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  • 51.
    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 immunohistochemistry2012Inngår i: Journal of Clinical Pathology, ISSN 0021-9746, E-ISSN 1472-4146, Vol. 65, nr 6, s. 496-502Artikkel i tidsskrift (Fagfellevurdert)
    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.

  • 52. Fiorentino, M.
    et al.
    Mucci, L.
    Fall, Katja
    Bailey, D.
    Fiore, C.
    Judson, G.
    Andrén, Ove
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Andersson, Swen-Olof
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Loda, M.
    Immunohistochemical Expression of BRCA1 in Prostate Cancer2009Inngår i: Laboratory Investigation, ISSN 0023-6837, E-ISSN 1530-0307, Vol. 89, s. 169A-169A, artikkel-id 760Artikkel i tidsskrift (Annet vitenskapelig)
    Abstract [en]

    Background: BRCA1 is a multifunctional protein involved in DNA repair, gene transcription and the regulation of cell-cycle check-points. While germline mutations of BRCA1 are rare in prostate cancer and seem to play a limited role in tumor susceptibility, BRCA1 expression has not been investigated to date.

    Design: We analyzed the immunohistochemical expression of BRCA1 in paraffin embedded samples from 524 men with prostate cancer belonging to the Physicians’ Health Study and the Swedish Watchful Waiting cohorts of prostate cancer patients. High density tissue micro-arrays (TMA) including at least three tumor cores for each case were utilized for the immunohistochemical staining with the monoclonal MS110 antibody specific for the N-terminus of the 220 kDa BRCA1 protein. Cases were scored as negative or positive for BRCA1 immunostaining. The Ki67 proliferation index was also assessed on the same TMAs and evaluated by quantitative image analysis.

    Results: A positive nuclear immunostaining for BRCA1 was revealed in 62 of 524 (11.9%) patients while normal prostate control cores were all negative. BRCA1 positive tumors were associated with 4 times greater proliferation rate compared to BRCA1 negative tumors (p ∼ 0.0003). In addition, we found a linear trend such that tumors with greater number of TMA cores expressing BRCA1 had stronger extent of proliferation. Men with BRCA1 positive tumors had a slightly higher Gleason’s score (mean 7.5) compared to those negative for BRCA1 (mean 7) No significant correlation was found between BRCA1 staining and cancer-specific death.

    Conclusions: BRCA1 protein is expressed in a small subset of prostate cancers characterized by high proliferation index but not in normal prostate tissue. Expression of BRCA1 might be acquired in selected tumors to prevent DNA damage in actively replicating cells. A different role independent of germline mutations might be disclosed for BRCA1 as cell cycle regulator in prostate cancer.

  • 53. Fiorentino, M.
    et al.
    Mucci, L.
    Fall, Katja
    Bailey, D.
    Fiore, C.
    Judson, G.
    Andrén, Ove
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Andersson, Swen-Olof
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Loda, M.
    Immunohistochemical Expression of BRCA1 in Prostate Cancer2009Inngår i: Modern Pathology, ISSN 0893-3952, E-ISSN 1530-0285, Vol. 22, s. 169A-169A, artikkel-id 760Artikkel i tidsskrift (Annet vitenskapelig)
    Abstract [en]

    Background: BRCA1 is a multifunctional protein involved in DNA repair, gene transcription and the regulation of cell-cycle check-points. While germline mutations of BRCA1 are rare in prostate cancer and seem to play a limited role in tumor susceptibility, BRCA1 expression has not been investigated to date.

    Design: We analyzed the immunohistochemical expression of BRCA1 in paraffin embedded samples from 524 men with prostate cancer belonging to the Physicians’ Health Study and the Swedish Watchful Waiting cohorts of prostate cancer patients. High density tissue micro-arrays (TMA) including at least three tumor cores for each case were utilized for the immunohistochemical staining with the monoclonal MS110 antibody specific for the N-terminus of the 220 kDa BRCA1 protein. Cases were scored as negative or positive for BRCA1 immunostaining. The Ki67 proliferation index was also assessed on the same TMAs and evaluated by quantitative image analysis.

    Results: A positive nuclear immunostaining for BRCA1 was revealed in 62 of 524 (11.9%) patients while normal prostate control cores were all negative. BRCA1 positive tumors were associated with 4 times greater proliferation rate compared to BRCA1 negative tumors (p ∼ 0.0003). In addition, we found a linear trend such that tumors with greater number of TMA cores expressing BRCA1 had stronger extent of proliferation. Men with BRCA1 positive tumors had a slightly higher Gleason’s score (mean 7.5) compared to those negative for BRCA1 (mean 7) No significant correlation was found between BRCA1 staining and cancer-specific death.

    Conclusions: BRCA1 protein is expressed in a small subset of prostate cancers characterized by high proliferation index but not in normal prostate tissue. Expression of BRCA1 might be acquired in selected tumors to prevent DNA damage in actively replicating cells. A different role independent of germline mutations might be disclosed for BRCA1 as cell cycle regulator in prostate canc

  • 54.
    Fiorentino, Michelangelo
    et al.
    Department of Pathology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, USA.
    Judson, Gregory
    Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, USA; Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Penney, Kathryn
    Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, USA; Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Flavin, Richard
    Department of Pathology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, USA.
    Stark, Jennifer
    Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, USA; Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Fiore, Christopher
    Department of Pathology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, USA.
    Fall, Katja
    Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, USA; Department of Epidemiology, Harvard School of Public Health, Boston, USA; Uppsala University Hospital, Uppsala, Sweden.
    Martin, Neil
    Department of Epidemiology, Harvard School of Public Health, Boston, USA; Radiation Oncology, Brigham and Women's Hospital, Boston, USA.
    Ma, Jing
    Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, USA.
    Sinnott, Jennifer
    Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, USA; Department of Biostatistics, Harvard School of Public Health, Boston, USA.
    Giovannucci, Edward
    Department of Medicine, Brigham and Women's Hospital, 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.
    Stampfer, Meir
    Department of Medicine, Brigham and Women's Hospital, 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.
    Sesso, Howard D.
    Department of Epidemiology, Harvard School of Public Health, Boston, USA; Division of Preventive Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, USA.
    Kantoff, Philip W.
    Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, USA; Broad Institute, Cambridge, USA.
    Finn, Stephen
    Department of Pathology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, USA.
    Loda, Massimo
    Department of Pathology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, USA; Broad Institute, Cambridge, USA.
    Mucci, Lorelei
    Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, USA; Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Immunohistochemical expression of BRCA1 and lethal prostate cancer2010Inngår i: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 70, nr 8, s. 3136-9Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BRCA1 functions as a tumor suppressor; recent work suggests that BRCA1 may also induce cell cycle arrest to allow for DNA repair. We hypothesized that BRCA1 expression in prostate tumor tissue may be associated with prostate cancer progression through regulation of the cell cycle. We used immunohistochemistry to evaluate BRCA1 protein expression in archival tumor samples from 393 prostate cancer cases in the Physicians' Health Study. The men were followed prospectively from diagnosis to development of metastases and mortality. Fifteen percent of tumors stained positive for BRCA1. BRCA1-positive tumors had substantially increased tumor proliferation index compared with negative tumors (47.0 Ki67-positive nuclei versus 10.3, P = 0.0016) and were more likely to develop lethal cancer compared with BRCA1-negative tumors (hazard ratio, 4.6; 95% confidence interval, 2.4-8.7). These findings strengthen the hypothesis that BRCA1 plays a role in cell cycle control and show that BRCA1 is a marker of clinical prostate cancer prognosis. Cancer Res; 70(8); 3136-9. (c)2010 AACR.

  • 55.
    Flavin, Richard
    et al.
    Center for Molecular Oncologic Pathology, Dana Farber Cancer Institute, Boston, USA; Departments of Medical Oncology, Dana Farber Cancer Institute, Boston, USA.
    Pettersson, Andreas
    Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, USA; Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Hendrickson, Whitney K.
    Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, USA; Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Fiorentino, Michelangelo
    Center for Molecular Oncologic Pathology, Dana Farber Cancer Institute, Boston, USA.
    Finn, Stephen
    Center for Molecular Oncologic Pathology, Dana Farber Cancer Institute, Boston, USA; Department of Histopathology, St. James's Hospital, Trinity College Dublin Medical School, Dublin, Ireland.
    Kunz, Lauren
    Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, USA; Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Judson, Gregory L.
    Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, USA; Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Lis, Rosina
    Center for Molecular Oncologic Pathology, Dana Farber Cancer Institute, Boston, USA.
    Bailey, Dyane
    Center for Molecular Oncologic Pathology, Dana Farber Cancer Institute, Boston, USA.
    Fiore, Christopher
    Center for Molecular Oncologic Pathology, Dana Farber Cancer Institute, Boston, USA.
    Nuttall, Elizabeth
    Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, USA; Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Martin, Neil E.
    Departments of Radiation Oncology, Dana Farber Cancer Institute, Boston, USA.
    Stack, Edward
    Center for Molecular Oncologic Pathology, Dana Farber Cancer Institute, Boston, USA.
    Penney, Kathryn L.
    Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, USA; Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Rider, Jennifer R.
    Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, USA; Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Sinnott, Jennifer
    Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, USA; Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Sweeney, Christopher
    Departments of Medical Oncology, Dana Farber Cancer Institute, Boston, USA.
    Sesso, Howard D
    Division of Preventive Medicine, Brigham and Women's Hospital, Boston, USA.
    Fall, Katja
    Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, USA; Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Giovannucci, Edward
    Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, USA; Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Kantoff, Philip
    Departments of Medical Oncology, Dana Farber Cancer Institute, Boston, USA.
    Stampfer, Meir
    Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, USA; Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Loda, Massimo
    Center for Molecular Oncologic Pathology, Dana Farber Cancer Institute, Boston, USA; Departments of Medical Oncology, Dana Farber Cancer Institute, Boston, USA.
    Mucci, Lorelei A.
    Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, USA; Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    SPINK1 protein expression and prostate cancer progression2014Inngår i: Clinical Cancer Research, ISSN 1078-0432, E-ISSN 1557-3265, Vol. 20, nr 18, s. 4904-11Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Purpose: SPINK1 overexpression has been described in prostate cancer and is linked with poor prognosis in many cancers. The objective of this study was to characterize the association between SPINK1 overexpression and prostate cancer-specific survival.

    Experimental design: The study included 879 participants in the U.S. Physicians' Health Study and Health Professionals Follow-Up Study, diagnosed with prostate cancer (1983-2004) and treated by radical prostatectomy. Protein tumor expression of SPINK1 was evaluated by immunohistochemistry on tumor tissue microarrays.

    Results: Seventy-four of 879 (8%) prostate cancer tumors were SPINK1 positive. Immunohistochemical data were available for PTEN, p-Akt, pS6, stathmin, androgen receptor (AR), and ERG (as a measure of the TMPRSS2:ERG translocation). Compared with SPINK1-negative tumors, SPINK1-positive tumors showed higher PTEN and stathmin expression, and lower expression of AR (P < 0.01). SPINK1 overexpression was seen in 47 of 427 (11%) ERG-negative samples and in 19 of 427 (4%) ERG-positive cases (P = 0.0003). We found no significant associations between SPINK1 status and Gleason grade or tumor stage. There was no association between SPINK1 expression and biochemical recurrence (P = 0.56). Moreover, there was no association between SPINK1 expression and prostate cancer mortality (there were 75 lethal cases of prostate cancer during a mean of 13.5 years follow-up; HR = 0.71; 95% confidence interval, 0.29-1.76).

    Conclusions: Our results suggest that SPINK1 protein expression may not be a predictor of recurrence or lethal prostate cancer amongst men treated by radical prostatectomy. SPINK1 and ERG protein expression do not seem to be entirely mutually exclusive, as some previous studies have suggested.

  • 56.
    Hiyoshi, Ayako
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Bergh, Cecilia
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län.
    Montgomery, Scott
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. Clinical Epidemiology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology and Public Health, University College London, London, United Kingdom.
    Comorbidity trajectories in working age cancer survivors: A national study of Swedish men2017Inngår i: Cancer Epidemiology, ISSN 1877-7821, E-ISSN 1877-783X, Vol. 48, s. 48-55, artikkel-id S1877-7821(17)30039-5Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: A large proportion of cancer survivors are of working age, and maintaining health is of interest both for their working and private life. However, patterns and determinants of comorbidity over time among adult cancer survivors are incompletely described. We aimed to identify distinct comorbidity trajectories and their potential determinants.

