sweden.
    Fall, Katja
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Sparen, P.
    Karolinska Institutet, Stockholm, Sweden.
    Ye, W.
    Karolinska Institutet, Stockholm, Sweden.
    Adami, H-O
    Karolinska Institutet, Stockholm, Sweden; Harvard University, Boston, USA .
    Valdimarsdottir, U.
    Harvard University, Boston, USA; University of Iceland, Reykjavík, Iceland .
    Fang, F.
    Karolinska Institutet, Stockholm, Sweden.
    Suicide and suicide attempt after a cancer diagnosis among young individuals2013In: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 24, no 12, p. 3112-3117Article in journal (Refereed)
    Abstract [en]

    Background: Data are scarce on the potential change in suicidal behavior among adolescents and young adults after receiving a cancer diagnosis.

    Patients and methods: We conducted a population-based cohort study including 7 860 629 Swedes at the age of >= 15 during 1987-2009. Among the cohort participants, 12 669 received a first diagnosis of primary cancer between the age of 15 and 30. We measured the relative risks (RRs) of suicidal behavior (defined as completed suicides or suicide attempts) after cancer diagnosis. We also carried out a case-crossover study nested within the cohort to adjust for unmeasured confounders.

    Results: Twenty-two completed suicides (versus 14 expected) and 136 suicide attempts (versus 80 expected) were identified among the cancer patients. The RR of suicidal behavior was 1.6 [ 95% confidence interval (CI), 1.4-1.9] after a cancer diagnosis, compared with cancer-free individuals. Risk increase was greatest immediately after diagnosis; the RR was 2.5 (95% CI 1.7-3.5) during the first year after diagnosis and was 1.5 (95% CI 1.2-1.8) thereafter. This pattern was similar for completed suicide and suicide attempts. The elevated risks were evident for majority of the main cancer types, except for cancer in thyroid, testis and melanoma. The case-crossover analysis of suicidal behavior during the first year after cancer diagnosis revealed similar results.

    Conclusions: Adolescents and young adults receiving a cancer diagnosis are at substantially increased risk of suicidal behavior, particularly during the first year after diagnosis. Although the absolute excess risk is modest, these findings emphasize the need to support and carefully monitor this vulnerable population.

  • 5.
    Matikas, A.
    et al.
    Oncol Pathol, Karolinska Inst, Stockholm, Sweden.
    Lovrot, J.
    Oncol Pathol, Karolinska Inst, Stockholm, Sweden.
    Ramberg, A.
    Clin Pathol & Cytol, Cent Hosp Karlstad, Karlstad, Sweden.
    Eriksson, M.
    Clin Pathol & Cytol, Cent Hosp Karlstad, Karlstad, Sweden.
    Lindsten, T.
    Clin Pathol & Cytol, Cent Hosp Karlstad, Karlstad, Sweden.
    Lekberg, T.
    Oncol Pathol, Karolinska Inst, Stockholm, Sweden.
    Hedenfalk, I.
    Oncol Pathol, Lund Univ, Lund, Sweden.
    Loman, N.
    Oncol Pathol, Lund Univ, Lund, Sweden.
    Bergh, J.
    Oncol Pathol, Karolinska Inst, Stockholm, Sweden.
    Erlandsson, Ann
    Örebro University, School of Medical Sciences.
    Hatschek, T.
    Oncol Pathol, Karolinska Inst, Stockholm, Sweden.
    Foukakis, T.
    Oncol Pathol, Karolinska Inst, Stockholm, Sweden.
    Immune function and response to neoadjuvant chemotherapy in hormone receptor positive, HER2-negative breast cancer2017In: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 28, no Suppl. 5, article id 219PArticle in journal (Other academic)
  • 6.
    Thomsen, F. B.
    et al.
    Copenhagen Prostate Cancer Center, Department of Urology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
    Brasso, K.
    Copenhagen Prostate Cancer Center, Department of Urology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
    Berg, K. D.
    Copenhagen Prostate Cancer Center, Department of Urology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
    Gerds, T. A.
    Department of Biostatistics, University of Copenhagen, Copenhagen, Denmark.
    Johansson, J-E
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Department of Urology, Faculty of Medicine and Health.
    Angelsen, A.
    Faculty of Medicine, Norwegian University of Technology and Science, Trondheim, Norway.
    Tammela, T. L. J.
    Department of Surgery, Tampere University Hospital and School of Medicine, University of Tampere, Tampere, Finland.
    Iversen, P.
    Copenhagen Prostate Cancer Center, Department of Urology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
    Association between PSA kinetics and cancer-specific mortality in patients with localised prostate cancer: analysis of the placebo arm of the SPCG-6 study2016In: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 27, no 3, p. 460-466Article in journal (Refereed)
    Abstract [en]

