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  • 1.
    Adams, Charleen
    et al.
    MRC Integrative Epidemiology Unit at the University of Bristol, Bristol, United Kingdom.; University of Bristol, Bristol, United Kingdom..
    Richmond, Rebecca C.
    Santos Ferreira, Diana L
    Spiller, Wes
    Tan, Vanessa Y
    Zheng, Jie
    Wurtz, Peter
    Donovan, Jenny L
    Hamdy, Freddie C
    Neal, David E
    Lane, J Athene
    Davey Smith, George
    Relton, Caroline L
    Eeles, Rosalind A
    Henderson, Brian E
    Haiman, Christopher A
    Kote-Jarai, Zsofia
    Schumacher, Fredrick R
    Amin Al Olama, Ali
    Benlloch, Sara
    Muir, Kenneth
    Berndt, Sonja I
    Conti, David V
    Wiklund, Fredrik
    Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden..
    Chanock, Stephen J
    Gapstur, Susan M
    Stevens, Victoria L
    Tangen, Catherine M
    Batra, Jyotsna
    Clements, Judith A
    Grönberg, Henrik
    Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden..
    Pashayan, Nora
    Schleutker, Johanna
    Albanes, Demetrius
    Wolk, Alicja
    Division of Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden..
    West, Catharine M L
    Mucci, Lorelei A
    Cancel-Tassin, Geraldine
    Koutros, Stella
    Sørensen, Karina D
    Maehle, Lovise
    Travis, Ruth C
    Hamilton, Robert
    Ingles, Sue Ann
    Rosenstein, Barry S
    Lu, Yong-Jie
    Giles, Graham G
    Kibel, Adam S
    Vega, Ana
    Kogevinas, Manolis
    Penney, Kathryn L
    Park, Jong Y
    Stanford, Janet L
    Cybulski, Cezary
    Nordestgaard, Borge G
    Brenner, Hermann
    Maier, Christiane
    Kim, Jeri
    John, Esther M
    Teixeira, Manuel R
    Neuhausen, Susan L
    DeRuyck, Kim
    Razack, Azad
    Newcomb, Lisa F
    Lessel, Davor
    Kaneva, Radka P
    Usmani, Nawaid
    Claessens, Frank
    Townsend, Paul
    Gago Dominguez, Manuela
    Roobol, Monique J
    Menegaux, Florence
    Khaw, Kay-Tee
    Cannon-Albright, Lisa A
    Pandha, Hardev
    Thibodeau, Stephen N
    Martin, Richard M
    Circulating Metabolic Biomarkers of Screen-Detected Prostate Cancer in the ProtecT Study2019In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 28, no 1, p. 208-216Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Whether associations between circulating metabolites and prostate cancer are causal is unknown. We report on the largest study of metabolites and prostate cancer (2,291 cases and 2,661 controls) and appraise causality for a subset of the prostate cancer-metabolite associations using two-sample Mendelian randomization (MR).

    MATERIALS AND METHODS: The case-control portion of the study was conducted in nine UK centres with men aged 50-69 years who underwent prostate-specific antigen (PSA) screening for prostate cancer within the Prostate testing for cancer and Treatment (ProtecT) trial. Two data sources were used to appraise causality: a genome-wide association study (GWAS) of metabolites in 24,925 participants and a GWAS of prostate cancer in 44,825 cases and 27,904 controls within the Association Group to Investigate Cancer Associated Alterations in the Genome (PRACTICAL) consortium.

    RESULTS: Thirty-five metabolites were strongly associated with prostate cancer (p <0.0014, multiple-testing threshold). These fell into four classes: i) lipids and lipoprotein subclass characteristics (total cholesterol and ratios, cholesterol esters and ratios, free cholesterol and ratios, phospholipids and ratios, and triglyceride ratios); ii) fatty acids and ratios; iii) amino acids; iv) and fluid balance. Fourteen top metabolites were proxied by genetic variables, but MR indicated these were not causal.

    CONCLUSIONS: We identified 35 circulating metabolites associated with prostate cancer presence, but found no evidence of causality for those 14 testable with MR. Thus, the 14 MR-tested metabolites are unlikely to be mechanistically important in prostate cancer risk.

    IMPACT: The metabolome provides a promising set of biomarkers that may aid prostate cancer classification.

  • 2.
    Ahlin, Cecilia
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology.
    Zhou, Wenjing
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Endocrine Surgery.
    Holmqvist, Marit
    Holmberg, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Endocrine Surgery.
    Nilsson, Cecilia
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm , Centre for Clinical Research, County of Västmanland.
    Jirström, Karin
    Blomqvist, Carl
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology.
    Amini, Rose-Marie
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology.
    Fjällskog, Marie-Louise
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology.
    Cyclin A is a proliferative marker with good prognostic value in node-negative breast cancer2009In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 18, no 9, p. 2501-2506Article in journal (Refereed)
    Abstract [en]

    Background: Proliferative markers are not recommended as prognostic   factors for clinical use in breast cancer due to lack of   standardization in methodology. However, proliferation is driving   several gene expression signatures emphasizing the need for a reliable   proliferative marker IF or clinical use. Studies suggest that cyclin A   is a prognostic marker with satisfying reproducibility. We investigated   cyclin A as a prognostic marker in node-negative breast cancer using   previously defined cutoff values.   Patients and Methods: In a case-control study, we defined 190 women who   died from breast cancer as cases and 190 women alive at the time for   the corresponding case's death as controls. Inclusion criteria were   tumor size <= 50 mm, no lymph node metastases and no adjuvant   chemotherapy. Tumor tissues were immunostained for cyclin A using   commercially available antibodies.   Results: We found a statistically significant association between   expression of cyclin A and breast cancer death in a univariate model:   odds ratio for cyclin A(ave) 2.7 [95% confidence interval (CI),   1.7-4.3] and cyclin A(max) 3.4 (CI, 2.1-5.5). Corresponding odds ratio   for Ki67 were Ki67(ave) 1.9 (CI, 1.2-3.1) and Ki67(max) 1.7 (CI,   1.1-2.7) and for grade 3.1 (CI, 1.8-5.1). Cyclin A was strongly   correlated to Ki67 and grade why a model including all was not   appropriate.   Conclusions: Cyclin A is a prognostic factor for breast cancer death in   node-negative patients using standardized methodology regarding scoring   and cutoff values. Adding cyclin A as a proliferative marker to established clinicopathologic factors will improve the separation of  low and high risk breast cancer.