    METHODS: In a cohort study of Swedish men born between 1952 and 1956, men diagnosed with cancer between 2000 and 2003 (n=878) were matched with cancer-free men (n=4340) and followed over five years after their first year of survival. Comorbid diseases were identified using hospital diagnoses and included in the analysis using group-based trajectory modelling. The association of socioeconomic and developmental characteristics were assessed using multinomial logit models.

    RESULTS: Four distinct comorbidity trajectories were identified. As many as 84% of cancer survivors remained at very low levels of comorbidity, and the distribution of trajectories was similar among the cancer survivors and the cancer-free men. Increases in comorbidity were seen among those who had comorbid disease at baseline and among those with poor summary disease scores in adolescence. Socioeconomic characteristics and physical, cognitive and psychological function were associated with types of trajectory in unadjusted models but did not retain independent relationships with them after simultaneous adjustment.

    CONCLUSIONS: Among working-age male cancer survivors, the majority remained free or had very low levels of comorbidity. Those with poorer health in adolescence and pre-existing comorbid diseases at cancer diagnosis may, however, benefit from follow-up to prevent further increases in comorbidity.

    Fulltekst (pdf)
    Comorbidity trajectories in working age cancer survivors: a national study of Swedish men
  • 57.
    Hiyoshi, Ayako
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Fall, Katja
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Netuveli, G.
    International Centre for Life Course Studies in Society and Health, University College London, London, United Kingdom: Institute for Health and Human Development (IHHD), University of East London, London, United Kingdom.
    Montgomery, Scott
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Clinical Epidemiology Unit, Department of Medicine, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology and Public Health, University College London, London, United Kingdom.
    Remarriage after divorce and depression risk2015Inngår i: Social Science and Medicine, ISSN 0277-9536, E-ISSN 1873-5347, Vol. 141, s. 109-114Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    As marriage is associated with lower depression rates compared with being single in men, we aimed to examine if remarriage compared with remaining divorced is also associated with a reduced depression risk. Swedish register data were used to define a cohort of men who were born between 1952 and 1956 and underwent a compulsory military conscription assessment in adolescence. This study population comprised men who were divorced in 1985 (n = 72,246). The risk of pharmaceutically treated depression from 2005 to 2009 was compared for those who remarried or remained divorced between 1986 and 2004. Cox proportional hazards analysis was used to estimate hazard ratios for the risk of depression identified by pharmaceutical treatment, with adjustment for a range of potential confounding factors including childhood and adulthood socioeconomic circumstances, cognitive, physical, psychological and medical characteristics at the conscription assessment. The results showed that, even though divorced men who remarried had markers of lower depression risk in earlier life such as higher cognitive and physical function, higher stress resilience and socioeconomic advantages than men who remained divorced, remarriage was associated with a statistically significant elevated risk of depression with an adjusted hazard ratio (and 95% confidence interval) of 1.27(1.03 1.55), compared with men who remained divorced. Remarriage following divorce is not associated with a reduced risk of depression identified by pharmaceutical treatment, compared with remaining divorced. Interpersonal or financial difficulties resulting from remarriage may outweigh the benefits of marriage in terms of depression risk.

  • 58.
    Hiyoshi, Ayako
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Udumyan, Ruzan
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Osika, Walter
    Center for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden; Centre for Social Sustainability (CSS), Department of Neurobiology, Care Sciences and Society, Karolinska Institute Huddinge, Stocholm, Sweden.
    Bihagen, Erik
    Swedish Institute for Social Research (SOFI), Stockholm University, Stockholm, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Clinical Epidemiology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
    Montgomery, Scott
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Clinical Epidemiology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology and Public Health, University College London, London, United Kingdom.
    Stress resilience in adolescence and subsequent antidepressant and anxiolytic medication in middle aged men: Swedish cohort study2015Inngår i: Social Science and Medicine, ISSN 0277-9536, E-ISSN 1873-5347, Vol. 134, s. 43-49Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    It is unclear whether psychological resilience to stress in adolescence represents a persistent characteristic relevant to the subsequent risk for depression and anxiety in later adulthood. We aimed to test whether low psychological stress resilience assessed in adolescence is associated with an increased risk of receiving medication for depression and anxiety in middle age. We utilized Swedish register-based cohort study. Men born between 1952 and 1956 (n = 175,699), who underwent compulsory assessment for military conscription in late adolescence were followed to examine subsequent risk of pharmaceutically-treated depression and anxiety in middle age, from 2006 to 2009 corresponding to ages between 50 and 58 years, using Cox regression. The associations of stress resilience with prescription of antidepressant and anxiolytics medication through potential mediating factors cognitive and physical function and adult socioeconomic factors were calculated. Low stress resilience was associated with elevated risks for antidepressant (hazard ratio (HR):1.5 (95% CI 1.4 1.6)) and anxiolytics (HR:2.4 (CI 2.0 2.7)) medication. Adjustment for measures of childhood living circumstances attenuated the associations somewhat. Around a third of association with low stress resilience, and a half of that with moderate resilience, was mediated through cognitive and physical function in adolescence and adult socioeconomic factors. The magnitude of the inverse association of higher cognitive function with antidepressant medication was eliminated among those with low stress resilience. These results indicate that low stress resilience in adolescence is associated with an increased risk for antidepressant and anxiolytics medication over 30 years later, in part mediated through developmental factors in adolescence and socioeconomic circumstances in adulthood, and low stress resilience can diminish or eliminate the inverse association of higher cognitive function with antidepressant medication.

  • 59. Huang, Jiaqi
    et al.
    Valdimarsdttir, Unnur
    Fall, Katja
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Ye, Weimin
    Fang, Fang
    Pancreatic cancer risk after loss of a child: a register-based study in Sweden during 1991-20092013Inngår i: American Journal of Epidemiology, ISSN 0002-9262, E-ISSN 1476-6256, Vol. 178, nr 4, s. 582-589Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The potential role of psychological stress in pancreatic cancer has rarely been investigated in epidemiologic studies. During 1991-2009, we conducted a nested case-control study based on Swedish national population and health registers to investigate whether severe psychological stress induced by the death of a child was associated with subsequent risk of pancreatic cancer. The study included 16,522 cases and 82,107 controls who were matched to the cases on sex and year of birth. Conditional logistic regression was used to estimate odds ratios and 95% confidence intervals. Overall, loss of a child was associated with an odds ratio of 1.09 for pancreatic cancer (95% confidence interval (CI): 1.02, 1.17). The risk elevation was mainly seen during the first 5 years after the loss (odds ratio (OR) = 1.27, 95% CI: 1.12, 1.45) and for loss of a child due to suicide (OR = 1.23, 95% CI: 1.03, 1.46). The association was statistically significant among women but not among men, and it appeared stronger for early-onset pancreatic cancer. Persons with a history of psychiatric illness had the greatest risk increase after child loss (OR = 1.43, 95% CI: 1.17, 1.76). Although other explanations are possible, our findings provide some evidence that psychological stress may be associated with pancreatic cancer.

  • 60.
    Hálfdánarson, Óskar Ö.
    et al.
    Centre of Public Health Sciences, Faculty of Medicine, University of Iceland, Reykjavík, Iceland.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper. Clinical Epidemiology and Biostatistics, School of Medical Sciences, Örebro University, Örebro, Sweden; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Ogmundsdottir, Margret H.
    Department of Biochemistry and Molecular Biology, BioMedical Center, Faculty of Medicine, University of Iceland, Reykjavik, Iceland.
    Lund, Sigrún H.
    Centre of Public Health Sciences, Faculty of Medicine, University of Iceland, Reykjavík, Iceland.
    Steingrímsson, Eiríkur
    Department of Biochemistry and Molecular Biology, BioMedical Center, Faculty of Medicine, University of Iceland, Reykjavik, Iceland.
    Ogmundsdottir, Helga M.
    Cancer Research Laboratory, BioMedical Center, Faculty of Medicine, University of Iceland, Reykjavik, Iceland.
    Zoega, Helga
    Centre of Public Health Sciences, Faculty of Medicine, University of Iceland, Reykjavík, Iceland; Medicines Policy Research Unit, Centre for Big Data Research in Health, University of New South Wales, Sydney, Australia.
    Proton pump inhibitor use and risk of breast cancer, prostate cancer, and malignant melanoma: An Icelandic population-based case-control study2019Inngår i: Pharmacoepidemiology and Drug Safety, ISSN 1053-8569, E-ISSN 1099-1557, Vol. 28, nr 4, s. 471-478Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Purpose: Increased expression of Vacuolar-type H+ ATPases (V-ATPases), in the plasma membrane of cancer cells has been suggested to contribute to the development of aggressive cancer phenotypes by promoting acidic tumor microenvironments. Accumulating data suggest that proton pump inhibitors (PPIs) may elicit a chemopreventive effect via V-ATPase inhibition in some cancers, but evidence is still limited. Therefore, we aimed to explore a potential preventive role of PPIs in this study.

    Methods: In this population-based case-control study, we identified incident cases of breast cancer (n=1739), prostate cancer (n=1897), and malignant melanoma (n=385) in Iceland between 2005 and 2014 from the Icelandic Cancer Registry. We assessed varying levels of PPI use through record linkages to the Icelandic Medicines Registry. For each case, we selected up to 10 age-matched, sex-matched, and calendar-matched population controls using risk-set sampling. Using conditional logistic regression, we calculated odds ratios (ORs) and 95% confidence intervals (CIs) controlling for NSAID use.

    Results: Adjusted ORs associated with ever use of PPIs were 1.03 (95% CI: 0.92-1.16) for breast cancer, 1.12 (95% CI: 1.00-1.25) for prostate cancer, and 0.84 (95% CI: 0.69-1.12) for malignant melanoma. Analyses of high use of PPIs (>= 1000 DDDs) yielded ORs of 0.97 (95% CI: 0.78-1.19), 1.20 (0.99-1.47), and 0.59 (0.40-1.13) for breast cancer, prostate cancer, and malignant melanoma, respectively. Analyses of cumulative exposure to PPIs did not support a dose-response relationship for any of the three cancer types.

    Conclusions: Our findings do not support a chemopreventive effect of PPI use on breast cancer, prostate cancer, or malignant melanoma.

  • 61.
    Jakobsson, Hedvig
    et al.
    Department of Bacteriology, Swedish Institute for Infectious Disease Control, Stockholm; Departments of Microbiology, Tumuor and Cell Biology, Karolinska Institute, Stockholm.
    Wreiber, Karin
    Department of Bacteriology, Swedish Institute for Infectious Disease Control, Stockholm.
    Fall, Katja
    Department of Medical Epidemiology, Karolinska Institute, Stockholm.
    Fjelstad, Björn
    Mora County Hospital, Mora.
    Nyrén, Olof
    Department of Medical Epidemiology, Karolinska Institute, Stockholm.
    Engstrand, Lars
    Department of Bacteriology, Swedish Institute for Infectious Disease Control, Stockholm.
    Macrolide resistance in the normal microbiota after Helicobacter pylori treatment2007Inngår i: Scandinavian Journal of Infectious Diseases, ISSN 0036-5548, E-ISSN 1651-1980, Vol. 39, nr 9, s. 757-63Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Large-scale chemoprevention of peptic ulcer disease and gastric cancer through eradication of Helicobacter pylori would expose large population groups to antibiotics, which raises concerns about possible dissemination of antibiotic resistance. The objective of this cohort study was to determine whether a triple therapy, containing omeprazole, clarithromycin, and metronidazole, of H. pylori infection increases the prevalence of macrolide resistance in the normal microbiota. 85 patients with a peptic ulcer disease with verified H. pylori infection and 12 dyspeptic patients without positive findings upon endoscopy were included. Minimal inhibitory concentrations of clarithromycin for Staphylococcus, Streptococcus, Enterococcus and Bacteroides spp. were determined from samples taken before and after treatment, and 1 y later. Before treatment, macrolide resistance was observed in 11%, 31%, 9% and 11% of the staphylococci, streptococci, enterococci and Bacteroides, respectively. The number of resistant isolates remained elevated after 1 y, most notably for staphylococci and streptococci. No development of persistent resistance was detected in the untreated control group. Triple therapy including clarithromycin leads to persistent macrolide resistance in the normal microbiota. A prevalent pool of resistance genes in the normal microbiota constitutes an ecological hazard that needs to be considered before global treatment programmes for eradication of H. pylori are implemented.