    Background: The prognostic value of prostate-specific antigen (PSA) kinetics in untreated prostate cancer (PCa) patients is debatable. We investigated the association between PSA doubling time (PSAdt), PSA velocity (PSAvel) and PSAvel risk count (PSAvRC) and PCa mortality in a cohort of patients with localised PCa managed on watchful waiting.

    Patients and methods: Patients with clinically localised PCa managed observationally, who were randomised to and remained on placebo for minimum 18 months in the SPCG-6 study, were included. All patients survived at least 2 years and had a minimum of three PSA determinations available. The prognostic value of PSA kinetics was analysed and patients were stratified according to their PSA at consent: ≤10, 10.1-25, and >25 ng/ml. Cumulative incidences of PCa-specific mortality were estimated with the Aalen-Johansen method.

    Results: Two hundred and sixty-three patients were included of which 116, 76 and 71 had a PSA at consent ≤10, 10.1-25, and >25 ng/ml, respectively. Median follow-up was 13.6 years. For patients with PSA at consent between 10.1 and 25 ng/ml, the 13-year risks of PCa mortality were associated with PSA kinetics: PSAdt ≤3 years: 62.0% versus PSAdt >3 years: 16.3% (Gray's test: P < 0.0001), PSAvel ≥2 ng/ml/year: 48.0% versus PSAvel <2 ng/ml/year: 11.0% (Gray's test: P = 0.0008), and PSAvRC 2: 45.0% versus 0-1: 3.8% (Gray's test: P = 0.001). In contrast, none of the PSA kinetics were significantly associated with changes of 13-year risks of PCa mortality in patients with PSA at consent ≤10 or >25 ng/ml.

    Conclusion: We found that magnitude changes in 13-year risks of PCa mortality that can be indicated by PSA kinetics depend on PSA level in patients with localised PCa who were managed observationally. Our results question PSA kinetics as surrogate marker for PCa mortality in patients with low and high PSA values.

  • 7.
    Vingeliene, Snieguole
    et al.
    Örebro University, School of Medical Sciences. Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK.
    Chan, Doris
    Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK.
    Vieira, Ana Rita
    Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK.
    Polemiti, Elli
    Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK.
    Stevens, Christophe A.T.
    Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK.
    Abar, Leila
    Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK.
    Navarro Rosenblatt, Deborah A.
    Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK.
    Greenwood, Darren C.
    Division of Biostatistics, University of Leeds, Leeds, UK.
    Norat, Teresa
    Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK.
    An update of the WCRF/AICR systematic literature review and meta-analysis on dietary and anthropometric factors and esophageal cancer risk2017In: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 28, no 10, p. 2409-2419Article, review/survey (Refereed)
    Abstract [en]

    Background: In the 2007 World Cancer Research Fund/American Institute for Cancer Research Second Expert Report, the expert panel judged that there was strong evidence that alcoholic drinks and body fatness increased esophageal cancer risk, whereas fruits and vegetables probably decreased its risk. The judgments were mainly based on case-control studies. As part of the Continuous Update Project, we updated the scientific evidence accumulated from cohort studies in this topic.

    Methods: We updated the Continuous Update Project database up to 10 January 2017 by searching in PubMed and conducted dose-response meta-analyses to estimate summary relative risks (RRs) and 95% confidence intervals (CIs) using random effects model.