  • 3.
    Argirion, Ilona
    et al.
    NCI, Div Canc Epidemiol & Genet, Rockville, MD USA..
    Pfeiffer, Ruth M.
    NCI, Div Canc Epidemiol & Genet, Rockville, MD USA..
    Proietti, Carla
    James Cook Univ, Australian Inst Trop Hlth & Med, Ctr Mol Therapeut, Cairns, Qld, Australia..
    Coghill, Anna E.
    NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.;H Lee Moffitt Canc Ctr & Res Inst, Canc Epidemiol Program, Div Populat Sci, Tampa, FL USA..
    Yu, Kelly J.
    NCI, Div Canc Epidemiol & Genet, Rockville, MD USA..
    Middeldorp, Jaap M.
    Vrije Univ Amsterdam Med Ctr, Amsterdam, Netherlands..
    Sarathkumara, Yomani D.
    James Cook Univ, Australian Inst Trop Hlth & Med, Ctr Mol Therapeut, Cairns, Qld, Australia..
    Hsu, Wan-Lun
    Fu Jen Catholic Univ, Coll Med, Master Program Big Data Biomed, New Taipei, Taiwan.;Fu Jen Catholic Univ, Coll Med, Data Sci Ctr, New Taipei, Taiwan..
    Chien, Yin-Chu
    Acad Sinica, Genom Res Ctr, Taipei, Taiwan.;Natl Hlth Res Inst, Natl Inst Canc Res, Miaoli, Taiwan..
    Lou, Pei-Jen
    Natl Taiwan Univ Hosp & Coll Med, Dept Otolaryngol, Taipei, Taiwan..
    Wang, Cheng-Ping
    Natl Taiwan Univ Hosp & Coll Med, Dept Otolaryngol, Taipei, Taiwan..
    Rothman, Nathaniel
    NCI, Div Canc Epidemiol & Genet, Rockville, MD USA..
    Lan, Qing
    NCI, Div Canc Epidemiol & Genet, Rockville, MD USA..
    Chen, Chien-Jen
    Acad Sinica, Genom Res Ctr, Taipei, Taiwan.;Natl Taiwan Univ, Grad Inst Epidemiol & Prevent Med, Coll Publ Hlth, Taipei, Taiwan..
    Mbulaiteye, Sam M.
    NCI, Div Canc Epidemiol & Genet, Rockville, MD USA..
    Jarrett, Ruth F.
    Univ Glasgow, MRC, Ctr Virus Res, Glasgow, Lanark, Scotland..
    Glimelius, Ingrid
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology.
    Smedby, Karin E.
    Karolinska Inst, Dept Med Solna, Div Clin Epidemiol, Stockholm, Sweden..
    Hjalgrim, Henrik
    Statens Serum Inst, Copenhagen, Denmark.;Rigshosp, Dept Haematol, Copenhagen, Denmark..
    Hildesheim, Allan
    NCI, Div Canc Epidemiol & Genet, Rockville, MD USA..
    Doolan, Denise L.
    James Cook Univ, Australian Inst Trop Hlth & Med, Ctr Mol Therapeut, Cairns, Qld, Australia..
    Liu, Zhiwei
    NCI, Div Canc Epidemiol & Genet, Rockville, MD USA..
    Comparative Analysis of the Humoral Immune Response to the EBV Proteome across EBV-Related Malignancies2023In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 32, no 5, p. 687-696Article in journal (Refereed)
    Abstract [en]

    Background: Epstein-Barr virus (EBV) is linked to multiple cancers, including classical Hodgkin lymphoma (cHL), endemic Burkitt lymphoma (eBL), nasopharyngeal carcinoma (NPC), and extranodal natural killer/T-cell lymphoma (NKTCL).

    Methods: Anti-EBV IgG and IgA antibody responses target-ing 202 sequences from 86 EBV proteins were measured using the same EBV whole proteome array across four case-control studies investigating EBV-positive cHL, eBL, NPC, and NKTCL (407 cases/620 controls). We grouped EBV-targeted antibodies into pathways by immunoglobulin type (IgA and IgG) and life-cycle stage (latent, immediate early lytic, early lytic, late lytic, and glycoprotein) and evaluated their associ-ation with each cancer type. In an additional analysis, we focused on the subset of 46 individual antibodies repre-senting the top candidates for each cancer and compared their associations across the four cancer types using multivariable linear regression models.

    Results: IgA antibody responses targeting all EBV life-cycle stages were associated with NPC but limited to anti-early lytic stage for cHL. NPC and eBL were associated with IgG antibodies across the viral life cycle; cHL with antibodies in the early lytic, late lytic and glyco-protein stages; and NKTCL with antibodies in the latent, immediate early lytic and early lytic phases. EBNA3A, BBLF1, BDLF4, and BLRF2 IgG antibodies were associated with all cancer types.Conclusions: Our observed similarities and differences across four EBV-associated cancers may inform EBV-related oncogenesis.

    Impact: Understanding the comparative humoral immune response across EBV-related cancers may aid in identifying shared etiologic roles of EBV proteins and inform unique pathogenic processes for each cancer.

  • 4.
    Blom, Johannes
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Colorectal Surgery.
    Yin, Li
    Lidén, Annika
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Colorectal Surgery.
    Dolk, Anders
    Jeppsson, Bengt
    Påhlman, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Colorectal Surgery.
    Holmberg, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Endocrine Surgery.
    Nyrén, Olof
    A 9-year follow-up study of participants and nonparticipants in sigmoidoscopy screening: importance of self-selection2008In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 17, no 5, p. 1163-1168Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Self-selection may compromise cost-effectiveness of screening programs. We hypothesized that nonparticipants have generally higher morbidity and mortality than participants. METHODS: A Swedish population-based random sample of 1,986 subjects ages 59 to 61 years was invited to sigmoidoscopy screening and followed up for 9 years by means of multiple record linkages to health and population registers. Gender-adjusted cancer incidence rate ratio (IRR) and overall and disease group-specific and mortality rate ratio (MRR) with 95% confidence intervals (95% CI) were estimated for nonparticipants relative to participants. Cancer and mortality rates were also estimated relative to the age-matched, gender-matched, and calendar period-matched Swedish population using standardized incidence ratios and standardized mortality ratios. RESULTS: Thirty-nine percent participated. The incidence of colorectal cancer (IRR, 2.2; 95% CI, 0.8-5.9), other gastrointestinal cancer (IRR, 2.7; 95% CI, 0.6-12.8), lung cancer (IRR, 2.2; 95% CI, 0.8-5.9), and smoking-related cancer overall (IRR, 1.4; 95% CI, 0.7-2.5) tended to be increased among nonparticipants relative to participants. Standardized incidence ratios for most of the studied cancers tended to be >1.0 among nonparticipants and <1.0 among participants. Mortality from all causes (MRR, 2.4; 95% CI, 1.7-3.4), neoplastic diseases (MRR, 1.9; 95% CI, 1.1-3.5), gastrointestinal cancer (MRR, 4.7; 95% CI, 1.1-20.7), and circulatory diseases (MRR, 2.3; 95% CI, 1.2-4.2) was significantly higher among nonparticipants than among participants. Standardized mortality ratio for the studied outcomes tended to be increased among nonparticipants and was generally decreased among participants. CONCLUSION: Individuals who might benefit most from screening are overrepresented among nonparticipants. This self-selection may attenuate the cost-effectiveness of screening programs on a population level.

  • 5. Bonn, Stephanie E
    et al.
    Sjölander, Arvid
    Lagerros, Ylva Trolle
    Wiklund, Fredrik
    Stattin, Pär
    Department of Surgical and Perioperative Sciences, Urology and Andrology, Umeå University, Umeå, Sweden.
    Holmberg, Erik
    Grönberg, Henrik
    Bälter, Katarina
    Physical activity and survival among men diagnosed with prostate cancer2015In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 24, no 1, p. 57-64Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Few studies have investigated the association between post-diagnosis physical activity and mortality among men diagnosed with prostate cancer. The aim of this study was to investigate the effect of physical activity after a prostate cancer diagnosis on both overall and prostate cancer-specific mortality in a large cohort.

    METHODS: Data from 4,623 men diagnosed with localized prostate cancer 1997-2002 and followed-up until 2012 were analyzed. HRs with 95% confidence intervals (CI) were estimated using Cox proportional hazards models to examine the association between post-diagnosis recreational MET-h/d, time spent walking/bicycling, performing household work or exercising, and time to overall and prostate cancer-specific death. All models were adjusted for potential confounders.

    RESULTS: During the follow-up, 561 deaths of any cause and 194 deaths from prostate cancer occurred. Statistically significantly lower overall mortality rates were found among men engaged in ≥5 recreational MET-h/d (HR, 0.63; 95% CI, 0.52-0.77), walking/bicycling ≥20 min/d (HR, 0.70; 95% CI, 0.57-0.86), performing household work ≥1 h/d (HR, 0.71; 95% CI, 0.59-0.86), or exercising ≥1 h/wk (HR, 0.74; 95% CI, 0.61-0.90), compared with less active men within each activity type. For prostate cancer-specific mortality, statistically significantly lower mortality rates were seen among men walking/bicycling ≥20 min/d (HR, 0.61; 95% CI, 0.43-0.87) or exercising ≥1 h/wk (HR, 0.68; 95% CI, 0.48-0.94).

    CONCLUSIONS: Higher levels of physical activity were associated with reduced rates of overall and prostate cancer-specific mortality.