  • 62.
    Jansson, Stefan P. O.
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Region Örebro län. Family Medicine Research Centre, Region Örebro County, Örebro, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
    Brus, O.
    Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
    Magnuson, A.
    Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
    Wändell, P.
    Department of Neurobiology, Care Sciences and Society, Unit of Family Medicine, Karolinska Institutet, Huddinge, Sweden.
    Östgren, C. J.
    Division of Community Medicine, Department of Medicine and Health Sciences, Faculty of Health Sciences, Linköping University, Linköping, Sweden; Department of Local Care West, County Council of Östergötland, Linköping, Sweden.
    Rolandsson, O.
    Department of Public Health and Clinical Medicine, Family Medicine, Umeå University, Umeå, Sweden.
    Prevalence and incidence of diabetes mellitus: a nationwide population-based pharmaco-epidemiological study in Sweden2015Inngår i: Diabetic Medicine, ISSN 0742-3071, E-ISSN 1464-5491, Vol. 32, nr 10, s. 1319-1328Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Aim: To investigate the changes in prevalence and incidence of pharmacologically and non-pharmacologically treated diabetes in Sweden during 2005 to 2013.

    Methods: We obtained data on gender, date of birth and pharmacologically and non-pharmacologically treated diabetes from national registers for all Swedish residents.

    Results: During the study period a total of 240 871 new cases of pharmacologically treated diabetes was found. The age-standardized incidence during the follow-up was 4.34 and 3.16 per 1000 individuals in men and women, respectively. A decreasing time trend in incidence for men of 0.6% per year (0.994, 95% CI 0.989-0.999) and for women of 0.7% per year (0.993, 95% CI 0.986-0.999) was observed. The age-standardized prevalence increased from 41.9 and 29.9 per 1000 in 2005/2006 to 50.8 and 34.6 in 2012/2013 in men and women, respectively. This corresponds to an annually increasing time trend for both men (1.024, 95% CI 1.022-1.027) and women (1.019, 95% CI 1.016-1.021). The total age-standardized prevalence of pharmacologically and non-pharmacologically treated diabetes (2012) was 46.9 per 1000 (55.6 for men and 38.8 for women). This corresponds to an annually increasing time trend (2010-2012) for both men (1.017, 95% CI 1.013-1.021) and women (1.012, 95% CI 1.008-1.016).

    Conclusions: The prevalence of pharmacologically treated diabetes increased moderately during 8 years of follow-up, while the incidence decreased modestly. This is in contrast to the results reported by most other studies. The total prevalence of diabetes (both pharmacologically and non-pharmacologically treated) in Sweden is relatively low, from a global viewpoint.

  • 63.
    Jansson, Stefan P. O.
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper. University Health Care Research Center, Region Örebro County, Örebro, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Brus, O.
    Magnuson, A.
    Wändell, P.
    Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Huddinge, Sweden.
    Östgren, C. J.
    Division of Community Medicine, Department of Medicine and Health Sciences, Linköping University, Linköping, Sweden; Department of Local Care West, County Council of Östergötland, Linköping, Sweden.
    Rolandsson, O.
    Department of Public Health and Clinical Medicine, Umea University, Umeå, Sweden.
    Response to Carlsson et al.: Prevalence and incidence of diabetes mellitus: a nationwide population-based pharmaco-epidemiological study in Sweden2016Inngår i: Diabetic Medicine, ISSN 0742-3071, E-ISSN 1464-5491, Vol. 33, nr 8, s. 1150-1152Artikkel i tidsskrift (Fagfellevurdert)
  • 64.
    Jerlström, Tomas
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Urology.
    Ruoqing, Chen
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Liedberg, Fredrik
    Department of Urology, Skåne University Hospital, Malmö, Sweden; Department of Translational Medicine, Lund University, Malmö, Sweden.
    Andrén, Ove
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Urology.
    Ströck, Viveka
    Sahlgrenska Academy, Institute of Clinical Sciences, Gothenburg, Sweden; Sahlgrenska Academy, Institute of Clinical Sciences, Gothenburg, Sweden.
    Aljabery, Firas A. S.
    Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
    Hosseini, Abolfazl
    Section of Urology, Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
    Sherif, Amir
    Department of Surgical and Perioperative Sciences, Urology and Andrology, Umeå University, Umeå, Sweden.
    Malmström, Per-Uno
    Department of Urology, Institute of Surgical Sciences, Uppsala, Sweden.
    Ullén, Anders
    PO Bäckencancer, Theme Cancer, Karolinska University Hospital and Department of Oncology-Pathology, Karolinska Institutet, Solna, Sweden.
    Gårdmark, Truls
    Department of Clinical Sciences, Danderyd Hospital, Karolinska Institutet, Stockholm, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Urology, Faculty of Medicine and Health, Örebro University, Örebro, Sweden; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    No increased risk of short-term complications after radical cystectomy for muscle-invasive bladder cancer among patients treated with preoperative chemotherapy: a nation-wide register-based study2020Inngår i: World journal of urology, ISSN 0724-4983, E-ISSN 1433-8726, Vol. 38, nr 2, s. 381-388Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    PURPOSE: Preoperative chemotherapy is underused in conjunction with radical cystectomy (RC) for muscle-invasive bladder cancer (MIBC) due to concerns for complications and delay of surgery. Prospective data on short-term complications from population-based settings with frequent use of preoperative chemotherapy and standardised reporting of complications is lacking.

    METHODS: We identified 1,340 patients who underwent RC between 2011 and 2015 in Sweden due to MIBC according to the Swedish Cystectomy Register. These individuals were followed through linkages to several national registers. Propensity score adjusted logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs) for complications and death within 90 days of surgery, comparing patients receiving preoperative chemotherapy or not.

    RESULTS: Minimum two cycles of preoperative chemotherapy were given to 519 (39%) of the patients, who on average tended to be younger, have higher education, better physical status, and more advanced bladder cancer than patients not receiving chemotherapy. After adjusting for these and other parameters, there was no association between treatment with preoperative chemotherapy and short-term complications (OR 1.06 95% CI 0.82-1.39) or mortality (OR 0.75 95% CI 0.36-1.55). We observed a risk reduction for gastrointestinal complications among patients who received preoperative chemotherapy compared with those who did not (OR 0.49 95% CI 0.30-0.81).

    CONCLUSION: This nation-wide population-based observational study does not suggest that preoperative chemotherapy, in a setting with high utilisation of such treatment, is associated with an increased risk of short-term complications in MIBC patients treated with radical cystectomy.

  • 65.
    Jerlström, Tomas
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Urology.
    Ruoqing, Chen
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. Clinical Epidemiology Unit, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden.
    Liedberg, Fredrik
    Department of Urology, Skåne University Hospital, Malmö, Sweden; Department of Translational Medicine, Lund University, Malmö, Sweden.
    Ströck, Viveka
    Department of Urology, Sahlgrenska University Hospital, Gothenburg, Sweden; Sahlgrenska Academy, institute of Clinical Sciences, Gothenburg, Sweden.
    Aljabery, Firas A.S.
    Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
    Hosseini, Abolfazl
    Section of Urology, Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
    Sherif, Amir
    Department of Surgical and Perioperative Sciences, Urology and Andrology, Umeå University, Umeå, Sweden.
    Malmström, Per-Uno
    1Department of Urology, Institute of surgical Sciences, Uppsala, Sweden.
    Ullén, Anders
    PO Bäckencancer, Theme Cancer, Karolinska University Hospita, Solna, Sweden; Department of Oncology-Pathology, Karolinska Institutet, Solna, Sweden.
    Gårdmark, Truls
    Department of Clinical Sciences, Danderyd Hospital, Karolinska Institutet, Stockholm, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    No increased risk of short-term complications after radical cystectomy for muscle invasive bladder cancer among patients treated with preoperative chemotherapy: a nationwide register-based studyManuskript (preprint) (Annet vitenskapelig)
  • 66.
    Kantor, Elizabeth D.
    et al.
    Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, New York, USA; Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, Massachusetts, USA.
    Udumyan, Ruzan
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Giovannucci, Edward L.
    Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, Massachusetts, USA; Department of Nutrition, Harvard T. H. Chan School of Public Health, Boston, Massachusetts, USA; Channing Division of Network Medicine, Brigham and Women's Hospital, Boston, Massachusetts, USA.
    Valdimarsdottir, Unnur A.
    Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, Massachusetts, USA; Center of Public Health Sciences, Faculty of Medicine, School of Health Sciences, University of Iceland, Reykjavik, Iceland; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Signorello, Lisa B.
    Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, Massachusetts, USA; Division of Cancer Prevention, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
    Montgomery, Scott
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Epidemiology and Public Health, University College London, London, United Kingdom; Clinical Epidemiology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, Massachusetts, USA; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Association of Blood Marker of Inflammation in Late Adolescence With Premature Mortality2019Inngår i: JAMA pediatrics, ISSN 2168-6203, E-ISSN 2168-6211, Vol. 173, nr 11, s. 1095-1097Artikkel i tidsskrift (Fagfellevurdert)
  • 67.
    Kantor, Elizabeth D.
    et al.
    Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Udumyan, Ruzan
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Signorello, Lisa B.
    Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Giovannucci, Edward L.
    Department of Epidemiology, Harvard School of Public Health, Boston, USA; Department of Nutrition, Harvard School of Public Health, Boston, USA; Channing Division of Network Medicine, Brigham and Women’s Hospital, Boston, USA.
    Montgomery, Scott
    Örebro universitet, Institutionen för medicinska vetenskaper. Research Department of Epidemiology and Public Health, University College London, London, United Kingdom; Clinical Epidemiology Unit, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Epidemiology, Harvard School of Public Health, Boston, USA; Clinical Epidemiology Unit, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Adolescent body mass index and erythrocyte sedimentation rate in relation to colorectal cancer risk2016Inngår i: Gut, ISSN 0017-5749, E-ISSN 1468-3288, Vol. 65, nr 8, s. 1289-1295Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objective: Adult obesity and inflammation have been associated with risk of colorectal cancer (CRC); however, less is known about how adolescent body mass index (BMI) and inflammation, as measured by erythrocyte sedimentation rate (ESR), relate to CRC risk. We sought to evaluate these associations in a cohort of 239 658 Swedish men who underwent compulsory military enlistment examinations in late adolescence (ages 16-20 years).

    Design: At the time of the conscription assessment (1969-1976), height and weight were measured and ESR was assayed. By linkage to the national cancer registry, these conscripts were followed for CRC through 1 January 2010. Over an average of 35 years of follow-up, 885 cases of CRC occurred, including 501 colon cancers and 384 rectal cancers. Cox regression was used to estimate adjusted HRs and corresponding 95% CIs.

    Results: Compared with normal weight (BMI 18.5 to <25 kg/m(2)) in late adolescence, upper overweight (BMI 27.5 to <30 kg/m(2)) was associated with a 2.08-fold higher risk of CRC (95% CI 1.40 to 3.07) and obesity (BMI 30+ kg/m(2)) was associated with a 2.38-fold higher risk of CRC (95% CI 1.51 to 3.76) (p-trend: <0.001). Male adolescents with ESR (15+ mm/h) had a 63% higher risk of CRC (HR 1.63; 95% CI 1.08 to 2.45) than those with low ESR (<10 mm/h) (p-trend: 0.006). Associations did not significantly differ by anatomic site.

    Conclusions: Late-adolescent BMI and inflammation, as measured by ESR, may be independently associated with future CRC risk. Further research is needed to better understand how early-life exposures relate to CRC.

  • 68. Kasperzyk, Julie L.
    et al.
    Fall, Katja
    Mucci, Lorelei A.
    Håkansson, Niclas
    Wolk, Alicja
    Johansson, Jan-Erik
    Örebro universitet, Hälsoakademin.
    Andersson, Swen-Olof
    Andrén, Ove
    One-carbon metabolism-related nutrients and prostate cancer survival2009Inngår i: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 90, nr 3, s. 561-569Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Folate and other one-carbon metabolism nutrients may influence prostate cancer pathogenesis. Prior studies of these nutrients in relation to prostate cancer incidence have been inconclusive, and none have explored prostate cancer survival. OBJECTIVE: The objective was to assess whether dietary intakes of folate, riboflavin, vitamin B-6, vitamin B-12, and methionine measured around the time of prostate cancer diagnosis are associated with prostate cancer survival. DESIGN: This population-based prospective study comprised 525 men from Orebro, Sweden, who received a diagnosis of incident prostate cancer between 1989 and 1994 and completed a self-administered food-frequency questionnaire. Record linkages to the Swedish Death Registry enabled all cases to be followed for up to 20 y after diagnosis, and the cause of death was assigned via medical record review. Cox proportional hazards regression was used to calculate multivariable hazard ratios (HRs) and 95% CIs. During a median of 6.4 y of follow-up, 218 men (42%) died of prostate cancer and 257 (49%) of other causes. RESULTS: A comparison of the highest with the lowest quartile showed that vitamin B-6 intake was inversely associated with prostate cancer-specific death (HR: 0.71; 95% CI: 0.46, 1.10; P for trend = 0.08), especially in men with a diagnosis of localized-stage disease (HR; 0.05; 95% CI: 0.01, 0.26; P for trend = 0.0003). However, vitamin B-6 intake was not associated with improved prostate cancer survival among advanced-stage cases (HR: 1.04; 95% CI: 0.64, 1.72; P for trend = 0.87). Folate, riboflavin, vitamin B-12, and methionine intakes were not associated with prostate cancer survival. CONCLUSION: A high vitamin B-6 intake may improve prostate cancer survival among men with a diagnosis of localized-stage disease.

