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  • 1.
    Akre [Fall], Katja
    et al.
    Department of Medical Epidemiology, Karolinska Institute, Stockholm.
    Signorello, Lisa B.
    Engstrand, Lars
    Bergström, Reinhold
    Larsson, Sune
    Eriksson, Bengt I.
    Nyrén, Olof
    Risk for gastric cancer after antibiotic prophylaxis in patients undergoing hip replacement2000In: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 60, no 22, p. 6376-80Article in journal (Refereed)
    Abstract [en]

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

  • 2.
    Blattner, Mirjam
    et al.
    Weill Cornell Med Coll, New York NY, USA.
    Lee, Daniel
    Weill Cornell Med Coll, New York NY, USA.
    O'Reilly, Catherine
    Weill Cornell Med Coll, New York NY, USA.
    Park, Kyung
    Weill Cornell Med Coll, New York NY, USA.
    MacDonald, Theresa Y.
    Weill Cornell Med Coll, New York NY, USA.
    Khani, Francesca
    Weill Cornell Med Coll, New York NY, USA.
    Turner, Kevin
    Weill Cornell Med Coll, New York NY, USA.
    Wild, Peter J.
    Univ Zurich Hosp, Zurich, Switzerland.
    Hieronymus, Haley
    Mem Sloan Kettering Canc Ctr, New York NY, USA.
    Sawyers, Charles L.
    Mem Sloan Kettering Canc Ctr, New York NY, USA.
    Tewari, Ashutosh K.
    Weill Cornell Med Coll, New York, USA.
    Moch, Holger
    Univ Zurich Hosp, Zurich, Switzerland.
    Yoon, Ghil Suk
    Sch Med, Kyungpook Natl Univ, Daegu, South Korea.
    Andrén, Ove
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Fall, Katja
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Mosquera, Juan Miguel
    Weill Cornell Med Coll, New York NY, USA.
    Robinson, Brian D.
    Weill Cornell Med Coll, New York NY, USA.
    Sboner, Andrea
    Weill Cornell Med Coll, New York NY, USA.
    Barbierie, Christopher E.
    Weill Cornell Med Coll, New York NY, USA.
    Rubin, Mark A.
    Weill Cornell Med Coll, New York NY, USA.
    SPOP mutations in prostate cancer across demographically diverse patient cohorts2014In: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 74, no 19, article id 2244Article in journal (Other academic)
  • 3.
    Fang, Fang
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fall, Katja
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology, Harvard School of Public Health, Boston, USA; Centre of Public Health Sciences, School of Health Sciences, University of Iceland, Reykjavík, Iceland.
    Sparén, Pär
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Adami, Hans-Olov
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology, Harvard School of Public Health, Boston, USA.
    Valdimarsdóttir, Heiddis B.
    Department of Psychology, University of Iceland, Reykjavík, Iceland; Department of Oncological Sciences, Mount Sinai School of Medicine, New York, USA.
    Lambe, Mats
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Regional Oncologic Center, Uppsala, Sweden.
    Valdimarsdóttir, Unnur
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology, Harvard School of Public Health, Boston, USA; Centre of Public Health Sciences, School of Health Sciences, University of Iceland, Reykjavík, Iceland.
    Risk of infection-related cancers after the loss of a child: a follow-up study in Sweden2011In: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 71, no 1, p. 116-22Article in journal (Refereed)
    Abstract [en]

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

  • 4.
    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 cancer2010In: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 70, no 8, p. 3136-9Article in journal (Refereed)
    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.