    IMPACT: Our study further strengthens previous results indicating beneficial effects of physical activity on survival among men with prostate cancer.

  • 6. Campbell, Peter T
    et al.
    Newton, Christina C
    Kitahara, Cari M
    Patel, Alpa V
    Hartge, Patricia
    Koshiol, Jill
    McGlynn, Katherine A
    Adami, Hans-Olov
    Berrington de González, Amy
    Beane Freeman, Laura E
    Bernstein, Leslie
    Buring, Julie E
    Freedman, Neal D
    Gao, Yu-Tang
    Giles, Graham G
    Gunter, Marc J
    Jenab, Mazda
    Liao, Linda M
    Milne, Roger L
    Robien, Kim
    Sandler, Dale P
    Schairer, Catherine
    Sesso, Howard D
    Shu, Xiao-Ou
    Weiderpass, Elisabete
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Xiang, Yong-Bing
    Zeleniuch-Jacquotte, Anne
    Zheng, Wei
    Gapstur, Susan M
    Body Size Indicators and Risk of Gallbladder Cancer: Pooled Analysis of Individual-Level Data from 19 Prospective Cohort Studies.2017In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 26, no 4, p. 597-606Article in journal (Refereed)
    Abstract [en]

    Background: There are few established risk factors for gallbladder cancer beyond gallstones. Recent studies suggest a higher risk with high body mass index (BMI), an indicator of general heaviness, but evidence from other body size measures is lacking.Methods: Associations of adult BMI, young adult BMI, height, adult weight gain, waist circumference (WC), waist-height ratio (WHtR), hip circumference (HC), and waist-hip ratio (WHR) with gallbladder cancer risk were evaluated. Individual-level data from 1,878,801 participants in 19 prospective cohort studies (14 studies had circumference measures) were harmonized and included in this analysis. Multivariable Cox proportional hazards regression estimated hazard ratios (HR) and 95% confidence intervals (CI).Results: After enrollment, 567 gallbladder cancer cases were identified during 20.1 million person-years of observation, including 361 cases with WC measures. Higher adult BMI (per 5 kg/m2, HR: 1.24; 95% CI, 1.13-1.35), young adult BMI (per 5 kg/m2, HR: 1.12; 95% CI, 1.00-1.26), adult weight gain (per 5 kg, HR: 1.07; 95% CI, 1.02-1.12), height (per 5 cm, HR: 1.10; 95% CI, 1.03-1.17), WC (per 5 cm, HR: 1.09; 95% CI, 1.02-1.17), WHtR (per 0.1 unit, HR: 1.24; 95% CI, 1.00-1.54), and HC (per 5 cm, HR: 1.13; 95% CI, 1.04-1.22), but not WHR (per 0.1 unit, HR: 1.03; 95% CI, 0.87-1.22), were associated with higher risks of gallbladder cancer, and results did not differ meaningfully by sex or other demographic/lifestyle factors.Conclusions: These findings indicate that measures of overall and central excess body weight are associated with higher gallbladder cancer risks.Impact: Excess body weight is an important, and potentially preventable, gallbladder cancer risk factor. Cancer Epidemiol Biomarkers Prev; 26(4); 597-606. ©2017 AACR.

  • 7.
    Carlander, Christina
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Centre for Clinical Research, County of Västmanland. Karolinska Inst, Infect Dis Unit, Dept Med, Huddinge, Sweden.;Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Lagheden, Camilla
    Karolinska Inst, Div Clin Pathol, Dept Lab Med, Stockholm, Sweden..
    Eklund, Carina
    Karolinska Inst, Div Clin Pathol, Dept Lab Med, Stockholm, Sweden..
    Kleppe, Sara Nordqvist
    Karolinska Inst, Div Clin Pathol, Dept Lab Med, Stockholm, Sweden..
    Dzabic, Mensur
    Karolinska Inst, Div Clin Pathol, Dept Lab Med, Stockholm, Sweden..
    Wagner, Philippe
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Centre for Clinical Research, County of Västmanland.
    Yilmaz, Aylin
    Univ Gothenburg, Sahlgrenska Acad, Inst Biomed, Dept Infect Dis, Gothenburg, Sweden..
    Elfgren, Kristina
    Karolinska Univ Hosp, CLINTEC, Dept Obstet & Gynaecol, Stockholm, Sweden..
    Sönnerborg, Anders
    Karolinska Inst, Infect Dis Unit, Dept Med, Huddinge, Sweden..
    Sparén, Pär
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Dillner, Joakim
    Karolinska Inst, Div Clin Pathol, Dept Lab Med, Stockholm, Sweden..
    HPV Types in Cervical Precancer by HIV Status and Birth Region: A Population-Based Register Study2020In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 29, no 12, p. 2662-2668Article in journal (Refereed)
    Abstract [en]

    Background: Data are lacking regarding which human papillomavirus (HPV) types cause high-grade cervical neoplasia (CIN2+) in people with HIV in Europe. We assessed which HPV types are associated with CIN2+ in women living in Sweden by HIV status.

    Methods: The Swedish National HIV Registry, the Swedish Population Registry, and the Swedish National Cervical Screening Registry were linked. CIN2+ tissue blocks of 130 women living with HIV (WLWH) and 234 HIV-negative women, matched for country of birth (1:2), were retrieved from bio-banks and HPV genotyped. Adjusted ORs (adjOR), stratified by country of birth, were calculated using conditional logistic regression. Matching was broken for cross-group comparisons.

    Results: WLWH with CIN2 were less likely to have HPV16 [14% vs. 40%; adjOR 0.1; 95% confidence interval (CI), 0.04-0.56] than HIV-negative women, but among women with CIN3, there was no difference in HPV16 prevalence by HIV status (adjOR 0.9; 95% CI, 0.51-1.70). WLWH were six times more likely to have HPV35 in CIN3 than HIV-negative women (adjOR 6.2; 95% CI, 1.3-30.4). WLWH from sub-Saharan Africa (SSA) had less 9-valent vaccine types, compared with both HIV-negative women born in Sweden (adjOR 0.1; 95% CI, 0.02-0.44) and WLWH born in Sweden (adjOR 0.1; 95% CI, 0.01-0.73), mostly because of decreased HPV16 and increased HPV35.

    Conclusions: WLWH from SSA were less likely to be covered by the 9-valent vaccine, mostly due to less HPV16 and more HPV35. Impact: This could have implications for HPV vaccines, currently not including HPV35, and for HPV-screening algorithms in women with origin from SSA.

  • 8. Chang, Ellen T.
    et al.
    Smedby, Karin Ekström
    Zhang, Shumin M.
    Hjalgrim, Henrik
    Melbye, Mads
    Öst, Åke
    Glimelius, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology.
    Wolk, Alicja
    Adami, Hans-Olov
    Dietary factors and risk of non-hodgkin lymphoma in men and women2005In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 14, no 2, p. 512-20Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The incidence of non-Hodgkin lymphoma (NHL) has increased worldwide in recent decades. Diet could influence NHL risk by modulating the immune system, although evidence is limited. We did a population-based case-control study to determine whether differences in diet were associated with NHL risk. METHODS: A total of 597 NHL cases and 467 population controls in Sweden completed a semiquantitative food frequency questionnaire evaluating their dietary habits 2 years before the interview. Unconditional logistic regression was used to estimate the odds ratios (OR) and corresponding 95% confidence intervals (95% CI) for associations between food intake and risk of NHL. RESULTS: High consumption of dairy products and fried red meat was associated with increased risk of NHL. The OR of NHL for individuals in the highest quartile compared with the lowest quartile of dairy intake was 1.5 (95% CI, 1.1-2.2; P(trend) = 0.003). The OR for the highest versus lowest quartile of fried red meat intake was 1.5 (95% CI, 1.0-2.1; P(trend) = 0.02). In contrast, high consumption of fruits and vegetables was associated with reduced risk of NHL, particularly follicular lymphoma, among women but not men. Compared with the lowest quartile of vegetable intake, the OR of follicular lymphoma among women in the highest quartile of vegetable intake was 0.3 (95% CI, 0.1-0.7; P(trend) = 0.002). CONCLUSIONS: The positive associations of NHL risk with dairy products and fried red meat and the inverse association with fruits and vegetables suggest that diet affects NHL risk and could explain the increase of some histopathogic subtypes.