  • 69.
    Kennedy, Beatrice
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Fang, Fang
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Valdimarsdottir, Unnur
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Centre of Public Health Sciences, Faculty of Medicine, School of Health Sciences, University of Iceland, Reykjavík, Iceland; Department of Epidemiology, Harvard Chan School of Public Health, Boston MA, USA.
    Udumyan, Ruzan
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Montgomery, Scott
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Epidemiology and Public Health, University College London, London, UK; Clinical Epidemiology Unit, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Stress resilience and cancer risk: a nationwide cohort study2017Inngår i: Journal of Epidemiology and Community Health, ISSN 0143-005X, E-ISSN 1470-2738, Vol. 71, nr 10, s. 947-953Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Stress resilience is recognised as a determinant of both psychiatric and somatic health, but the potential link between stress resilience and cancer development has not been explored.

    Methods: In this nationwide cohort study, we examined the association between stress resilience in adolescence and subsequent cancer risk. We identified a cohort of 284 257 Swedish men, born 1952-1956, who underwent compulsory military enlistment examinations including measures of psychological stress resilience (median age 18 years). The resulting score was categorised as low, moderate and high stress resilience. Individuals diagnosed with cancer during the follow-up time were identified through data linkage to the Swedish Cancer Register.

    Results: Lowest stress resilience, compared with the highest, was associated with increased risks of liver (HR: 4.73, 95% CI 2.73 to 8.19) and lung (HR: 2.75, 95% CI 2.02 to 3.74) cancer after adjusting for markers of socioeconomic circumstances in childhood (p for trend <0.001 for both cancer types). Further adjustment for cognitive and physical fitness at conscription assessment had a marginal influence. In contrast, men with low stress resilience had a decreased risk of being diagnosed with prostate cancer (HR: 0.65, 95% CI 0.56 to 0.76) and malignant melanoma (HR: 0.65, 95% CI 0.55 to 0.76).

    Conclusion: We conclude that adolescent stress resilience, plausibly by influencing behavioural choices and social patterns, constitutes an important determinant of adult cancer occurrence. Increased awareness of longterm consequences in susceptible individuals may help direct future efforts to reduce cancer burden in adults.

  • 70.
    Kennedy, Beatrice
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper. Uppsala University, Uppsala, Sweden.
    Ruoqing, Chen
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. Karolinska institutet, Stockholm, Sweden.
    Fang, Fang
    Karolinska Institutet, Stockholm, Sweden.
    Valdimarsdottir, Unnur
    Karolinska Institutet, Stockholm, Sweden; Centre of Public Health Sciences, Faculty of Medicine, School of Health Sciences, University of Iceland, Reykjavík, Iceland; Department of Epidemiology, Harvard Chan School of Public Health, Boston MA, USA.
    Montgomery, Scott
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. Clinical Epidemiology and Biostatistics, School of Medical Sciences, Örebro University, Örebro, Sweden; Department of Epidemiology and Public Health, University College London, London, UK: Clinical Epidemiology Unit, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Larsson, Henrik
    Örebro universitet, Institutionen för medicinska vetenskaper. Karolinska Institutet, Stockholm, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper. Karolinska institutet, Stockholm, Sweden.
    Low stress resilience and use of addictive substancesManuskript (preprint) (Annet vitenskapelig)
  • 71.
    Kennedy, Beatrice
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Medical Sciences, Molecular Epidemiology and Science for Life Laboratory, Uppsala University, Uppsala, Sweden.
    Ruoqing, Chen
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fang, Fang
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Valdimarsdottir, Unnur
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Centre of Public Health Sciences, Faculty of Medicine, School of Health Sciences, University of Iceland, Reykjavík, Iceland; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA.
    Montgomery, Scott
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Epidemiology and Public Health, University College London, London, UK; Clinical Epidemiology Unit, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Larsson, Henrik
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Low stress resilience in late adolescence and risk of smoking, high alcohol consumption and drug use later in life2019Inngår i: Journal of Epidemiology and Community Health, ISSN 0143-005X, E-ISSN 1470-2738, Vol. 73, nr 6, s. 469-501Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: While compromised stress resilience constitutes a recognised risk factor for somatic and psychiatric disease development in general, the knowledge about how individual variation in vulnerability to stress may specifically influence the long-term risks of disadvantageous health behaviours is limited.

    METHODS: In this Swedish cohort study, we aimed to investigate the association between stress resilience in late adolescence and adult use of addictive substances. We included 9381 men with information on psychological stress resilience measured during military conscription examinations, who later responded to an extensive health survey (mean age 34.0±7.2 years) including detailed information on substance use. We modelled continuous outcomes using linear regression, binary outcomes with logistic regression and other categorical outcomes with multinomial logistic regression.

    RESULTS: We found that low stress resilience in adolescence conferred increased risks of all studied measures of addictive behaviour. After adjusting for childhood socioeconomic information, low stress resilience was associated with adult current regular smoking (relative risk ratio: 5.85, 95% CI 4.32 to 7.93), higher nicotine dependence scores (beta: 0.76, 95% CI 0.29 to 1.23), hazardous use of alcohol (>14 alcoholic drink-equivalents per week, OR: 1.72, 95% CI 1.37 to 2.16), DSM-IV criteria for alcohol dependence (OR: 1.74, 95% CI 1.35 to 2.25), and drug use (OR: 1.77, 95% CI 1.51 to 2.08). The results remained largely unchanged after further adjustments for adult educational attainment and occupation as well as for additional conscription covariates.

    CONCLUSION: Low stress resilience in late adolescence appears to be associated with an increased risk of disadvantageous and addictive health behaviours in adulthood.

  • 72.
    Kennedy, Beatrice
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Ruoqing, Chen
    Med Epidemiol & Biostat, Karolinska Inst, Stockholm, Sweden.
    Valdimarsdottir, Unnur
    Publ Hlth Sci, Univ Iceland, Reykjavik, Iceland.
    Fang, Fang
    Med Epidemiol & Biostat, Karolinska Inst, Stockholm, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Childhood Bereavement And Reduced Stress Resilience In Late Adolescence2017Inngår i: Psychosomatic Medicine, ISSN 0033-3174, E-ISSN 1534-7796, Vol. 79, nr 4, s. A3-A3Artikkel i tidsskrift (Fagfellevurdert)
  • 73.
    Kennedy, Beatrice
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper. Uppsala University, Uppsala, Sweden.
    Ruoqing, Chen
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. Karolinska institutet, Stockholm, Sweden.
    Valdimarsdottir, Unnur
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Centre of Public Health Sciences, Faculty of Medicine, School of Health Sciences, University of Iceland, Reykjavík, Iceland; Department of Epidemiology, Harvard Chan School of Public Health, Boston MA, USA.
    Montgomery, Scott
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Epidemiology and Public Health, University College London, London, UK: Clinical Epidemiology Unit, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Fang, Fang
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper. Karolinska institutet, Stockholm, Sweden.
    Childhood Bereavement and Increased Sensitivity to Stress in Late AdolescenceManuskript (preprint) (Annet vitenskapelig)
  • 74.
    Kennedy, Beatrice
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Medical Sciences, Molecular Epidemiology and Science for Life Laboratory, Uppsala University, Uppsala, Sweden.
    Ruoqing, Chen
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Valdimarsdóttir, Unnur
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Centre of Public Health Sciences, Faculty of Medicine, School of Health Sciences, University of Iceland, Reykjavík, Iceland; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, USA.
    Montgomery, Scott
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Epidemiology and Public Health, University College London, London, UK; Clinical Epidemiology Unit, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Fang, Fang
    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.
    Childhood Bereavement and Lower Stress Resilience in Late Adolescence2018Inngår i: Journal of Adolescent Health, ISSN 1054-139X, E-ISSN 1879-1972, Vol. 63, nr 1, s. 108-114Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    PURPOSE: Although childhood traumatic experiences are recognized as important determinants for adolescent psychiatric health in general, our objective was to explore the specific influence of childhood bereavement on the stress resilience development trajectory.

    METHODS: In this national register-based cohort study, we identified 407,639 men born in Sweden between 1973 and 1983, who underwent compulsory military enlistment examinations in late adolescence, including measures of psychological stress resilience. We defined exposure as loss of a first-degree family member in childhood, and estimated relative risk ratios (RRRs) for reduced (moderate or low), compared with high, stress resilience with 95% confidence intervals (CIs) using multinomial logistic regression.

    RESULTS: Loss of a parent or sibling in childhood conferred a 49% increased risk of subsequent low stress resilience (RRR, 1.49, 95% CI, 1.41-1.57) and an 8% increased risk of moderate stress resilience (RRR, 1.08, 95% CI, 1.03-1.13) in late adolescence. There was also a graded increase in risk with increasing age at loss; teenagers were at higher risk for low resilience (RRR, 1.64, 95% CI, 1.52-1.77) than children aged 7-12 (RRR, 1.47, 95% CI, 1.34-1.61) and ≤6 years (RRR, 1.16 95% CI, 1.02-1.32). The excess risk was observed for all causes of death, including suicide and unexpected deaths as well as deaths due to other illnesses. The associations remained after exclusion of parents with a history of hospitalization for psychiatric diagnoses.

    CONCLUSIONS: The long-term consequences of childhood bereavement may include lower stress resilience in late adolescence.

  • 75.
    Kennedy, Beatrice
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Clinical Epidemiology and Biostatistics Unit, Örebro University Hospital, Örebro, Sweden.
    Valdimarsdóttir, Unnur
    Faculty of Medicine, School of Health Sciences, University of Iceland, Reykjavík, Iceland.
    Sundström, Karin
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Sparén, Pär
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Lambe, Mats
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Regional Cancer Centre, Uppsala University Hospital, Uppsala, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Faculty of Medicine, School of Health Sciences, University of Iceland, Reykjavík, Iceland.
    Fang, Fang
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Loss of a parent and the risk of cancer in early life: a nationwide cohort study2014Inngår i: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 25, nr 4, s. 499-506Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

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

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

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

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

  • 76.
    Landberg, Anna
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Urology.
    Fält, Anna
    School of Medical Sciences, Örebro University, Örebro, Sweden.
    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.
    Sundqvist, Pernilla
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Urology.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden.
    Overweight and obesity during adolescence increases the risk of renal cell carcinoma2019Inngår i: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 145, nr 5, s. 1232-1237Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    While overweight among adults has been linked with renal cell carcinoma (RCC) risk, little is known about the potential influence of overweight and obesity during adolescence. To ascertain if adolescent body mass index is associated with subsequent risk of RCC, we identified a cohort of 238,788 Swedish men who underwent mandatory military conscription assessment between 1969 and 1976 at a mean age of 18.5 years. At the time of conscription assessment, physical and psychological tests were performed including measurements of height and weight. Participants were followed through linkage to the Swedish Cancer Registry to identify incident diagnoses of RCC. The association between body mass index (BMI, kg/m(2)) at conscription assessment and subsequent RCC was evaluated using multivariable Cox regression. During a follow-up of up to 37 years, 266 men were diagnosed with RCC. We observed a trend for higher RCC risk with increasing BMI during adolescence, where one-unit increase in BMI conferred a 6% increased risk of RCC (95% CI 1.01-1.10). compared to normal weight men (BMI 18.5- < 25), men with overweight (BMI 25- < 30) or obesity (BMI >= 30) had hazard ratios for RCC of 1.76 (95% CI 1.16-2.67) and 2.87 (95% CI 1.26-6.25), respectively. The link between overweight/obesity and RCC appear to be already established during late adolescence. Prevention of unhealthy weight gain during childhood and adolescence may thus be a target in efforts to decrease the burden of RCC in the adult population.