  • 5.
    Gnosa, Sebastian
    et al.
    Linköping University, Linköping, Sweden.
    Brodin, Veronika Patcha
    Linköping University, Linköping, Sweden.
    Ticha, Ivana
    Linköping University, Linköping, Sweden.
    Adell, Gunnar
    Linköping University, Linköping, Sweden.
    Arbman, Gunnar
    Vrinnevi Hospital, Norrköping, Sweden.
    Zhang, Hong
    Örebro University, School of Medicine, Örebro University, Sweden.
    Sun, Xiao-Feng
    Linköping University, Linköping, Sweden.
    Genetic variants and expression of AEG-1 in relation to clinical outcome and radiotherapy response in colorectal cancer patients and cell lines2014In: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 74, no 19Article in journal (Other academic)
  • 6.
    Hilvo, Mika
    et al.
    Bio and Process Technology, VTT Technical Research Centre of Finland, Espoo, Finland.
    Denkert, Carsten
    Institute of Pathology, Berlin, Germany.
    Lehtinen, Laura
    Bio and Process Technology, VTT Technical Research Centre of Finland, Turku, Finland.
    Müller, Berit
    Institute of Pathology, Berlin, Germany.
    Brockmöller, Scarlet
    Institute of Pathology, Berlin, Germany.
    Seppänen-Laakso, Tuulikki
    Bio and Process Technology, VTT Technical Research Centre of Finland, Espoo, Finland.
    Budczies, Jan
    Institute of Pathology, Berlin, Germany.
    Bucher, Elmar
    Bio and Process Technology, VTT Technical Research Centre of Finland, Turku, Finland.
    Yetukuri, Laxman
    Bio and Process Technology, VTT Technical Research Centre of Finland, Espoo, Finland.
    Castillo, Sandra
    Bio and Process Technology, VTT Technical Research Centre of Finland, Espoo, Finland.
    Berg, Emilia
    Bio and Process Technology, VTT Technical Research Centre of Finland, Espoo, Finland.
    Nygren, Heli
    Bio and Process Technology, VTT Technical Research Centre of Finland, Espoo, Finland.
    Sysi-Aho, Marko
    Bio and Process Technology, VTT Technical Research Centre of Finland, Espoo, Finland.
    Griffin, Julian L.
    Department of Biochemistry, University of Cambridge, Cambridge, United Kingdom.
    Fiehn, Oliver
    Genome Center, University of California, Davis CA, United States.
    Loibl, Sibylle
    German Breast Group, GBG-Forschungs GmbH, Neu-Isenburg, Germany.
    Richter-Ehrenstein, Christiane
    cBreast Cancer Center, Charité University Hospital, Berlin, Germany.
    Radke, Cornelia
    Institute of Pathology, DRK Klinikum Berlin Köpenick, Berlin, Germany.
    Hyötyläinen, Tuulia
    Örebro University, School of Science and Technology. Bio and Process Technology, VTT Technical Research Centre of Finland, Espoo, Finland.
    Kallioniemi, Olli
    Bio and Process Technology, VTT Technical Research Centre of Finland, Turku, Finland.
    Iljin, Kristiina
    Bio and Process Technology, VTT Technical Research Centre of Finland, Turku, Finland.
    Oresic, Matej
    Bio and Process Technology, VTT Technical Research Centre of Finland, Espoo, Finland.
    Novel theranostic opportunities offered by characterization of altered membrane lipid metabolism in breast cancer progression2011In: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 71, no 9, p. 3236-45Article in journal (Refereed)
    Abstract [en]

    Activation of lipid metabolism is an early event in carcinogenesis and a central hallmark of many cancers. However, the precise molecular composition of lipids in tumors remains generally poorly characterized. The aim of the present study was to analyze the global lipid profiles of breast cancer, integrate the results to protein expression, and validate the findings by functional experiments. Comprehensive lipidomics was conducted in 267 human breast tissues using ultraperformance liquid chromatography/ mass spectrometry. The products of de novo fatty acid synthesis incorporated into membrane phospholipids, such as palmitate-containing phosphatidylcholines, were increased in tumors as compared with normal breast tissues. These lipids were associated with cancer progression and patient survival, as their concentration was highest in estrogen receptor-negative and grade 3 tumors. In silico transcriptomics database was utilized in investigating the expression of lipid metabolism related genes in breast cancer, and on the basis of these results, the expression of specific proteins was studied by immunohistochemistry. Immunohistochemical analyses showed that several genes regulating lipid metabolism were highly expressed in clinical breast cancer samples and supported also the lipidomics results. Gene silencing experiments with seven genes [ACACA (acetyl-CoA carboxylase α), ELOVL1 (elongation of very long chain fatty acid-like 1), FASN (fatty acid synthase), INSIG1 (insulin-induced gene 1), SCAP (sterol regulatory element-binding protein cleavage-activating protein), SCD (stearoyl-CoA desaturase), and THRSP (thyroid hormone-responsive protein)] indicated that silencing of multiple lipid metabolism-regulating genes reduced the lipidomic profiles and viability of the breast cancer cells. Taken together, our results imply that phospholipids may have diagnostic potential as well as that modulation of their metabolism may provide therapeutic opportunities in breast cancer treatment.