  • 9.
    Chen, Lingjing
    et al.
    Karolinska Inst, Dept Med Solna, Clin Epidemiol Unit, Stockholm, Sweden..
    Glimelius, Ingrid
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Experimental and Clinical Oncology. Karolinska Inst, Dept Med Solna, Clin Epidemiol Unit, Stockholm, Sweden..
    Neovius, Martin
    Karolinska Inst, Dept Med Solna, Clin Epidemiol Unit, Stockholm, Sweden..
    Ekberg, Sara
    Karolinska Inst, Dept Med Solna, Clin Epidemiol Unit, Stockholm, Sweden.;Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Martling, Anna
    Karolinska Inst, Dept Mol Med & Surg, Stockholm, Sweden..
    Eloranta, Sandra
    Karolinska Inst, Dept Med Solna, Clin Epidemiol Unit, Stockholm, Sweden..
    Smedby, Karin E.
    Karolinska Inst, Dept Med Solna, Clin Epidemiol Unit, Stockholm, Sweden..
    Work Loss Duration and Predictors Following Rectal Cancer Treatment among Patients with and without Prediagnostic Work Loss2016In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 25, no 6, p. 987-994Article in journal (Refereed)
    Abstract [en]

    Background: The number of working-age rectal cancer survivors is increasing due to early detection and improved treatment. However, work loss duration and predictors among them have not been studied thoroughly. Methods: We identified 3,438 patients with stage I-III rectal cancer, 18 to 61 years of age in the Swedish Colorectal Cancer Register 1996-2009. Information on work loss due to sick leave or disability pension was collected from 2 years before diagnosis to 5 years after (until December 31st, 2013). Incidence rate ratios (IRR) of work loss were estimated in a negative binominal model by clinical characteristics for the 1st and 2nd-5th years after diagnosis. Patients were stratified by prediagnostic work loss. Results: Patients without prediagnostic work loss (74%) experienced median 147 days (25th and 75th percentile: 55 and 281) of work loss during the 1st year after diagnosis. Work loss rates (2nd-5th years) were significantly increased among relapse-free patients diagnosed in stage III [IRR = 1.92; 95% confidence interval (CI), 1.52-2.43], operated with abdominoperineal resection (IRR = 1.26; 95% CI, 1.03-1.56), and treated with neoadjuvant (chemo) radiotherapy (IRR = 1.46; 95% CI, 1.06-2.02). Patients with prediagnostic work loss (26%) experienced median 336 days (25th and 75th percentile: 183 and 365) of work loss during the 1st year, and rates did not vary clinically till 5 years. Conclusion: Without prediagnostic work loss, disease-and treatment-related factors could help identify rectal cancer patients in need of early interventions to facilitate return to work. Impact: Clinical awareness around prediagnostic and postdiagnostic work loss and individualized cancer rehabilitation programs should be emphasized among cancer survivors.

  • 10. Cnattingius, Sven
    et al.
    Eloranta, Sandra
    Adami, Hans-Olov
    Axelsson, Ove
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health.
    Dickman, Paul W.
    Hsieh, Chung-cheng
    Mucci, Lorelei A.
    Trichopoulus, Dimitrius
    Lambe, Mats
    Johansson, Anna L. V.
    Placental weight and risk of invasive epithelial ovarian cancer with an early age of onset2008In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 17, no 9, p. 2344-2349Article in journal (Refereed)
    Abstract [en]

    Background: Epithelial ovarian cancer is associated with reproductive factors, but we lack knowledge if hormonal factors during pregnancy influence the mother's risk. Because pregnancy hormones are primarily produced by the placenta, placental weight may be an indirect marker of hormone exposure during pregnancy. Methods: In a nationwide Swedish cohort study, we included women with singleton births from 1982 to 1989. Women were followed for occurrence of invasive epithelial ovarian cancer, death, or emigration through 2004. Hazard ratios (HR) with 95% confidence intervals (95% CI) from Cox models were used to estimate associations between pregnancy exposures and epithelial ovarian cancer. Results: Among 395,171 women with information on placental weight in their first recorded birth, 316 women developed invasive epithelial ovarian cancer. Mean age at diagnosis was 44 years. Compared with women with a placental weight of 500 to 699 g, women with a high (>= 700 g) placental weight had an increased risk of developing epithelial ovarian cancer (HR, 1.47, 95% CI, 1.14-1.90). Compared with women with term pregnancies (40-41 weeks), women with post-term (>= 42 weeks) pregnancies had an increased risk of developing epithelial ovarian cancer (HR, 1.48, 95% CI, 1.00-2.19). These associations were slightly stronger when we included information about women's overall first birth, and slightly weaker when we included information about last recorded birth or ever last birth from 1982 to 1989. Conclusions: Because pregnancy hormone levels increase with placental weight, our study supports the hypothesis that hormone exposures during pregnancy influence the risk of invasive epithelial ovarian cancer among young women.