  • 77.
    Li, Yuchen
    et al.
    Mental Health Center, West China Hospital of Sichuan University, Chengdu, China; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Wang, Yue
    Mental Health Center, West China Hospital of Sichuan University, Chengdu, China.
    Jiang, Jingwen
    West China Biomedical Big Data Center, West China Hospital, Sichuan University, Chengdu, China.
    Valdimarsdóttir, Unnur A.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Center 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.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper. Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Fang, Fang
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Song, Huan
    West China Biomedical Big Data Center, West China Hospital, Sichuan University, Chengdu, China; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Center of Public Health Sciences, Faculty of Medicine, University of Iceland, Reykjavík, Iceland.
    Lu, Donghao
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA; Clinical Research Center for Breast Diseases, West China Hospital, Sichuan University, Chengdu, China; Channing Division of Network Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
    Zhang, Wei
    Mental Health Center, West China Hospital of Sichuan University, Chengdu, China; West China Biomedical Big Data Center, West China Hospital, Sichuan University, Chengdu, China.
    Psychological distress among health professional students during the COVID-19 outbreak2020Inngår i: Psychological Medicine, ISSN 0033-2917, E-ISSN 1469-8978, s. 1-12Artikkel i tidsskrift (Fagfellevurdert)
  • 78.
    Lu, Donghao
    et al.
    Department of Medical Epidemiology & Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Andersson, Therese M. -L.
    Department of Medical Epidemiology & Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Hultman, Christina M.
    Department of Medical Epidemiology & Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Czene, Kamila
    Department of Medical Epidemiology & Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Valdimarsdottir, Unnur
    Center of Public Health Sciences, School of Health Sciences, University of Iceland, Reykjavík, Iceland.
    Fang, Fang
    Department of Medical Epidemiology & Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Increased risk for psychiatric disorders immediately before and after cancer diagnosis: A nationwide matched cohort study in Sweden2015Inngår i: Psychoneuroendocrinology, ISSN 0306-4530, E-ISSN 1873-3360, Vol. 61, s. 50-50Artikkel i tidsskrift (Annet vitenskapelig)
    Abstract [en]

    Purpose: To examine whether undergoing diagnostic workup leading up to a cancer diagnosis entrails increased risks for depression, anxiety disorder, substance use disorder, somatoform/conversion disorder, severe stress and adjustment disorder.

    Methods: Based on the nationwide health registers in Sweden, we conducted a matched cohort study during 2001–2010, including 304,118 cancer patients and five cancer-free individuals per cancer patient randomly selected from the Swedish population and matched on year of birth and sex. Flexible parametric survival models were used to estimate the time-varying hazard ratios [HRs] of any first in-/outpatient diagnosis of the studied psychiatric disorders from two years before cancer diagnosis (Year−2), through the time at diagnosis (Year 0), until ten years after diagnosis (Year 10).

    Results: The overall risk for the studied psychiatric disorders started to increase from Year−1 (HR 1.2, 95% confidence interval [CI] 1.0–1.5), peaked immediately after diagnosis (Week 1: HR 12.9, 95% CI 9.4–17.8), and decreased rapidly thereafter to be comparable with cancer-free individuals at approximately Year 10 (HR 1.0, 95% CI 0.8–1.3). The risk elevation was clear for all main cancer types except for non-melanoma skin cancer; and was stronger for cancers of relatively poor prognosis after (P= 0.0005) but not before diagnosis (P= 0.47).

    Conclusion: Patients recently diagnosed with cancer experience a dramatic increase in risks of psychiatric disorders. The clear risk elevation during the year before diagnosis suggests an impact of cancer symptoms pre-diagnosis as well as the stress of undergoing clinical evaluation for a suspected malignancy. This work is supported by Cancerfonden and FORTE.

  • 79.
    Lu, Donghao
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Andersson, Therese M. L.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Hultman, Christina M.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Czene, Kamila
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Valdimarsdóttir, Unnur
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Faculty of Medicine, Center of Public Health Sciences, School of Health Sciences, University of Iceland, Reykjavik, Iceland; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, USA.
    Fang, Fang
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Clinical Diagnosis of Mental Disorders Immediately Before and After Cancer Diagnosis: A Nationwide Matched Cohort Study in Sweden2016Inngår i: JAMA oncology, ISSN 2374-2445, Vol. 2, nr 9, s. 1188-1196Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Importance: Psychiatric comorbidities are common among patients with cancer. However, whether or not there is increased risk of mental disorders during the diagnostic workup leading to a cancer diagnosis was unknown.

    Objective: To examine the relative risks of depression, anxiety, substance abuse, somatoform/conversion disorder, and stress reaction/adjustment disorder during the periods before and after cancer diagnosis compared with individuals without cancer.

    Design, Setting, and Participants: Nationwide matched cohort study from January 1, 2001, to December 31, 2010, in a Swedish population and health registers.

    Main Outcomes and Measures: We estimated the time-varying hazard ratios (HRs) of the first clinical diagnosis of the studied mental disorders from 2 years before cancer diagnosis, through the time of diagnosis, and until 10 years after diagnosis, adjusting for age, sex, calendar period, and educational level. To assess milder mental conditions and symptoms, we further assessed the use of related psychiatric medications for patients with cancer diagnosed during 2008-2009.

    Results: The study included 304 118 patients with cancer and 3 041 174 cancer-free individuals who were randomly selected from the Swedish population and individually matched to the patients with cancer on year of birth and sex. The median age at diagnosis for the patients with cancer was 69 years, and 46.9% of the patients were female. The relative rate for all studied mental disorders started to increase from 10 months before cancer diagnosis (HR, 1.1; 95% CI, 1.1-1.2), peaked during the first week after diagnosis (HR, 6.7; 95% CI, 6.1-7.4), and decreased rapidly thereafter but remained elevated 10 years after diagnosis (HR, 1.1; 95% CI, 1.1-1.2). The rate elevation was clear for all main cancers except nonmelanoma skin cancer and was stronger for cancers of poorer prognosis. Compared with cancer-free individuals, increased use of psychiatric medications was noted from 1 month before cancer diagnosis and peaked around 3 months after diagnosis among patients with cancer.

    Conclusions and Relevance: Patients diagnosed as having cancer had increased risks of several common mental disorders from the year before diagnosis. These findings support the existing guidelines of integrating psychological management into cancer care and further call for extended vigilance for multiple mental disorders starting from the time of the cancer diagnostic workup.

  • 80.
    Lu, Donghao
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Faculty of Medicine, Center of Public Health Sciences, School of Health Sciences, University of Iceland, Reykjavík, Iceland.
    Andrae, Bengt
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Centre for Research and Development, Uppsala University/Region of Gävleborg, Gävle, Sweden.
    Valdimarsdottir, Unnur
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Faculty of Medicine, Center of Public Health Sciences, School of Health Sciences, University of Iceland, Reykjavík, Iceland; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, United States.
    Sundström, Karin
    Department of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper. Clinical Epidemiology and Biostatistics.
    Sparen, Par
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fang, Fang
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Psychologic Distress Is Associated with Cancer-Specific Mortality among Patients with Cervical Cancer2019Inngår i: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 79, nr 15, s. 3965-3972Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Emerging evidence suggests a role of psychologic factors in the progression of different cancer types. However, it is unclear whether psychologic distress around the time of diagnosis of invasive cervical cancer places patients at a higher risk of cancer-specific mortality, independently of tumor characteristics and treatment modalities. We conducted a nationwide cohort study, including 4,245 patients with newly diagnosed cervical cancer during 2002-2011 in Sweden. Psychologic distress was indicated by a clinical diagnosis of depression, anxiety, or stress reaction and adjustment disorders, or the experience of a stressful life event, including death or severe illness of a family member, divorce, or between jobs, from one year before cancer diagnosis and onwards. We calculated the HRs of cancer-specific mortality among the patients exposed to psychologic distress, compared with unexposed patients, controlling for socioeconomic characteristics and other known prognostic indicators such as tumor and treatment characteristics. We found that patients exposed to psychologic distress had an increased risk of cancer-specific mortality (HR 1.33; 95% CI, 1.14-1.54). The association was primarily driven by distress experienced within one year before or after diagnosis (HR 1.30; 95% CI, 1.11-1.52), but not thereafter (HR 1.12; 95% CI, 0.84-1.49). In summary, our study shows that psychiatric disorders and stressful life events around cancer diagnosis are associated with increased cancer-specific mortality among patients with cervical cancer, independent of tumor characteristics and treatment modality.

    Significance: These findings support the integration of psychologic screening and intervention in the clinical management of patients with cervical cancer, particularly around the time of cancer diagnosis.

  • 81.
    Lu, Donghao
    et al.
    Department of Medical Epidemiology & Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Carlsson, Jessica
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Penney, Kathryn L.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, USA; Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston MA, USA.
    Davidsson, Sabina
    Region Örebro län. Örebro universitet, Institutionen för medicinska vetenskaper. Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Andersson, Swen-Olof
    Department of Urology, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
    Mucci, Lorelei A.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, USA; Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston MA, USA.
    Valdimarsdóttir, Unnur
    Department of Medical Epidemiology & Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, USA; Faculty of Medicine, Center of Public Health Sciences, School of Health Sciences, University of Iceland, Reykjavík, Iceland.
    Andrén, Ove
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Urology, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
    Fang, Fang
    Department of Medical Epidemiology & Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Medical Epidemiology & Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Expression and Genetic Variation in Neuroendocrine Signaling Pathways in Lethal and Nonlethal Prostate Cancer among Men Diagnosed with Localized Disease2017Inngår i: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 26, nr 12, s. 1781-1787Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Recent data suggest that neuroendocrine signaling pathways may play a role in the progression of prostate cancer, particularly for early-stage disease. We aimed to explore whether expression of selected genes in the adrenergic, serotoninergic, glucocorticoid, and dopaminergic pathways differs in prostate tumor tissue from men with lethal disease compared to men with nonlethal disease.

    METHODS: Based on the Swedish Watchful Waiting Cohort, we included 511 men diagnosed with incidental prostate cancer through TURP during 1977-1998 with follow-up up to 30 years. For those with tumor tissue (N=262), we measured mRNA expression of 223 selected genes included in neuroendocrine pathways. Using DNA from normal prostate tissue (N=396), we genotyped 36 SNPs from 14 receptor genes. Lethal prostate cancer was the primary outcome in analyses with pathway gene expression and genetic variants.

    RESULTS: Differential expression of genes in the serotoninergic pathway was associated with risk of lethal prostate cancer (P=0.007); similar but weaker associations were noted for the adrenergic (P=0.014) and glucocorticoid (P=0.020) pathways. Variants of the HTR2A (rs2296972; P=0.002) and NR3CI (rs33388; P=0.035) genes (within the serotoninergic and glucocorticoid pathways) were associated with lethal cancer in over-dominant models. These genetic variants were correlated with expression of several genes in corresponding pathways (P<0.05).

    CONCLUSIONS: Our findings lend support to hypothesis that the neuroendocrine pathways, particularly serotoninergic pathway, are associated with lethal outcome in the natural course of localized prostate cancer.

    IMPACT: The current study provides evidence of the role of neuroendocrine pathways in prostate cancer progression which may have clinical utility.

  • 82.
    Lu, Donghao
    et al.
    Karolinska Institutet, Stockholm, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    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 individuals2013Inngår i: Annals of Oncology, ISSN 0923-7534, E-ISSN 1569-8041, Vol. 24, nr 12, s. 3112-3117Artikkel i tidsskrift (Fagfellevurdert)
    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.