  • 7.
    Jerby, Livnat
    et al.
    School of Computer Sciences, Tel Aviv University, Tel Aviv, Israel.
    Wolf, Lior
    School of Computer Sciences, Tel Aviv University, Tel Aviv, Israel.
    Denkert, Carsten
    Institute of Pathology, Charité Hospital, Berlin, Germany.
    Stein, Gideon Y.
    Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel; Department of Internal Medicine B, Beilinson Hospital, Rabin Medical Center, Petah-Tikva, Israel.
    Hilvo, Mika
    VTT Technical Research Centre of Finland, Espoo, Finland.
    Oresic, Matej
    VTT Technical Research Centre of Finland, Espoo, Finland.
    Geiger, Tamar
    Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
    Ruppin, Eytan
    School of Computer Sciences, Tel Aviv University, Tel Aviv, Israel; Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
    Metabolic associations of reduced proliferation and oxidative stress in advanced breast cancer2012In: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 72, no 22, p. 5712-5720Article in journal (Refereed)
    Abstract [en]

    Aberrant metabolism is a hallmark of cancer, but whole metabolomic flux measurements remain scarce. To bridge this gap, we developed a novel metabolic phenotypic analysis (MPA) method that infers metabolic phenotypes based on the integration of transcriptomics or proteomics data within a human genome-scale metabolic model. MPA was applied to conduct the first genome-scale study of breast cancer metabolism based on the gene expression of a large cohort of clinical samples. The modeling correctly predicted cell lines' growth rates, tumor lipid levels, and amino acid biomarkers, outperforming extant metabolic modeling methods. Experimental validation was obtained in vitro. The analysis revealed a subtype-independent "go or grow" dichotomy in breast cancer, where proliferation rates decrease as tumors evolve metastatic capability. MPA also identified a stoichiometric tradeoff that links the observed reduction in proliferation rates to the growing need to detoxify reactive oxygen species. Finally, a fundamental stoichiometric tradeoff between serine and glutamine metabolism was found, presenting a novel hallmark of estrogen receptor (ER)(+) versus ER(-) tumor metabolism. Together, our findings greatly extend insights into core metabolic aberrations and their impact in breast cancer.

  • 8.
    Lee, Jung Eun
    et al.
    Sookmyung Women's University, Seoul, Republic of Korea.
    Kim, Nayeon
    Sookmyung Women's University, Seoul, Republic of Korea.
    Adami, Hans-Olov
    Harvard School of Public Health, Boston MA, USA.
    Lindblad, Per
    Örebro University, School of Medical Sciences.
    Body mass, smoking habit, and hypertension and renal cell cancer survival2015In: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 75, article id 883Article in journal (Other academic)
  • 9.
    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 University, School of Medical Sciences. 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 Cancer2019In: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 79, no 15, p. 3965-3972Article in journal (Refereed)
    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.