  • 11. Couch, Fergus J.
    et al.
    Gaudet, Mia M.
    Antoniou, Antonis C.
    Ramus, Susan J.
    Kuchenbaecker, Karoline B.
    Soucy, Penny
    Beesley, Jonathan
    Chen, Xiaoqing
    Wang, Xianshu
    Kirchhoff, Tomas
    McGuffog, Lesley
    Barrowdale, Daniel
    Lee, Andrew
    Healey, Sue
    Sinilnikova, Olga M.
    Andrulis, Irene L.
    Ozcelik, Hilmi
    Mulligan, Anna Marie
    Thomassen, Mads
    Gerdes, Anne-Marie
    Jensen, Uffe Birk
    Skytte, Anne-Bine
    Kruse, Torben A.
    Caligo, Maria A.
    von Wachenfeldt, Anna
    Barbany-Bustinza, Gisela
    Loman, Niklas
    Soller, Maria
    Ehrencrona, Hans
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Medical Genetics.
    Karlsson, Per
    Nathanson, Katherine L.
    Rebbeck, Timothy R.
    Domchek, Susan M.
    Jakubowska, Ania
    Lubinski, Jan
    Jaworska, Katarzyna
    Durda, Katarzyna
    Zlowocka, Elzbieta
    Huzarski, Tomasz
    Byrski, Tomasz
    Gronwald, Jacek
    Cybulski, Cezary
    Gorski, Bohdan
    Osorio, Ana
    Duran, Mercedes
    Isabel Tejada, Maria
    Benitez, Javier
    Hamann, Ute
    Hogervorst, Frans B. L.
    van Os, Theo A.
    van Leeuwen, Flora E.
    Meijers-Heijboer, Hanne E. J.
    Wijnen, Juul
    Blok, Marinus J.
    Kets, Marleen
    Hooning, Maartje J.
    Oldenburg, Rogier A.
    Ausems, Margreet G. E. M.
    Peock, Susan
    Frost, Debra
    Ellis, Steve D.
    Platte, Radka
    Fineberg, Elena
    Evans, D. Gareth
    Jacobs, Chris
    Eeles, Rosalind A.
    Adlard, Julian
    Davidson, Rosemarie
    Eccles, Diana M.
    Cole, Trevor
    Cook, Jackie
    Paterson, Joan
    Brewer, Carole
    Douglas, Fiona
    Hodgson, Shirley V.
    Morrison, Patrick J.
    Walker, Lisa
    Porteous, Mary E.
    Kennedy, M. John
    Side, Lucy E.
    Bove, Betsy
    Godwin, Andrew K.
    Stoppa-Lyonnet, Dominique
    Fassy-Colcombet, Marion
    Castera, Laurent
    Cornelis, Francois
    Mazoyer, Sylvie
    Leone, Melanie
    Boutry-Kryza, Nadia
    Bressac-de Paillerets, Brigitte
    Caron, Olivier
    Pujol, Pascal
    Coupier, Isabelle
    Delnatte, Capucine
    Akloul, Linda
    Lynch, Henry T.
    Snyder, Carrie L.
    Buys, Saundra S.
    Daly, Mary B.
    Terry, MaryBeth
    Chung, Wendy K.
    John, Esther M.
    Miron, Alexander
    Southey, Melissa C.
    Hopper, John L.
    Goldgar, David E.
    Singer, Christian F.
    Rappaport, Christine
    Tea, Muy-Kheng M.
    Fink-Retter, Anneliese
    Hansen, Thomas V. O.
    Nielsen, Finn C.
    Arason, Adalgeir
    Vijai, Joseph
    Shah, Sohela
    Sarrel, Kara
    Robson, Mark E.
    Piedmonte, Marion
    Phillips, Kelly
    Basil, Jack
    Rubinstein, Wendy S.
    Boggess, John
    Wakeley, Katie
    Ewart-Toland, Amanda
    Montagna, Marco
    Agata, Simona
    Imyanitov, Evgeny N.
    Isaacs, Claudine
    Janavicius, Ramunas
    Lazaro, Conxi
    Blanco, Ignacio
    Feliubadalo, Lidia
    Brunet, Joan
    Gayther, Simon A.
    Pharoah, Paul P. D.
    Odunsi, Kunle O.
    Karlan, Beth Y.
    Walsh, Christine S.
    Olah, Edith
    Teo, Soo Hwang
    Ganz, Patricia A.
    Beattie, Mary S.
    van Rensburg, Elizabeth J.
    Dorfling, Cecelia M.
    Diez, Orland
    Kwong, Ava
    Schmutzler, Rita K.
    Wappenschmidt, Barbara
    Engel, Christoph
    Meindl, Alfons
    Ditsch, Nina
    Arnold, Norbert
    Heidemann, Simone
    Niederacher, Dieter
    Preisler-Adams, Sabine
    Gadzicki, Dorothea
    Varon-Mateeva, Raymonda
    Deissler, Helmut
    Gehrig, Andrea
    Sutter, Christian
    Kast, Karin
    Fiebig, Britta
    Heinritz, Wolfram
    Caldes, Trinidad
    de la Hoya, Miguel
    Muranen, Taru A.
    Nevanlinna, Heli
    Tischkowitz, Marcd.
    Spurdle, Amanda B.
    Neuhausen, Susan L.
    Ding, Yuan Chun
    Lindor, Noralane M.
    Fredericksen, Zachary
    Pankratz, V. Shane
    Peterlongo, Paolo
    Manoukian, Siranoush
    Peissel, Bernard
    Zaffaroni, Daniela
    Barile, Monica
    Bernard, Loris
    Viel, Alessandra
    Giannini, Giuseppe
    Varesco, Liliana
    Radice, Paolo
    Greene, Mark H.
    Mai, Phuong L.
    Easton, Douglas F.
    Chenevix-Trench, Georgia
    Offit, Kenneth
    Simard, Jacques
    Common Variants at the 19p13.1 and ZNF365 Loci Are Associated with ER Subtypes of Breast Cancer and Ovarian Cancer Risk in BRCA1 and BRCA2 Mutation Carriers2012In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 21, no 4, p. 645-657Article in journal (Refereed)
    Abstract [en]

    Background: Genome-wide association studies (GWAS) identified variants at 19p13.1 and ZNF365 (10q21.2) as risk factors for breast cancer among BRCA1 and BRCA2 mutation carriers, respectively. We explored associations with ovarian cancer and with breast cancer by tumor histopathology for these variants in mutation carriers from the Consortium of Investigators of Modifiers of BRCA1/2 (CIMBA).

    Methods: Genotyping data for 12,599 BRCA1 and 7,132 BRCA2 mutation carriers from 40 studies were combined.

    Results: We confirmed associations between rs8170 at 19p13.1 and breast cancer risk for BRCA1 mutation carriers [HR, 1.17; 95% confidence interval (CI), 1.07-1.27; P = 7.42 x 10(-4)] and between rs16917302 at ZNF365 (HR, 0.84; 95% CI, 0.73-0.97; P = 0.017) but not rs311499 at 20q13.3 (HR, 1.11; 95% CI, 0.94-1.31; P = 0.22) and breast cancer risk for BRCA2 mutation carriers. Analyses based on tumor histopathology showed that 19p13 variants were predominantly associated with estrogen receptor (ER)-negative breast cancer for both BRCA1 and BRCA2 mutation carriers, whereas rs16917302 at ZNF365 was mainly associated with ER-positive breast cancer for both BRCA1 and BRCA2 mutation carriers. We also found for the first time that rs67397200 at 19p13.1 was associated with an increased risk of ovarian cancer for BRCA1 (HR, 1.16; 95% CI, 1.05-1.29; P = 3.8 x 10(-4)) and BRCA2 mutation carriers (HR, 1.30; 95% CI, 1.10-1.52; P = 1.8 x 10(-3)).

    Conclusions: 19p13.1 and ZNF365 are susceptibility loci for ovarian cancer and ER subtypes of breast cancer among BRCA1 and BRCA2 mutation carriers.

    Impact: These findings can lead to an improved understanding of tumor development and may prove useful for breast and ovarian cancer risk prediction for BRCA1 and BRCA2 mutation carriers.

  • 12.
    Crump, Casey
    et al.
    Icahn Sch Med Mt Sinai, Dept Family Med & Community Hlth, New York, NY 10029 USA; Icahn Sch Med Mt Sinai, Dept Populat Hlth Sci & Policy, New York, NY 10029 USA.
    Stattin, Pär
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Urology.
    Brooks, James D.
    Stanford Univ, Sch Med, Dept Urol, Stanford, CA 94305 USA.
    Stocks, Tanja
    Lund Univ, Dept Clin Sci Lund, Lund, Sweden.
    Sundquist, Jan
    Icahn Sch Med Mt Sinai, Dept Family Med & Community Hlth, New York, NY 10029 USA; Icahn Sch Med Mt Sinai, Dept Populat Hlth Sci & Policy, New York, NY 10029 USA; Lund Univ, Ctr Primary Hlth Care Res, Malmö, Sweden.
    Sieh, Weiva
    Icahn Sch Med Mt Sinai, Dept Populat Hlth Sci & Policy, New York, NY 10029 USA; Icahn Sch Med Mt Sinai, Dept Genet & Genom Sci, New York, NY 10029 USA.
    Sundquist, Kristina
    Icahn Sch Med Mt Sinai, Dept Family Med & Community Hlth, New York, NY 10029 USA; Icahn Sch Med Mt Sinai, Dept Populat Hlth Sci & Policy, New York, NY 10029 USA; Lund Univ, Ctr Primary Hlth Care Res, Malmö, Sweden.
    Early-Life Cardiorespiratory Fitness and Long-term Risk of Prostate Cancer2020In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 29, no 11, p. 2187-2194Article in journal (Refereed)
    Abstract [en]

    Background: Adolescence is a period of rapid prostatic growth, yet is understudied for susceptibility for future risk of prostate cancer. We examined cardiorespiratory fitness (CRF) in late adolescence in relation to long-term prostate cancer risk.

    Methods: A population-based cohort study was conducted of all 699,125 Swedish military conscripts during 1972–1985 (97%–98% of 18-year-old men) in relation to risk of prostate cancer overall, aggressive prostate cancer, and prostate cancer mortality during 1998–2017 (ages 50–65 years). CRF was measured by maximal aerobic workload, and prostate cancer was ascertained using the National Prostate Cancer Register. Muscle strength was examined as a secondary predictor.