  • 83.
    Lu, Donghao
    et al.
    Department of Medical Epidemiology & Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Sinnott, Jennifer A.
    Department of Statistics, Ohio State University, Columbus OH, USA; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, USA.
    Valdimarsdóttir, Unnur
    Department of Medical Epidemiology & Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, USA; Faculty of Medicine, Center of Public Health Sciences, School of Health Sciences, University of Iceland, Reykjavík, Iceland.
    Fang, Fang
    Department of Medical Epidemiology & Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Gerke, Travis
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, USA; Department of Epidemiology, College of Medicine and College of Public Health and Health Professions, University of Florida, Gainesville, USA.
    Tyekucheva, Svitlana
    Department of Biostatistics and Computational Biology, Dana-Farber Cancer Institute, Boston, USA.
    Fiorentino, Michelangelo
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, USA; Center for Molecular Oncologic Pathology, Dana-Farber Cancer Institute, Boston, USA; Pathology Unit, Addarii Institute, S. Orsola-Malpighi Hospital, Bologna, Italy.
    Lambe, Mats
    Department of Medical Epidemiology & Biostatistics, Karolinska Institutet, Stockholm, Sweden; Regional Cancer Center, Uppsala University Hospital, Uppsala, Sweden.
    Sesso, Howard D.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, USA; Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, USA; Division of Aging, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, USA.
    Sweeney, Christopher J.
    Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, USA.
    Wilson, Kathryn M.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, USA; Faculty of Medicine, Center of Public Health Sciences, School of Health Sciences, University of Iceland, Reykjavík, Iceland.
    Giovannucci, Edward L.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, USA; Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, USA.
    Loda, Massimo
    Center for Molecular Oncologic Pathology, Dana-Farber Cancer Institute, Boston, USA; Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, USA.
    Mucci, Lorelei A.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, USA; Channing Division of Network Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, USA.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, USA; Department of Clinical Epidemology and Biostatistics, Örebro University Hospital, Örebro, Sweden.
    Stress-Related Signaling Pathways in Lethal and Nonlethal Prostate Cancer2016Inngår i: Clinical cancer research : an official journal of the American Association for Cancer Research, ISSN 1078-0432, Vol. 22, nr 3, s. 765-772Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Purpose: Recent data suggest that neuroendocrine signaling may influence progression in some cancers. We aimed to determine whether genes within the five major stress-related signaling pathways are differentially expressed in tumor tissue when comparing prostate cancer patients with lethal and nonlethal disease.

    Experimental design: We measured mRNA expression of 51 selected genes involved in predetermined stress-related signaling pathways (adrenergic, glucocorticoid, dopaminergic, serotoninergic, and muscarinic systems) in tumor tissue and normal prostate tissue collected from prostate cancer patients in the Physicians' Health Study (n = 150; n = 82 with normal) and the Health Professionals Follow-Up Study (n = 254; n = 120 with normal). We assessed differences in pathway expression in relation to prostate cancer lethality as the primary outcome and to biomarkers as secondary outcomes.

    Results: Differential mRNA expression of genes within the adrenergic (P = 0.001), glucocorticoid (P < 0.0001), serotoninergic (P = 0.0019), and muscarinic (P = 0.0045) pathways in tumor tissue was associated with the risk of lethality. The adrenergic pathway was also statistically significant (P = 0.001) when comparing against differential expression of genes not involved in the pathways. In adjacent normal prostate tissue, none of the pathways was clearly differentially expressed between lethal and nonlethal prostate cancer. The glucocorticoid and adrenergic pathways were associated with cell proliferation, while the glucocorticoid pathway was additionally associated with angiogenesis and perineural invasion.

    Conclusions: Our study suggests that stress-related signaling pathways, particularly the adrenergic and glucocorticoid, may be dysregulated in the tumors of men whose prostate cancer proves to be lethal, and motivates further investigation of these pathways in functional studies.

  • 84.
    Lu, Donghao
    et al.
    Department of Medical Epidemiology & Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Sundström, Karin
    Department of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden.
    Sparén, Pär
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, sweden.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston MA, USA.
    Sjölander, Arvid
    Department of Medical Epidemiology & Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Dillner, Joakim
    Department of Medical Epidemiology & Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden.
    Ylitalo Helm, Nathalie
    Division of Clinical Cancer Epidemiology, Department of Oncology, Sahlgrenska University Hospital, Gothenburg, 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 Massachusetts, USA.
    Valdimarsdottir, Unnur
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston Massachusetts, USA; Center of Public Health Sciences, University of Iceland, Reykjavik, Iceland.
    Fang, Fang
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Bereavement is associated with an increased risk of HPV infection and cervical cancer: an epidemiological study in Sweden2016Inngår i: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 76, nr 3, s. 643-651Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Grief over the loss of a family member may cause physical and mental illness, but an association between bereavement and cancer risk has not been established. Based on the Swedish National Cervical Screening Register (1969-2011) including 14,011,269 smears from 2,466,107 women, we conducted two nested case-control studies to examine the associations of bereavement (i.e., loss of a family member due to death) with abnormal cytology (390,310 first abnormal and 1,951,319 normal smears) and in situ/invasive cervical cancer (75,128 case and 375,640 control women), both individually matched on year of birth and screening adherence. Among 1,696 of the control women, we further investigated bereavement in association with HPV infection, both HPV16 and other HPV types. Bereavement was consistently associated with a 4-9% increased risk for first abnormal cytology, in situ and invasive cervical cancer (all P<0.02). The associations became stronger when multiple losses, loss of child, sibling or spouse, and loss due to unnatural cause were analyzed separately (P for trend or difference<0.0001), and for women with high screening adherence (P for difference<0.05). Among 1,696 women who had not developed cervical cancer, we further investigated the link between bereavement and HPV infection. Bereavement was associated with a 62% increased risk of HPV16 infection, high viral load, and recurrent infection, and was also more strongly associated with HPV infections designated as high-risk compared to low-risk determinants of cervical carcinogenesis. Collectively, our findings demonstrate that bereavement is associated with an increased risk of developing cervical cancer. Further, they suggest that this association may be attributed to stress-induced oncogenic HPV infections.

  • 85.
    Ludvigsson, Jonas F.
    et al.
    Department of Paediatrics, Örebro University Hospital, Örebro, Sweden; Clinical Epidemiology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Department of Epidemiology, Harvard School of Public Health, Boston, US.
    Montgomery, Scott M.
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Clinical Epidemiology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden; Department of Primary Care and Public Health, Charing Cross Hospital, Imperial College, London, UK.
    Risk of prostate cancer in a population-based cohort of men with coeliac disease2012Inngår i: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 106, nr 1, s. 217-221Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Prostate cancer (PC) is a leading cause of fatal cancer in men in developed countries. Coeliac disease (CD) has previously been linked to a raised cancer risk, and changes in some exposures following a CD diagnosis might hypothetically raise PC risk. METHODS: We identified 10 995 patients with CD who had undergone a small intestinal biopsy in 1969-2007. Statistics Sweden then identified 54 233 age-matched male reference individuals from the general population. PC data were obtained from the Swedish Cancer Register. Hazard ratios (HRs) for PC were estimated using Cox regression analysis. RESULTS: During follow-up, 185 individuals with CD (expected = 200) had an incident diagnosis of PC. This corresponds to a HR of 0.92 (0.79-1.08) (with 95% confidence interval) and an absolute risk reduction of 15/100 000 person-years among those with CD. An increased risk was not observed even when identification of PC began 5 years after biopsy. CONCLUSION: Our conclusion is that a CD diagnosis does not represent an increased risk for PC. 

  • 86.
    Lü, Donghao
    et al.
    Karolinska Institutet, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. Karolinska Institutet, Stockholm, Sweden; University of Nottingham, Nottingham, United Kingdom; Columbia University College of Physicians and Surgeons, New York NY, United States .
    Smedby, Karin Ekström
    Karolinska University Hospital, Stockholm, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper. Karolinska Institutet, Stockholm, Sweden.
    Valdimarsdóttir, Unnur
    Karolinska Institutet, Stockholm, Sweden; University of Iceland, Reykjavík, Iceland.
    Cnattingius, Sven
    Karolinska University Hospital, Stockholm, Sweden .
    Fang, Fang
    Karolinska Institutet, Stockholm, Sweden.
    Maternal Cancer During Pregnancy and Risks of Stillbirth and Infant Mortality2017Inngår i: Journal of Clinical Oncology, ISSN 0732-183X, E-ISSN 1527-7755, Vol. 35, nr 14, s. 1522-1529, artikkel-id JCO2016699439Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Purpose: To examine whether maternal cancer during pregnancy is associated with increased risks of stillbirth and infant mortality.

    Methods: On the basis of nationwide health registers, we conducted a study of 3,947,215 singleton births in Sweden from 1973 through 2012. Exposure was defined as maternal cancer diagnosed during pregnancy (number of births = 984) or during the year after pregnancy (number of births = 2,723). We calculated incidence rate ratios (IRRs) for stillbirth and infant mortality, comparing exposed births to unexposed births. Small-for-gestational-age (SGA) and preterm births were examined as secondary outcomes.

    Results: Maternal cancer diagnosed during pregnancy was positively associated with stillbirth (IRR, 2.5; 95% CI, 1.2 to 5.0), mainly stillbirths assessed as SGA (IRR, 4.9; 95% CI, 2.2 to 11.0), and with preterm SGA births (relative risk 3.0; 95% CI, 2.1 to 4.4). Positive associations of maternal cancer diagnosed during pregnancy or the year after pregnancy were noted for both neonatal mortality (deaths within 0 to 27 days; IRR, 2.7; 95% CI, 1.3 to 5.6 and IRR, 2.0; 95% CI, 1.2 to 3.2, respectively) and preterm birth (IRR, 5.8; 95% CI, 5.3 to 6.5 and IRR, 1.6; 95% CI, 1.4 to 1.8, respectively). The positive association with preterm birth was due to iatrogenic instead of spontaneous preterm birth. Preterm birth explained 89% of the association of maternal cancer during pregnancy with neonatal mortality.

    Conclusion: Maternal cancer during pregnancy is associated with increased risks of rare but fatal outcomes, including stillbirth and neonatal mortality. This may be due to conditions associated with fetal growth restriction and iatrogenic preterm birth. Careful monitoring of fetal growth and cautious decision making on preterm delivery should therefore be reinforced.

  • 87.
    Markt, Sarah C.
    et al.
    Department of Epidemiology, Harvard TH Chan School of Public Health, Boston, USA.
    Nuttall, Elizabeth
    Department of Epidemiology, Harvard TH Chan School of Public Health, Boston, USA.
    Turman, Constance
    Program in Molecular and Genetic Epidemiology, Harvard TH Chan School of Public Health, Boston, USA.
    Sinnott, Jennifer
    Department of Epidemiology, Harvard TH Chan School of Public Health, Boston, USA; Department of Statistics, Ohio State University, Columbus, USA.
    Rimm, Eric B.
    Department of Epidemiology, Harvard TH Chan School of Public Health, Boston, USA; Department of Nutrition, Harvard TH Chan School of Public Health, Boston, USA; Channing Division of Network Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, USA.
    Ecsedy, Ethan
    Cabot School, Newton, USA.
    Unger, Robert H.
    Department of Epidemiology, Harvard TH Chan School of Public Health, Boston, USA.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Epidemiology, Harvard TH Chan School of Public Health, Boston, USA; Division of Public Health Sciences, University of Iceland, Reykjavik, Iceland.
    Finn, Stephen
    Department of Pathology, Trinity College, Dublin, Republic of Ireland.
    Jensen, Majken K.
    Department of Nutrition, Harvard TH Chan School of Public Health, Boston, USA; Channing Division of Network Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, USA.
    Rider, Jennifer R.
    Department of Epidemiology, Harvard TH Chan School of Public Health, Boston, USA; Department of Epidemiology, Boston University School of Public Health, Boston, USA.
    Kraft, Peter
    Department of Epidemiology, Harvard TH Chan School of Public Health, Boston, USA; Department of Biostatistics, Harvard TH Chan School of Public Health, Boston, USA; Program in Molecular and Genetic Epidemiology, Harvard TH Chan School of Public Health, Boston, USA.
    Mucci, Lorelei A.
    Department of Epidemiology, Harvard TH Chan School of Public Health, Boston, USA; Channing Division of Network Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, US; Division of Public Health Sciences, University of Iceland, Reykjavik, Iceland.
    Sniffing out significant "Pee values": genome wide association study of asparagus anosmia2016Inngår i: BMJ-BRITISH MEDICAL JOURNAL, E-ISSN 1756-1833, Vol. 355, artikkel-id i6071Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objective: To determine the inherited factors associated with the ability to smell asparagus metabolites in urine.

    Design: Genome wide association study.

    Sstting: Nurses' Health Study and Health Professionals Follow-up Study cohorts.

    Participants: 6909 men and women of European-American descent with available genetic data from genome wide association studies.

    Main outcome measure: Participants were characterized as asparagus smellers if they strongly agreed with the prompt "after eating asparagus, you notice a strong characteristic odor in your urine," and anosmic if otherwise. We calculated per-allele estimates of asparagus anosmia for about nine million single nucleotide polymorphisms using logistic regression. P values <5×10(-8) were considered as genome wide significant.