  • 10.
    Lu, Donghao
    et al.
    Department of Medical Epidemiology & Biostatistics, Karolinska Institute, Stockholm, Sweden.
    Andrae, Bengt
    Dept of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden.
    Valdimarsdóttir, Unnur
    Faculty of Medicine, Center of Public Health Sciences, School of Health Sciences, University of Iceland, Reykjavik, Iceland.
    Sundström, Karin
    Laboratory Medicine, Karolinska Institute, Stockholm, Sweden.
    Fall, Katja
    Örebro University, School of Medical Sciences.
    Sparén, Pär
    Department of Medical Epidemiology & Biostatistics, Karolinska Institute, Stockholm, Sweden.
    Fang, Fang
    Department of Medical Epidemiology & Biostatistics, Karolinska Institute, Stockholm, Sweden.
    Psychological distress is associated with cancer-specific mortality among patients with cervical cancer2019In: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, article id canres.0116.2019Article in journal (Refereed)
    Abstract [en]

    Emerging evidence suggests a role of psychological factors in the progression of different cancer types. However, it is unclear whether psychological 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. Psychological 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 hazard ratios (HRs) of cancer-specific mortality among the patients exposed to psychological distress, compared to unexposed patients, controlling for socioeconomic characteristics and other known prognostic indicators such as tumor and treatment characteristics. We found that patients exposed to psychological distress had an increased risk of cancer-specific mortality (HR 1.33, 95% CI 1.14 to 1.54). The association was primarily driven by distress experienced within one year before or after diagnosis (HR 1.30, 95% CI 1.11 to 1.52), but not thereafter (HR 1.12, 95% CI 0.84 to 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.

  • 11.
    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 University, School of Medical Sciences. 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 Sweden2016In: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 76, no 3, p. 643-651Article in journal (Refereed)
    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.

  • 12.
    Rider, Jennifer R.
    et al.
    Boston University School of Public Health, Boston, MA, USA.
    Erlandsson, Ann
    Örebro University Hospital, Örebro, Sweden.
    Vyas, Chirag
    Boston University School of Public Health, Boston, MA, USA.
    Davidsson, Sabina
    Örebro University Hospital, Örebro, Sweden.
    Carlsson, Jessica
    Örebro University, School of Medical Sciences. Örebro University Hospital, Örebro, Sweden.
    Andersson, Swen-Olof
    Örebro University Hospital, Örebro, Sweden.
    Andren, Ove
    Örebro University Hospital, Örebro, Sweden.
    iNOS expression and lethal prostate cancer in patients with localized disease2017In: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, no 22S, article id B26Article in journal (Refereed)
    Abstract [en]

    Inducible nitric oxide synthase (iNOS) has demonstrated both tumor-promoting and tumor-inhibiting effects in prostate cancer. However, the relationship between iNOS protein expression and long-term prostate cancer outcomes is unclear. We evaluated iNOS expression in tumor epithelia and stroma in 300 men with localized tumors diagnosed incidentally by transurethral resection of the prostate (TURP) in Sweden. In this extreme case-control design, cases (N=132) died of prostate cancer and controls (N=168) survived at least 8 years following diagnosis without death from prostate cancer or a competing cause. Immunohistochemistry was undertaken with a polyclonal rabbit anti-human NOS2 antibody (Abcam) and the Ventana (Roche) semi-automated staining system. Two observers individually scored the staining according to intensity and number of positive cells from 0-3. The median value across cores in each patient were then categorized as <1, >1-<2, and >2, separately for epithelial and stromal compartments. Odds ratios for lethal prostate cancer were estimated with logistic regression controlling for the matching factors (age, calendar year of diagnosis), as well as tumor stage, Gleason score, and percent tumor. iNOS was expressed by stromal-associated M1 macrophages and fibroblasts, as well as tumor cells. Gleason score was positively associated with both stromal and epithelial iNOS staining. In the stroma, there was no statistically significant association between iNOS expression and lethal prostate cancer after adjustment for clinical covariates. However, the odds of lethal prostate cancer increased with tumor expression of iNOS in the fully adjusted model. Compared to patients with the lowest category of iNOS expression, the odds ratios for lethal prostate cancer were 2.96 (95% CI: 1.26-6.96) for patients in the second category and 3.80 (95% CI: 1.45-9.97) for patients in the top category. These results suggest that iNOS may help to identify patients with aggressive prostate cancer at the time of diagnosis, or may be a therapeutic target. Given previously reported in vitro data suggesting that iNOS promotes proliferation of androgen-independent prostate tumors, future analyses will investigate association between iNOS expression and time to castration-resistant prostate cancer in this patient population.