    Results: In 38.8 million person-years of follow-up, 10,782 (1.5%) men were diagnosed with prostate cancer. Adjusting for sociodemographic factors, height, weight, and family history of prostate cancer, high CRF was associated with a slightly increased risk of any prostate cancer [highest vs. lowest quintile: incidence rate ratio (IRR), 1.10; 95% CI, 1.03–1.19; P = 0.008], but was neither significantly associated with aggressive prostate cancer (1.01; 0.85–1.21; P = 0.90) nor prostate cancer mortality (1.24; 0.73–2.13; P = 0.42). High muscle strength also was associated with a modestly increased risk of any prostate cancer (highest vs. lowest quintile: IRR, 1.14; 95% CI, 1.07–1.23; P < 0.001), but neither with aggressive prostate cancer (0.88; 0.74–1.04; P = 0.14) nor prostate cancer mortality (0.81; 0.48–1.37; P = 0.43).

    Conclusions: High CRF or muscle strength in late adolescence was associated with slightly increased future risk of prostate cancer, possibly related to increased screening, but neither with risk of aggressive prostate cancer nor prostate cancer mortality.

    Impact: These findings illustrate the importance of distinguishing aggressive from indolent prostate cancer and assessing for potential detection bias.

  • 13. Delahaye-Sourdeix, Manon
    et al.
    Urayama, Kevin Y
    Gaborieau, Valérie
    Veenstra, Rianne
    Foll, Matthieu
    Chabrier, Amelie
    Benavente, Yolanda
    Nieters, Alexandra
    Becker, Nikolaus
    Foretova, Lenka
    Maynadié, Marc
    Staines, Anthony
    Smedby, Karin Ekstrom
    Glimelius, Ingrid
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Experimental and Clinical Oncology.
    Lightfoot, Tracy
    Cocco, Pierluigi
    Galan, Pilar
    Vatten, Lars J
    Duell, Eric J
    Kiemeney, Lambertus
    Roman, Eve
    de Sanjosé, Silvia
    Lathrop, Mark
    Melbye, Mads
    Brennan, Paul
    Diepstra, Arjan
    van den Berg, Anke
    Hjalgrim, Henrik
    Jarrett, Ruth F
    McKay, James D
    A Novel Risk Locus at 6p21.3 for Epstein-Barr Virus-Positive Hodgkin Lymphoma2015In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 24, no 12, p. 1838-1843Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: A proportion of the genetic variants involved in susceptibility to Hodgkin lymphoma differ by the tumor's Epstein-Barr virus (EBV) status, particularly within the MHC region.

    METHODS: We have conducted an SNP imputation study of the MHC region, considering tumor EBV status in 1,200 classical Hodgkin lymphoma (cHL) cases and 5,726 control subjects of European origin. Notable findings were genotyped in an independent study population of 468 cHL cases and 551 controls.

    RESULTS: We identified and subsequently replicated a novel association between a common genetic variant rs6457715 and cHL. Although strongly associated with EBV-positive cHL [OR, 2.33; 95% confidence interval (CI), 1.83-2.97; P = 7 × 10(-12)], there was little evidence for association between rs6457715 and the EBV-negative subgroup of cHL (OR, 1.06; 95% CI, 0.92-1.21), indicating that this association was specific to the EBV-positive subgroup (Phet < P = 10(-8)). Furthermore, the association was limited to EBV-positive cHL subgroups within mixed cell (MCHL) and nodular sclerosis subtypes (NSHL), suggesting that the association is independent of histologic subtype of cHL.

    CONCLUSIONS: rs6457715, located near the HLA-DPB1 gene, is associated with EBV-positive cHL and suggests this region as a novel susceptibility locus for cHL.

    IMPACT: This expands the number of genetic variants that are associated with cHL and provides additional evidence for a critical and specific role of EBV in the etiology of this disease. Cancer Epidemiol Biomarkers Prev; 24(12); 1838-43.

  • 14.
    Eaker, Sonja
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Endocrine Surgery.
    Dickman, Paul W.
    Hellström, Vivan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Transplantation Surgery.
    Zack, Matthew M.
    Ahlgren, Johan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Centre for Research and Development, Gävleborg.
    Holmberg, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Endocrine Surgery.
    Regional differences in breast cancer survival despite common guidelines2005In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 14, no 12, p. 2914-8Article in journal (Refereed)
    Abstract [en]

    PURPOSE: Despite a uniform regional breast cancer care program, breast cancer survival differs within regions. We therefore examined breast cancer survival in relation to differences in diagnostic activity, tumor characteristics, and treatment in seven Swedish counties within a single health care region. METHODS: We conducted a population-based observational study using a clinical breast cancer register in one Swedish health care region. Eligible women (n = 7,656) ages 40 to 69 years diagnosed with primary breast cancer between 1992 and 2002 were followed up until 2003. The 7-year relative survival ratio was used to estimate breast cancer survival. Excess mortality was modeled using Poisson regression to study differences in survival between counties. RESULTS: The 7-year relative survival for breast cancer patients was significantly lower (up to 7% in absolute risk difference) in one county (county A) compared with the others. This difference existed only among women diagnosed before 1998, ages 50 to 59 years, and was strongest among stage II breast cancer patients. Adjustment for amount of diagnostic activity eliminated the survival differences among the counties. The amount of diagnostic activity was also lower in county A during the same time period. After county A, during 1997-1998, began to adhere strictly to the regional breast cancer care program, neither any survival differences nor diagnostic activity differences were observed. INTERPRETATIONS: Markers of diagnostic activity explained survival differences within our region, and the underlying mechanisms may be several. Low diagnostic activity may entail later diagnosis or inadequate characterization of the tumor and thereby missed treatment opportunities. Strengthening of multidisciplinary management of breast cancer can improve survival.

  • 15. Engel, Christoph
    et al.
    Versmold, Beatrix
    Wappenschmidt, Barbara
    Simard, Jacques
    Easton, Douglas F.
    Peock, Susan
    Cook, Margaret
    Oliver, Clare
    Frost, Debra
    Mayes, Rebecca
    Evans, D. Gareth
    Eeles, Rosalind
    Paterson, Joan
    Brewer, Carole
    McGuffog, Lesley
    Antoniou, Antonis C.
    Stoppa-Lyonnet, Dominique
    Sinilnikova, Olga M.
    Barjhoux, Laure
    Frenay, Marc
    Michel, Cecile
    Leroux, Dominique
    Dreyfus, Helene
    Toulas, Christine
    Gladieff, Laurence
    Uhrhammer, Nancy
    Bignon, Yves-Jean
    Meindl, Alfons
    Arnold, Norbert
    Varon-Mateeva, Raymonda
    Niederacher, Dieter
    Preisler-Adams, Sabine
    Kast, Karin
    Deissler, Helmut
    Sutter, Christian
    Gadzicki, Dorothea
    Chenevix-Trench, Georgia
    Spurdle, Amanda B.
    Chen, Xiaoqing
    Beesley, Jonathan
    Olsson, Hakan
    Kristoffersson, Ulf
    Ehrencrona, Hans
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology.
    Liljegren, Annelie
    van der Luijt, Rob B.
    van Os, Theo A.
    van Leeuwen, Flora E.
    Domchek, Susan M.
    Rebbeck, Timothy R.
    Nathanson, Katherine L.
    Osorio, Ana
    Ramon y Cajal, Teresa
    Konstantopoulou, Irene
    Benitez, Javier
    Friedman, Eitan
    Kaufman, Bella
    Laitman, Yael
    Mai, Phuong L.
    Greene, Mark H.
    Nevanlinna, Heli
    Aittomaki, Kristiina
    Szabo, Csilla I.
    Caldes, Trinidad
    Couch, Fergus J.
    Andrulis, Irene L.
    Godwin, Andrew K.
    Hamann, Ute
    Schmutzler, Rita K.
    Association of the Variants CASP8 D302H and CASP10 V410I with Breast and Ovarian Cancer Risk in BRCA1 and BRCA2 Mutation Carriers2010In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 19, no 11, p. 2859-2868Article in journal (Refereed)
    Abstract [en]