    Results: 58.0% of men (n=1449/2500) and 61.5% of women (n=2712/4409) had anosmia. 871 single nucleotide polymorphisms reached genome wide significance for asparagus anosmia, all in a region on chromosome 1 (1q44: 248139851-248595299) containing multiple genes in the olfactory receptor 2 (OR2) family. Conditional analyses revealed three independent markers associated with asparagus anosmia: rs13373863, rs71538191, and rs6689553.

    Conclusion: A large proportion of people have asparagus anosmia. Genetic variation near multiple olfactory receptor genes is associated with the ability of an individual to smell the metabolites of asparagus in urine. Future replication studies are necessary before considering targeted therapies to help anosmic people discover what they are missing.

  • 88.
    Markt, Sarah C.
    et al.
    Sch Publ Hlth, Dept Epidemiol, Harvard Univ, Boston, USA.
    Rider, Jennifer R.
    Sch Publ Hlth, Dept Epidemiol, Harvard Univ, Boston, USA; Dept Med, Channing Div Network Med, Brigham & Womens Hosp, Boston, USA; Sch Med, Harvard Univ, Boston, USA .
    Penney, Kathryn L.
    Sch Publ Hlth, Dept Epidemiol, Harvard Univ, Boston, USA; Dept Med, Channing Div Network Med, Brigham & Womens Hosp, Boston, USA; Sch Med, Harvard Univ, Boston, USA .
    Schumacher, Fredrick R.
    Keck Sch Med, Dept Prevent Med, Univ So Calif, Los Angeles, USA.
    Epstein, Mara M.
    Sch Publ Hlth, Dept Epidemiol, Harvard Univ, Boston, USA; Dept Med, Channing Div Network Med, Brigham & Womens Hosp, Boston, USA; Sch Med, Harvard Univ, Boston, USA .
    Fall, Katja
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Department of Epidemiology, Harvard School of Public Health, Boston MA, United States.
    Sesso, Howard D.
    Dept Med, Div Prevent Med, Brigham & Womens Hosp, Boston, USA; Sch Med, Harvard Univ, Boston, USA .
    Stampfer, Meir J.
    Sch Publ Hlth, Dept Epidemiol, Harvard Univ, Boston, USA; Dept Med, Channing Div Network Med, Brigham & Womens Hosp, Boston, USA; Sch Med, Harvard Univ, Boston, USA .
    Mucci, Lorelei A.
    Sch Publ Hlth, Dept Epidemiol, Harvard Univ, Boston, USA; Dept Med, Channing Div Network Med, Brigham & Womens Hosp, Boston, USA; Sch Med, Harvard Univ, Boston, USA .
    Genetic Variation Across C-Reactive Protein and Risk of Prostate Cancer2014Inngår i: The Prostate, ISSN 0270-4137, E-ISSN 1097-0045, Vol. 74, nr 10, s. 1034-1042Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND. Inflammation has been hypothesized to play an important etiological role in the initiation or progression of prostate cancer. Circulating levels of the systemic inflammation marker C-reactive protein (CRP) have been associated with increased risk of prostate cancer. We investigated the role of genetic variation in CRP and prostate cancer, under the hypothesis that variants may alter risk of disease.

    METHODS. We undertook a case-control study nested within the prospective Physicians' Health Study among 1,286 men with incident prostate cancer and 1,264 controls. Four single-nucleotide polymorphisms (SNPs) were selected to capture the common genetic variation across CRP (r(2) > 0.8). We used unconditional logistic regression to assess the association between each SNP and risk of prostate cancer. Linear regression models explored associations between each genotype and plasma CRP levels.

    RESULTS. None of the CRP SNPs were associated with prostate cancer overall. Individuals with one copy of the minor allele (C) in rs1800947 had an increased risk of high-grade prostate cancer (OR: 1.7; 95% CI: 1.1-2.8), and significantly lower mean CRP levels (P-value < 0.001), however, we found no significant association with lethal disease. Mean CRP levels were significantly elevated in men with one or two copies of the minor allele in rs3093075 and rs1417939, but these were unrelated to prostate cancer risk.

    CONCLUSION. Our findings suggest that SNPs in the CRP gene are not associated with risk of overall or lethal prostate cancer. Polymorphisms in CRP rs1800947 may be associated with higher grade disease, but our results require replication in other cohorts.

  • 89.
    Melinder, Carren
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Hiyoshi, Ayako
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Halfvarson, Jonas
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. Department of Gastroenterology, Örebro University Hospital, Örebro, Sweden.
    Montgomery, Scott
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län.
    Stress resilience and the risk of inflammatory bowel disease: a cohort study of men living in Sweden2017Inngår i: BMJ Open, ISSN 2044-6055, E-ISSN 2044-6055, Vol. 7, nr 1, artikkel-id e014315Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    OBJECTIVE: To determine if low psychosocial stress resilience in adolescence (increasing chronic stress arousal throughout life) is associated with an increased inflammatory bowel disease (IBD) risk in adulthood. Subclinical Crohn's disease (CD) and ulcerative colitis (UC) can exist over many years and we hypothesise that psychosocial stress may result in conversion to symptomatic disease through its proinflammatory or barrier function effects.

    DESIGN: National register-based cohort study of men followed from late adolescence to middle age.

    SETTING: A general population cohort of men in Sweden.

    PARTICIPANTS: Swedish population-based registers provided information on all men born between 1952 and 1956 who underwent mandatory Swedish military conscription assessment (n=239 591). Men with any gastrointestinal diagnoses (except appendicitis) prior to follow-up were excluded.

    PRIMARY OUTCOME MEASURES: An inpatient or outpatient diagnosis of CD or UC recorded in the Swedish Patient Register (1970-2009).

    RESULTS: A total of 938 men received a diagnosis of CD and 1799 UC. Lower stress resilience in adolescence was associated with increased IBD risk, with unadjusted HRs (95% CIs) of 1.54 (1.26 to 1.88) and 1.24 (1.08 to 1.42), for CD and UC, respectively. After adjustment for potential confounding factors, including markers of subclinical disease activity in adolescence, they are 1.39 (1.13 to 1.71) and 1.19 (1.03 to 1.37).

    CONCLUSIONS: Lower stress resilience may increase the risk of diagnosis of IBD in adulthood, possibly through an influence on inflammation or barrier function.

  • 90.
    Melinder, Carren
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Hiyoshi, Ayako
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Kasiga, Teresa
    Halfvarson, Jonas
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Gastroenterology, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Montgomery, Scott
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Epidemiology and Public Health, University College London, London, UK; Clinical Epidemiology Unit, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Resilience to stress and risk of gastrointestinal infections2018Inngår i: European Journal of Public Health, ISSN 1101-1262, E-ISSN 1464-360X, Vol. 28, nr 2, s. 364-369Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Exposure to psychological stress can elicit a physiological response that may influence characteristics of the gastrointestinal mucosa, including increased intestinal permeability, in turn possibly increasing susceptibility to gastrointestinal infections. We investigated whether low stress resilience in adolescence is associated with an 'increased' risk of gastrointestinal infections in subsequent adulthood.

    Methods: Data were provided by Swedish registers for a cohort of 237 577 men who underwent military conscription assessment in late adolescence (1969-76). As part of the assessment procedure, certified psychologists evaluated stress resilience through semi-structured interviews. The cohort was followed from conscription assessment until 31 December 2009 (up to age 57 years). Cox regression assessed the association of stress resilience with gastrointestinal infections (n = 5532), with adjustment for family background measures in childhood and characteristics in adolescence. Peptic ulcer disease (PUD) in adulthood was modelled as a time-dependent covariate.

    Results: Compared with high stress resilience, lower stress resilience was associated with a 'reduced' risk of gastrointestinal infections after adjustment for family background in childhood, characteristics in adolescence and PUD in adulthood, with hazard ratios (and 95% confidence intervals) of 0.88 (0.81-0.97) and 0.83 (0.77-0.88) for low and moderate stress resilience, respectively.

    Conclusion: Lower stress resilience in adolescence is associated with reduced risk of gastrointestinal infections in adulthood, rather than the hypothesized increased risk.

  • 91.
    Melinder, Carren
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Hiyoshi, Ayako
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Kasiga, Teresa
    School of Medical Sciences, Örebro University, Örebro, Sweden.
    Halfvarson, Jonas
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Gastroenterology.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Montgomery, Scott
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Epidemiology and Public Health, University College London, London, UK; Clinical Epidemiology Unit, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Resilience to stress and risk of gastrointestinal infectionsManuskript (preprint) (Annet vitenskapelig)
  • 92.
    Meyer, Mara S.
    et al.
    Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Penney, Kathryn L.
    Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Stark, Jennifer R.
    Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Schumacher, Fredrick R.
    Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, USA.
    Sesso, Howard D.
    Division of Preventive Medicine, Department of Medicine, Brigham and Women’s Hospital, Boston, USA.
    Loda, Massimo
    Harvard Radiation Oncology Program Brigham and Women’s Hospital/Dana-Farber Cancer Institute, Boston, USA.
    Fiorentino, Michelangelo
    Harvard Radiation Oncology Program Brigham and Women’s Hospital/Dana-Farber Cancer Institute, Boston, USA.
    Finn, Stephen
    Harvard Radiation Oncology Program Brigham and Women’s Hospital/Dana-Farber Cancer Institute, Boston, USA.
    Flavin, Richard J.
    Harvard Radiation Oncology Program Brigham and Women’s Hospital/Dana-Farber Cancer Institute, Boston, USA.
    Kurth, Tobias
    Department of Epidemiology, Harvard School of Public Health, Boston, USA; Division of Preventive Medicine, Department of Medicine, Brigham and Women’s Hospital, Boston, USA.
    Price, Alkes L.
    Department of Epidemiology, Harvard School of Public Health, Boston, USA; Department of Biostatistics, Harvard School of Public Health, Boston, USA.
    Giovannucci, Edward L.
    Department of Epidemiology, Harvard School of Public Health, Boston, USA; Department of Nutrition, Harvard School of Public Health, Boston,USA.
    Fall, Katja
    Department of Epidemiology, Harvard School of Public Health, Boston, USA; Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden.
    Stampfer, Meir 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.
    Ma, Jing
    Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, USA.
    Mucci, Lorelei 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.
    Genetic variation in RNASEL associated with prostate cancer risk and progression2010Inngår i: Carcinogenesis, ISSN 0143-3334, E-ISSN 1460-2180, Vol. 31, nr 9, s. 1597-603Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Variation in genes contributing to the host immune response may mediate the relationship between inflammation and prostate carcinogenesis. RNASEL at chromosome 1q25 encodes ribonuclease L, part of the interferon-mediated immune response to viral infection. We therefore investigated the association between variation in RNASEL and prostate cancer risk and progression in a study of 1286 cases and 1264 controls nested within the prospective Physicians' Health Study. Eleven single-nucleotide polymorphisms (SNPs) were selected using the web-based 'Tagger' in the HapMap CEPH panel (Utah residents of Northern and Western European Ancestry). Unconditional logistic regression models assessed the relationship between each SNP and incident advanced stage (T(3)/T(4), T(0)-T(4)/M(1) and lethal disease) and high Gleason grade (>/=7) prostate cancer. Further analyses were stratified by calendar year of diagnosis. Cox proportional hazards models examined the relationship between genotype and prostate cancer-specific survival. We also explored associations between genotype and serum inflammatory biomarkers interleukin-6 (IL-6), C-reactive protein (CRP) and tumor necrosis factor-alpha receptor 2 using linear regression. Individuals homozygous for the variant allele of rs12757998 had an increased risk of prostate cancer [AA versus GG; odds ratio (OR): 1.63, 95% confidence interval (CI): 1.18-2.25), and more specifically, high-grade tumors (OR: 1.90, 95% CI: 1.25-2.89). The same genotype was associated with increased CRP (P = 0.02) and IL-6 (P = 0.05) levels. Missense mutations R462Q and D541E were associated with an increased risk of advanced stage disease only in the pre-prostate-specific antigen era. There were no significant associations with survival. The results of this study support a link between RNASEL and prostate cancer and suggest that the association may be mediated through inflammation. These novel findings warrant replication in future studies.