  • 13.
    Stopsack, Konrad H.
    et al.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, USA; Department of Internal Medicine, Mayo Clinic, Rochester, USA.
    Gerke, Travis A.
    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 FL, USA.
    Sinnott, Jennifer A.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, USA; Department of Statistics, Ohio State University, Columbus OH, USA.
    Penney, Kathryn L.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, USA; Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, USA; Channing Division of Network Medicine, Department of Medicine, Harvard Medical School, Boston, USA.
    Tyekucheva, Svitlana
    Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, USA; Department of Biostatistics and Computational Biology, Dana-Farber Cancer Institute, Boston, USA.
    Sesso, Howard D.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, USA; Divisions of Preventive Medicine and Aging, Department of Medicine, Brigham and Women's Hospital, Boston, USA; Divisions of Preventive Medicine and Aging, Department of Medicine, Harvard Medical School, Boston, USA.
    Andersson, Swen-Olof
    Örebro University, School of Health Sciences. Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Andrén, Ove
    Örebro University, School of Medical Sciences. Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Cerhan, James R.
    Department of Health Sciences Research, Mayo Clinic, Rochester, USA.
    Giovannucci, Edward L.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, USA; Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, USA; Channing Division of Network Medicine, Department of Medicine, Harvard Medical School, Boston, USA; Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, USA.
    Mucci, Lorelei A.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, USA; Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Boston MA, USA; Channing Division of Network Medicine, Department of Medicine, Harvard Medical School, Boston MA, USA.
    Rider, Jennifer R.
    Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, USA; Department of Epidemiology, Boston University School of Public Health, Boston, USA.
    Cholesterol Metabolism and Prostate Cancer Lethality2016In: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 76, no 16, p. 4785-4790Article in journal (Refereed)
    Abstract [en]

    Cholesterol metabolism has been implicated in prostate cancer pathogenesis. Here, we assessed the association of intratumoral mRNA expression of cholesterol synthesis enzymes, transporters, and regulators in tumor specimen at diagnosis and lethal prostate cancer, defined as mortality or metastases from prostate cancer in contrast to nonlethal disease without evidence of metastases after at least 8 years of follow-up. We analyzed the prospective prostate cancer cohorts within the Health Professionals Follow-up Study (n = 249) and the Physicians' Health Study (n = 153) as well as expectantly managed patients in the Swedish Watchful Waiting Study (n = 338). The expression of squalene monooxygenase (SQLE) was associated with lethal cancer in all three cohorts. Men with high SQLE expression (>1 standard deviation above the mean) were 8.3 times (95% confidence interval, 3.5 to 19.7) more likely to have lethal cancer despite therapy compared with men with the mean level of SQLE expression. Absolute SQLE expression was associated with lethal cancer independently from Gleason grade and stage, as was a SQLE expression ratio in tumor versus surrounding benign prostate tissue. Higher SQLE expression was tightly associated with increased histologic markers of angiogenesis. Collectively, this study establishes the prognostic value of intratumoral cholesterol synthesis as measured via SQLE, its second rate-limiting enzyme. SQLE expression at cancer diagnosis is prognostic for lethal prostate cancer both after curative-intent prostatectomy and in a watchful waiting setting, possibly by facilitating micrometastatic disease.

  • 14.
    Udumyan, Ruzan
    et al.
    Örebro University, School of Medical Sciences.
    Montgomery, Scott
    Örebro University, School of Medical Sciences. Örebro University Hospital. Clinical Epidemiology Unit, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology and Public Health, University College London, London, United Kingdom.
    Fang, Fang
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Almroth, Henrik
    Department of Cardiology, Department of Medical and Health Sciences, Linköping University, Linköping, Sweden.
    Valdimarsdottir, Unnur
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Center of Public Health Sciences, University of Iceland, Reykjavik, Iceland; Department of Epidemiology, Harvard School of Public Health, Boston MA, United States.
    Ekbom, Anders
    Clinical Epidemiology Unit, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Smedby, Karin E.
    Clinical Epidemiology Unit, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden; Hematology Center, Karolinska University Hospital, Stockholm, Sweden.
    Fall, Katja
    Örebro University, School of Medical Sciences. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Beta-Blocker Drug Use and Survival among Patients with Pancreatic Adenocarcinoma2017In: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 77, no 13, p. 3700-3707Article in journal (Refereed)
    Abstract [en]