    Background: The genes caspase-8 (CASP8) and caspase-10 (CASP10) functionally cooperate and play a key role in the initiation of apoptosis. Suppression of apoptosis is one of the major mechanisms underlying the origin and progression of cancer. Previous case-control studies have indicated that the polymorphisms CASP8 D302H and CASP10 V410I are associated with a reduced risk of breast cancer in the general population. Methods: To evaluate whether the CASP8 D302H (CASP10 V410I) polymorphisms modify breast or ovarian cancer risk in BRCA1 and BRCA2 mutation carriers, we analyzed 7,353 (7,227) subjects of white European origin provided by 19 (18) study groups that participate in the Consortium of Investigators of Modifiers of BRCA1/2 (CIMBA). A weighted cohort approach was used to estimate hazard ratios (HR) and 95% confidence intervals (95% CI). Results: The minor allele of CASP8 D302H was significantly associated with a reduced risk of breast cancer (per-allele HR, 0.85; 95% CI, 0.76-0.97; P-trend = 0.011) and ovarian cancer (per-allele HR, 0.69; 95% CI, 0.53-0.89; P-trend = 0.004) for BRCA1 but not for BRCA2 mutation carriers. The CASP10 V410I polymorphism was not associated with breast or ovarian cancer risk for BRCA1 or BRCA2 mutation carriers. Conclusions: CASP8 D302H decreases breast and ovarian cancer risk for BRCA1 mutation carriers but not for BRCA2 mutation carriers. Impact: The combined application of these and other recently identified genetic risk modifiers could in the future allow better individual risk calculation and could aid in the individualized counseling and decision making with respect to preventive options in BRCA1 mutation carriers.

  • 16. Fall, Katja
    et al.
    Garmo, Hans
    Gudbjornsdottir, Soffia
    Stattin, Par
    Zethelius, Björn
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Geriatrics.
    Diabetes Mellitus and Prostate Cancer Risk; A Nationwide Case-Control Study within PCBaSe Sweden2013In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 22, no 6, p. 1102-1109Article in journal (Refereed)
    Abstract [en]

    Background: Diabetes mellitus (DM) increases the risk for cancer at almost all sites, but data on the association with prostate cancer are inconsistent. Methods: We assessed the risk of a prostate cancer diagnosis among men with type 2 (T2)DM in a nationwide population-based case-control study including 44,352 men with prostate cancer identified through the Prostate Cancer data Base Sweden (PCBaSe) between 2002 and 2006 and 221,495 age-matched men from the general population. Results: Overall, the risk of prostate cancer among men with T2DM was lower than among men without T2DM [OR, 0.80; 95% confidence interval (CI), 0.76-0.85]. The risk decreased with longer disease duration and was observed across all tumor risk categories, although most clearly among men with low risk tumors (OR, 0.71; 95% CI, 0.64-0.80). The risk for prostate cancer was reduced among diabetic men on dietary treatment only (OR, 0.89; 95% CI, 0.80-0.99) but more markedly among men on oral hypoglycemic agents (OR, 0.80; 95% CI, 0.74-0.87) and insulin (OR, 0.72; 95% CI, 0.69-0.81). Obese diabetic men (BMI > 30 kg/m(2)) showed a reduced risk (OR, 0.72; 95% CI, 0.65-0.80) compared with men without diabetes. There was a trend of decreasing risk with increasing levels of HbA1c (P < 0.05). Conclusions: This nationwide study confirmed a reduced risk of being diagnosed with prostate cancer among men with T2DM, especially for low-risk tumors. An altered hormonal milieu is a plausible explanation, although the possibility of decreased prostate cancer detection among diabetic men cannot be ruled out. Impact: This is the largest study to examine the association between T2DM and prostate cancer accounting for tumor risk group and diabetes treatment.

  • 17. Fletcher, Olivia
    et al.
    Johnson, Nichola
    Dos Santos Silva, Isabel
    Kilpivaara, Outi
    Aittomäki, Kristiina
    Blomqvist, Carl
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology, Oncology.
    Nevanlinna, Heli
    Wasielewski, Marijke
    Meijers-Heijerboer, Hanne
    Broeks, Annegien
    Schmidt, Marjanka K.
    Van't Veer, Laura J.
    Bremer, Michael
    Dörk, Thilo
    Chekmariova, Elena V.
    Sokolenko, Anna P.
    Imyanitov, Evgeny N.
    Hamann, Ute
    Rashid, Muhammad U.
    Brauch, Hiltrud
    Justenhoven, Christina
    Ashworth, Alan
    Peto, Julian
    Family history, genetic testing, and clinical risk prediction: pooled analysis of CHEK2 1100delC in 1,828 bilateral breast cancers and 7,030 controls2009In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 18, no 1, p. 230-4Article in journal (Refereed)
    Abstract [en]

    If breast cancers arise independently in each breast the odds ratio (OR) for bilateral breast cancer for carriers of CHEK2 1100delC should be approximately 5.5, the square of the reported OR for a first primary (OR, 2.34). In the subset of bilateral cases with one or more affected relatives, the predicted carrier OR should be approximately 9. We have tested these predictions in a pooled set of 1,828 cases with 2 primaries and 7,030 controls from 8 studies. The second primary OR for CHEK2 1100delC carriers was 6.43 (95% confidence interval, 4.33-9.56; P < 0.0001), significantly greater than the published estimate for a first primary (P < 0.001) but consistent with its square. The predicted increase in carrier OR with increasing numbers of affected relatives was seen using bilateral cases from the UK (P(trend) = 0.0003) and Finland (P(trend) = 0.37), although not using those from the Netherlands and Russia (P = 0.001 for heterogeneity between countries). Based on a standard genetic model, we predict lifetime risks for CHEK2 1100delC carrier and noncarrier daughters of bilateral breast cancer cases of 37% and 18%, respectively. Our results imply that clinical management of the daughter of a woman with bilateral breast cancer should depend on her CHEK2 1100delC carrier status. This and other moderate penetrance breast cancer susceptibility alleles, together with family history data, will thus identify increasing numbers of women at potentially very high risk. Before such predictions are accepted by clinical geneticists, however, further population-based evidence is needed on the effect of CHEK2 1100delC and other moderate penetrance alleles in women with a family history of breast cancer.