  • 93.
    Montgomery, Scott
    et al.
    Region Örebro län. Örebro universitet, Institutionen för medicinska vetenskaper.
    Bergh, Cecilia
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län.
    Udumyan, Ruzan
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Eriksson, Mats
    Örebro universitet, Institutionen för hälsovetenskaper.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Hiyoshi, Ayako
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län.
    Sex of older siblings and cognitive function2017Konferansepaper (Fagfellevurdert)
    Abstract [en]

    Background : Number of older siblings is associated with lower cognitive function, possibly as marker of material disadvantage. Sex differences may signal an influence of inter-sibling interactions.

    Methods: The study used a national Swedish register-based cohort of men (n=644,603), born between 1970 and 1992 who undertook military conscription assessments in adolescence that included cognitive function measured on a normally-distributed scale of 1-9. Associations with siblings were investigated using linear regression.

    Results: After adjustment for numbers of younger siblings, year of conscription assessment, age/year of birth, sex, European socioeconomic classification for parents and maternal age at delivery; the regression coefficients (and 95% confidence intervals) for cognitive function are -0.26 (-0.27, -0.25), -0.42 (-0.44, -0.40), and -0.72 (-0.76, -0.67) for one, two and three or more male older siblings, respectively, compared with none; and -0.22 (-0.23, -0.21), -0.39 (-.41, -0.37), -0.62 (-0.67, -0.58) for one two and three or more female older siblings, respectively, compared with none. A larger number of younger siblings is not associated with lower cognitive function in the adjusted model.

    Conclusions: Family size is associated with cognitive function: older male siblings may have greater implications than females due to their demands on familial resources or through inter-sibling interactions.

  • 94.
    Montgomery, Scott
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Bergh, Cecilia
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län.
    Udumyan, Ruzan
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Eriksson, Mats
    Örebro universitet, Institutionen för hälsovetenskaper.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Hiyoshi, Ayako
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Sex of older siblings and cognitive function2017Konferansepaper (Fagfellevurdert)
  • 95.
    Montgomery, Scott
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. Karolinska Institutet, Stockholm, Sweden; University College London, London, UK.
    Bergh, Cecilia
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län.
    Udumyan, Ruzan
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Eriksson, Mats
    Örebro universitet, Institutionen för hälsovetenskaper.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Hiyoshi, Ayako
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Sex of older siblings and stress resilience2018Inngår i: Longitudinal and life course studies, ISSN 1124-9064, E-ISSN 1757-9597, Vol. 9, nr 4, s. 447-455Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The aim was to investigate whether older siblings are associated with development of stress resilience in adolescence and if there are differences by sex of siblings. The study used a Swedish register-based cohort of men (n=664 603) born between 1970 and 1992 who undertook military conscription assessments in adolescence that included a measure of stress resilience: associations were assessed using multinomial logistic regression. Adjusted relative risk ratios (95% confidence intervals) for low stress resilience (n=136 746) compared with high (n=142 581) are 1.33 (1.30, 1.35), 1.65 (1.59, 1.71) and 2.36 (2.18, 2.54) for one, two and three or more male older siblings, compared with none. Equivalent values for female older siblings do not have overlapping confidence intervals with males and are 1.19 (1.17, 1.21), 1.46 (1.40, 1.51) and 1.87 (1.73, 2.03). When the individual male and female siblings are compared directly (one male sibling compared with one female sibling, etc.) and after adjustment, including for cognitive function, there is a statistically significant (p<0.005) greater risk for low stress resilience associated with male siblings. Older male siblings may have greater adverse implications for psychological development, perhaps due to greater demands on familial resources or inter-sibling interactions.

  • 96.
    Montgomery, Scott
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Department of Epidemiology and Public Health, University College London, London, UK; Clinical Epidemiology Unit, Department of Medicine, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Brus, Ole
    Faculty of Medicine and Health, Örebro University, Sweden.
    Hiyoshi, Ayako
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Cao, Yang
    Rider, Jennifer
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, USA.
    Fall, Katja
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Clinical Epidemiology Unit, Department of Medicine, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Childhood exposures among mothers and Hodgkin's lymphoma in offspring2015Inngår i: Cancer Epidemiology, ISSN 1877-7821, E-ISSN 1877-783X, Vol. 39, nr 6, s. 1006-1009Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Childhood exposures in mothers, signaled by number of older and younger siblings, have lifelong consequences for aspects of immune function. We hypothesized that these may influence young adult-onset Hodgkin's lymphoma (HL) risk in offspring.

    Materials and methods: Swedish registers identified 2028 cases of young adult onset HL (diagnosed between ages 15-39 years) up to 2012 among those born since 1958; and 18,374 matched controls. Conditional logistic regression was used to assess HL risk associated with number of older and younger siblings of mothers.

    Results: Having a mother with more than two older siblings is associated with lower HL risk, and the association is statistically significant for mothers with three or more siblings, compared with none. The adjusted odds ratios (and 95% confidence intervals) are 1.04 (0.93-1.16); 0.95 (0.81-1.10); and 0.81 (0.66-0.98) for one, two, and three or more older siblings, respectively. There is no association between number of mothers' younger siblings and HL risk.

    Conclusions: Exposures during the childhood of mothers may influence young onset adult HL risk in offspring, perhaps through vertical transmission of infectious agents, or through other long-term influences on maternal immune function.

  • 97.
    Montgomery, Scott
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Region Örebro län. Karolinska Institutet, Stockholm, Sweden .
    Hassan, Ahmad
    School of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Bahmanyar, Shahram
    Karolinska Institutet, Stockholm, Sweden; Golestan University of Medical Sciences, Gorgan, Iran .
    Brus, Ole
    Örebro University Hospital, Örebro, Sweden.
    Hussein, Oula
    Örebro University Hospital, Örebro, Sweden.
    Hiyoshi, Ayako
    Region Örebro län.
    Hillert, Jan
    Karolinska University Hospital Huddinge, Karolinska Institutet, Stockholm, Sweden .
    Olsson, Tomas
    Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden .
    Fall, Katja
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Örebro University Hospital, Örebro, Sweden.
    Mortality following a brain tumour diagnosis in patients with multiple sclerosis2013Inngår i: BMJ Open, ISSN 2044-6055, E-ISSN 2044-6055, Vol. 3, nr 11, artikkel-id e003622Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objectives: As brain tumours and their treatment may theoretically have a poorer prognosis in inflammatory central nervous system diseases such as multiple sclerosis (MS), all-cause mortality following a brain tumour diagnosis was compared between patients with and without MS. The potential role of age at tumour diagnosis was also examined.

    Setting: Hospital inpatients in Sweden with assessment of mortality in hospital or following discharge.

    Participants: Swedish national registers identified 20 543 patients with an MS diagnosis (1969–2005) and they were matched individually to produce a comparison cohort of 204 163 members of the general population without MS. Everyone with a primary brain tumour diagnosis was selected for this study: 111 with MS and 907 without MS.

    Primary and secondary outcome measures: 5-year mortality risk following brain tumour diagnosis and age at brain tumour diagnosis.

    Results: A non-statistically significant lower mortality risk among patients with MS (lower for those with tumours of high-grade and uncertain-grade malignancy and no notable difference for low-grade tumours) produced an unadjusted HR (and 95% CI) of 0.75 (0.56 to 1.02). After adjustment for age at diagnosis, grade of malignancy, sex, region of residence and socioeconomic index, the HR is 0.91 (0.67–1.24). The change in estimate was largely due to adjustment for age at brain tumour diagnosis, as patients with MS were on average 4.7 years younger at brain tumour diagnosis than those in the comparison cohort (p<0.001).

    Conclusions: Younger age at tumour diagnosis may contribute to mortality reduction in those with highgrade and uncertain-grade brain tumours. Survival following a brain tumour is not worse in patients with MS; even after age at brain tumour diagnosis and grade of malignancy are taken into account.

  • 98.
    Montgomery, Scott
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Hiyoshi, Ayako
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Bergh, Cecilia
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län.
    Udumyan, Ruzan
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Eriksson, Mats
    Örebro universitet, Institutionen för hälsovetenskaper.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Foetal risks for low stress resilience are exacerbated by childhood exposures2017Konferansepaper (Fagfellevurdert)
  • 99.
    Mota Garcia, Teresa
    et al.
    Faculty of Health Sciences, University of Beira Interior, Covilhã, Portugal.
    Hiyoshi, Ayako
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Udumyan, Ruzan
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Sjöqvist, Hugo
    Örebro universitet, Handelshögskolan vid Örebro Universitet.
    Fall, Katja
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Montgomery, Scott
    Örebro universitet, Institutionen för medicinska vetenskaper. Clinical Epidemiology Unit, Department of Medicine, Karolinska University Hospital Solna, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology and Public Health, University College, London, London, UK.
    Acne in late adolescence is not associated with a raised risk of subsequent malignant melanoma among men2017Inngår i: Cancer Epidemiology, ISSN 1877-7821, E-ISSN 1877-783X, Vol. 51, s. 44-48Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: To evaluate the association of acne in late adolescence with the risk for subsequent malignant melanoma (MM) in men.

    METHODS: Swedish register-based cohort study of 242,096 males born between 1952 and 1956, who took part in compulsory assessments for Swedish military conscription in late adolescence between 1969 and 1975, with subsequent diagnoses of MM (n=1,058) up to December 31, 2009. Covariates included measures of childhood circumstances and information from adolescence on presence of acne, physical fitness, cognitive function, body mass index (BMI), and a summary of diagnoses. Cox regression was used for the analysis.

    RESULTS: In total 1,058 men were diagnosed with MM. Acne was not associated with subsequent MM, with an adjusted hazard ratio (and 95% confidence interval) of 0.95 (0.61 to 1.49). Men with parents who were agricultural workers, and men who lived in northern Sweden, had lower physical fitness, or lower cognitive function had a lower risk of MM. Overweight and obesity was associated with a raised risk, with an adjusted hazard ratio of 1.39 (1.14, 1.71).

    CONCLUSIONS: Acne in late adolescence is unlikely to represent a raised risk for subsequent MM in men. Overweight or obesity was identified as a raised risk for MM, possibly due to the associated increased skin surface area.

  • 100. Mucci, Lorelei A.
    et al.
    Markt, Sarah
    Sigurdardottir, Lara
    Lockley, Steven W.
    Fall, Katja
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Stampfer, Meir J.
    Gudnason, Vilmundur
    Kraft, Peter
    Rider, Jennifer R.
    Czeisler, Charles A.
    Valdimarsdottir, Unnur Anna
    Circadian dysrhythm and advanced prostate cancer2014Inngår i: Journal of Clinical Oncology, ISSN 0732-183X, E-ISSN 1527-7755, Vol. 32, nr 4Artikkel i tidsskrift (Annet vitenskapelig)
    Abstract [en]

    Background: The circadian rhythm regulates diverse biologic pathways including tumor oncogenes, metabolism, and cell proliferation. Dysregulation of the circadian rhythm arises from faulty input signals such as exposure to light at night, variability in core circadian rhythm genes, and variation in outputs that regulate circadian behavior including melatonin. There is compelling biologic rationale, but little human data, on circadian dysrhythm and advanced prostate cancer.

    Methods: We undertook an integrative molecular epidemiology study of circadian dysrhythm and advanced prostate cancer among men in the Icelandic AGES-Reykjavik cohort and the U.S. Health Professionals Follow-up Study, which allowed integration of questionnaire data, biorepositories, and long-term follow-up. We characterized circadian dysrhythm using complimentary approaches: information on sleep problems from questionnaires, prediagnostic melatonin (6-sulfatoxymelatonin) measured on first morning void urine samples, and genetic variation across twelve circadian clock genes. We used multivariable regression models to estimate relative risks (RR) and 95% confidence intervals (CI) of associations with advanced prostate cancer, adjusted for potential confounders.

    Results: Twenty percent of men reported sleep problems. Men who had trouble falling asleep (RR = 2.1; 95% CI 0.7-6.2) and staying asleep (RR=3.2, 95% CI 1.1-9.7) had an increased risk of developing advanced prostate cancer. Men with sleep problems had significantly lower melatonin levels compared to those without. Low melatonin levels were associated with a statistically significant 4-fold higher risk of advanced prostate cancer compared to those with high levels (95% CI: 1.25-10.0). Variant alleles in two SNPs in cryptochrome (CRY1), involved in generating and maintaining circadian rhythms, were significantly associated with risk of advanced prostate cancer in both cohorts, with a gene-level p-value<0.01.

    Conclusions: Our results suggest there are multiple nodes in the circadian rhythm that are associated with an increased risk of advanced prostate cancer. As such, there is the potential for complimentary strategies to target circadian disruption and reduce the risk of advanced prostate cancer.

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