    Results: A total of 57 cohort studies were included in 13 meta-analyses. Esophageal adenocarcinoma risk was inversely related to vegetable intake (RR per 100 g/day: 0.89, 95% CI: 0.80-0.99, n = 3) and directly associated with body mass index (RR per 5 kg/m2: 1.47, 95% CI: 1.34-1.61, n = 9). For esophageal squamous cell carcinoma, inverse associations were observed with fruit intake (RR for 100 g/day increment: 0.84, 95% CI: 0.75-0.94, n = 3) and body mass index (RR for 5 kg/m2 increment: 0.64, 95% CI: 0.56-0.73, n = 8), and direct associations with intakes of processed meats (RR for 50 g/day increment: 1.59, 95% CI: 1.11-2.28, n = 3), processed and red meats (RR for 100 g/day increment: 1.37, 95% CI: 1.04-1.82, n = 3) and alcohol (RR for 10 g/day increment: 1.25, 95% CI: 1.12-1.41, n = 6).

    Conclusions: Evidence from cohort studies suggested a protective role of vegetables and body weight control in esophageal adenocarcinomas development. For squamous cell carcinomas, higher intakes of red and processed meats and alcohol may increase the risk, whereas fruits intake may play a protective role.

  • 8.
    Wengström, Yvonne
    et al.
    Karolinska Inst, European Oncol Nursing Soc, Stockholm, Sweden.
    Costa, Alberto
    European Sch Oncol, Milan, Italy.
    Koedam, Jan
    Novartis, Oncology, Arnhem, The Netherlands.
    Georgiou, Vasoulla
    Adelphi International, Research, Bollington, United Kingdom.
    Women's experience and knowledge of adjuvant endocrine therapy (AET) for early breast cancer (BC): a European survey2006In: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 17, p. 99-99Article in journal (Refereed)
  • 9.
    Zhu, Jianwei
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fang, Fang
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Sjölander, Arvid
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fall, Katja
    Örebro University, School of Medical Sciences. 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 T.H. Chan School of Public Health, Boston, USA; Clinical Effectiveness Research Group, Institute of Health and Society, University of Oslo, Oslo, Norway .
    Valdimarsdottir, Unnur Anna
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, USA; Center of Public Health Sciences, School of Health Sciences, Faculty of Medicine, University of Iceland, Reykjavík, Iceland.
    First-onset mental disorders after cancer diagnosis and cancer-specific mortality: a nationwide cohort study2017In: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 28, no 8, p. 1964-1969Article in journal (Refereed)
    Abstract [en]

    Background: The diagnosis of cancer is strongly associated with the risk of mental disorders even in patients with no previous history of mental disorders. Accumulating data suggest that mental distress may accelerate tumor progression. We hypothesized therefore that mental disorders after a cancer diagnosis may increase the risk of cancer-specific mortality.

    Patients and methods: We conducted a nationwide cohort study including 244 261 cancer patients diagnosed in Sweden during 2004-2009 and followed them through 2010. Through the Swedish Patient Register, we obtained clinical diagnoses of all mental disorders and focused on mood-, anxiety-, and substance abuse disorders (ICD10: F10-F16, F18-F19, F32-F33, F40-F41, and F43-45) that are commonly diagnosed among patients with cancer. We further classified the studied mental disorders into first-onset or recurrent mental disorders. We used Cox regression to estimate multivariable hazard ratios (HRs) with 95% confidence intervals (CIs) as a measure of the association between mental disorders after cancer diagnosis and cancer-specific mortality, adjusting for age, sex, calendar period, educational level, cancer stage, and cancer type at diagnosis.

    Results: After cancer diagnosis, 11 457 patients were diagnosed with mood-, anxiety-, and substance abuse disorders; of which 7236 were first-onset mental disorders. Patients with a first-onset mental disorder were at increased risk of cancer-specific mortality (HR: 1.82, 95% CI: 1.71-1.92) while patients with a recurrent mental disorder had much lower risk elevation (HR: 1.14, 95% CI: 1.05-1.24). The increased cancer-specific mortality by first-onset mental disorders was observed for almost all cancer sites/groups and the association was stronger for localized cancers (HR: 2.00, 95% CI: 1.73-2.31) than for advanced cancers (HR: 1.49, 95% CI: 1.32-1.69).

    Conclusions: Patients with a first-onset common mood-, anxiety-, or substance abuse disorder after cancer diagnosis may be at increased risk of cancer-specific death.

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