    Preclinical studies have suggested that beta-adrenergic signaling is involved in pancreatic cancer progression. Prompted by such studies, we investigated an association between beta-blocker drug use with improved cancer-specific survival in a large, general population-based cohort of patients with pancreatic ductal adenocarcinoma (PDAC). All patients diagnosed with a first primary PDAC in Sweden between 2006 and 2009 were identified through the Swedish Cancer Register (n = 2,394). We obtained information about use of beta-blockers and other medications through linkage with the national Prescribed Drug Register. Cancer-specific mortality was assessed using the Swedish Cause of Death Register. We used multivariable Cox regression adjusted for sociodemographic factors, tumor characteristics, comorbidity score, and other medications to estimate HRs and 95% confidence intervals (CI) for cancer-specific mortality associated with beta-blocker use during the 90-day period before cancer diagnosis. A total of 2,054 (86%) died, with pancreatic cancer recorded as the underlying cause of death during a maximum of 5-year follow-up (median 5 months). Patients who used beta-blockers (n = 522) had a lower cancer-specific mortality rate than nonusers (adjusted HR, 0.79; 95% CI, 0.70-0.90; P < 0.001). This observed rate reduction was more pronounced among patients with localized disease at diagnosis (n = 517; adjusted HR, 0.60; 95% CI, 0.43-0.83; P = 0.002), especially for users with higher daily doses (HR, 0.54; 95% CI, 0.35-0.83; P = 0.005). No clear rate differences were observed by beta-blocker receptor selectivity. Our results support the concept that beta-blocker drugs may improve the survival of PDAC patients, particularly among those with localized disease.

  • 15.
    Valachis, Antonis
    et al.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Oncology.
    Carlsson, L.
    Department of Oncology, Sundsvall County Hospital, Sundsvall, Sweden.
    Sundqvist, M.
    Breast Unit, Department of Surgery, Kalmar County Hospital, Kalmar, Sweden.
    Li, B.
    Real World & Analytic Solutions (RWAS), IQVIA, Stockholm, Sweden.
    Chiesa, F.
    Real World & Analytic Solutions (RWAS), IQVIA, Stockholm, Sweden.
    Uhde, M.
    Real World & Analytic Solutions (RWAS), IQVIA, Stockholm, Sweden.
    Sanglier, T.
    PHC Data Science, F Hoffmann-La Roche Ltd, Basel, Switzerland.
    Use of subcutaneous and intravenous trastuzumab: Real-world experience from three hospitals in Sweden2019In: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 79, no 4, article id P6-17-24Article in journal (Other academic)
  • 16.
    Yang, Haomin
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Inst, Stockholm, Sweden.
    Brand, Judith S.
    Department of Medical Epidemiology and Biostatistics, Karolinska Inst, Stockholm, Sweden.
    Li, Jingmei
    Department of Medical Epidemiology and Biostatistics, Karolinska Inst, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Medical Epidemiology and Biostatistics, Karolinska Inst, Stockholm, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden.
    Ugalde-Morales, Emilio
    Department of Medical Epidemiology and Biostatistics, Karolinska Inst, Stockholm, Sweden.
    Chiesa, Flaminia
    Department of Medical Epidemiology and Biostatistics, Karolinska Inst, Stockholm, Sweden.
    Hall, Per
    Department of Medical Epidemiology and Biostatistics, Karolinska Inst, Stockholm, Sweden.
    Czene, Kamila
    Department of Medical Epidemiology and Biostatistics, Karolinska Inst, Stockholm, Sweden.
    Risk and predictors of psoriasis in breast cancer patients: A Swedish population based cohort study2018In: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 78, no 4Article in journal (Other academic)
1 - 16 of 16
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