  • 18.
    Fortner, Renee T.
    et al.
    German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany.;Deutsch Krebsforschungszentrum DKFZ, Neuenheimer Feld 280, D-69120 Heidelberg, Germany..
    Rice, Megan S.
    Massachusetts Gen Hosp, Dept Med, Clin & Translat Epidemiol Unit, Harvard Med Sch, Boston, MA USA..
    Knutsen, Synnove F.
    Loma Linda Univ, Sch Publ Hlth, Loma Linda, CA USA..
    Orlich, Michael J.
    Loma Linda Univ, Sch Publ Hlth, Loma Linda, CA USA..
    Visvanathan, Kala
    Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.;Johns Hopkins Bloomberg Sch Med, Baltimore, MD USA..
    Patel, Alpa, V
    Amer Canc Soc, Behav & Epidemiol Res Grp, Atlanta, GA USA..
    Gaudet, Mia M.
    Amer Canc Soc, Behav & Epidemiol Res Grp, Atlanta, GA USA..
    Tjønneland, Anne
    Univ Copenhagen, Dept Publ Hlth, Copenhagen, Denmark.;Danish Canc Soc Res Ctr, Diet Genes & Environm, Copenhagen, Denmark..
    Kvaskoff, Marina
    Univ Paris Saclay, Fac Med Univ Paris Sud, Fac Med UVSQ, INSERM,CESP, Villejuif, France.;Gustave Roussy, Villejuif, France..
    Kaaks, Rudolf
    German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany.;Deutsch Krebsforschungszentrum DKFZ, Neuenheimer Feld 280, D-69120 Heidelberg, Germany..
    Trichopolou, Antonia
    Hellen Hlth Fdn, Athens, Greece..
    Pala, Valeria
    Fdn IRCCS Ist Nazl Tumori Milano, Epidemiol & Prevent Unit, Milan, Italy..
    Onland-Moret, N. Charlotte
    Univ Utrecht, Univ Med Ctr Utrecht, Julius Ctr Hlth Sci & Primary Care, Utrecht, Netherlands..
    Gram, Inger T.
    Univ Tromso, Arctic Univ Norway, Fac Hlth Sci, Dept Community Med, Tromso, Norway..
    Amiano, Pilar
    BioDonostia Res Inst, Publ Hlth Div Gipuzkoa, Donostia San Sebastian, Spain.;CIBER Epidemiol & Salud Publ, Madrid, Spain..
    Idahl, Annika
    Umeå Univ, Dept Clin Sci Obstet & Gynecol, Umeå, Sweden..
    Allen, Naomi E.
    Univ Oxford, Nuffield Dept Populat Hlth, Oxford, England..
    Weiderpass, Elisabete
    Int Agcy Res Canc, Lyon, France..
    Poynter, Jenny N.
    Univ Minnesota, Div Pediat Epidemiol & Clin Res, Minneapolis, MN USA..
    Robien, Kim
    George Washington Univ, Milken Inst Sch Publ Hlth, Dept Exercise & Nutr Sci, Washington, DC USA..
    Giles, Graham G.
    Canc Council Victoria, Canc Epidemiol Div, Melbourne, Vic, Australia.;Univ Melbourne, Ctr Epidemiol & Biostat, Melbourne Sch Populat & Global Hlth, Melbourne, Vic, Australia.;Monash Univ, Sch Clin Sci Monash Hlth, Precis Med, Clayton, Vic, Australia..
    Milne, Roger L.
    Canc Council Victoria, Canc Epidemiol Div, Melbourne, Vic, Australia.;Univ Melbourne, Ctr Epidemiol & Biostat, Melbourne Sch Populat & Global Hlth, Melbourne, Vic, Australia.;Monash Univ, Sch Clin Sci Monash Hlth, Precis Med, Clayton, Vic, Australia..
    Setiawan, Veronica W.
    Univ Southern Calif, Los Angeles, CA 90007 USA..
    Merritt, Melissa A.
    Univ Hawaii, Canc Epidemiol Program, Canc Ctr, Honolulu, HI USA..
    van den Brandt, Piet A.
    Maastricht Univ, GROW Sch Oncol & Dev Biol, Dept Epidemiol, Maastricht, Netherlands..
    Zeleniuch-Jacquotte, Anne
    NYU, Sch Med, New York, NY USA..
    Arslan, Alan A.
    NYU, Sch Med, New York, NY USA..
    O'Brien, Katie M.
    Natl Inst Environm Hlth Sci, Epidemiol Branch, Durham, NC USA..
    Sandler, Dale P.
    Natl Inst Environm Hlth Sci, Epidemiol Branch, Durham, NC USA..
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics. Karolinska Inst, Inst Environm Med, Stockholm, Sweden..
    Håkansson, Niclas
    Karolinska Inst, Inst Environm Med, Stockholm, Sweden..
    Harris, Holly R.
    Fred Hutchinson Canc Res Ctr, Program Epidemiol, Washington, DC USA.;Univ Washington, Sch Publ Hlth, Dept Epidemiol, Washington, DC USA..
    Trabert, Britton
    NIH, Div Canc Epidemiol & Genet, NCI, Washington, DC USA..
    Wentzensen, Nicolas
    NIH, Div Canc Epidemiol & Genet, NCI, Washington, DC USA..
    Tworoger, Shelley S.
    H Lee Moffitt Canc Ctr & Res Inst, Dept Canc Epidemiol, Tampa, FL USA.;Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA..
    Schouten, Leo J.
    Maastricht Univ, GROW Sch Oncol & Dev Biol, Dept Epidemiol, Maastricht, Netherlands..
    Ovarian Cancer Risk Factor Associations by Primary Anatomic Site: The Ovarian Cancer Cohort Consortium2020In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 29, no 10, p. 2010-2018Article in journal (Refereed)
    Abstract [en]

    Background: Epithelial ovarian, fallopian tube, and primary peritoneal cancers have shared developmental pathways. Few studies have prospectively examined heterogeneity in risk factor associations across these three anatomic sites.

    Methods: We identified 3,738 ovarian, 337 peritoneal, and 176 fallopian tube incident cancer cases in 891,731 women from 15 prospective cohorts in the Ovarian Cancer Cohort Consortium. Associations between 18 putative risk factors and risk of ovarian, peritoneal, and fallopian tube cancer, overall and for serous and high-grade serous tumors, were evaluated using competing risks Cox proportional hazards regression. Heterogeneity was assessed by likelihood ratio tests.

    Results: Most associations did not vary by tumor site (P-het = 0.05). Associations between first pregnancy (P-het = 0.04), tubal ligation (P-het = 0.01), and early-adult (age 18-21 years) body mass index (BMI; P-het = 0.02) and risk differed between ovarian and peritoneal cancers. The association between early-adult BMI and risk further differed between peritoneal and fallopian tube cancer (P-het = 0.03). First pregnancy and tubal ligation were inversely associated with ovarian, but not peritoneal, cancer. Higher early-adult BMI was associated with higher risk of peritoneal, but not ovarian or fallopian tube, cancer. Patterns were generally similar when restricted to serous and high-grade serous cases.

    Conclusions: Ovarian, fallopian tube, and primary peritoneal cancers appear to have both shared and distinct etiologic pathways, although most risk factors appear to have similar associations by anatomic site.

    Impact: Further studies on the mechanisms underlying the differences in risk profiles may provide insights regarding the developmental origins of tumors arising in the peritoneal cavity and inform prevention efforts.

  • 19. Friberg, Emilie
    et al.
    Mantzoros, Christos S.
    Wolk, Alicja
    Diabetes and risk of endometrial cancer: A population-based prospective cohort study2007In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 16, no 2, p. 276-280Article in journal (Refereed)
    Abstract [en]

    Although there is accumulating evidence that hyperinsulinemia in the context of insulin resistance is associated with carcinogenesis, only one prospective study of endometrial cancer incidence, in relation to diabetes, addressed this issue and showed no significant positive association. No previous study has investigated whether physical activity can modify the association between diabetes and endometrial cancer. We examined the association between diabetes and incidence of endometrial cancer and the potential effect modification by obesity and physical activity in the Swedish Mammography Cohort, a prospective cohort of 36,773 women, including 225 incident endometrial adenocarcinoma cases. After adjustments, the relative risk (RR) for endometrial cancer among women with diabetes comparing with nondiabetic women was 1.94 [95% confidence interval (95% CI), 1.23-3.08]. Among obese diabetics, the RR was 6.39 (95% CI, 3.28-12.06) compared with nonobese nondiabetic women. Among diabetics with low physical activity, the RR for endometrial cancer was 2.80 (95% CI, 1.62-4.85) compared with physically active nondiabetic women. Obese diabetics with low physical activity had a RR of 9.61 (95% CI, 4.66-19.83) compared with normal weight nondiabetic women with high physical activity. Diabetes was associated with a 2-fold increased risk, and combination of diabetes with obesity and low physical activity was associated with a further increased risk for endometrial cancer. Interventions to reduce body weight and increase physical activity may have important implications in terms of prevention of endometrial cancer and future management of diabetic subjects.

  • 20. Friberg, Emilie
    et al.
    Mantzoros, Christos S.
    Wolk, Alicja
    Physical activity and risk of endometrial cancer: A population-based prospective cohort study2006In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 15, no 11, p. 2136-2140Article in journal (Refereed)
    Abstract [en]

    Physical activity is involved in the regulation of metabolic and hormonal pathways and is one of the factors important for the maintenance of body weight; obesity is a risk factor for endometrial cancer. A connection between physical activity and endometrial cancer risk through hormonal mechanisms, possibly mediated by body weight, is biologically plausible. Only one study has investigated total physical activity, and no previous study has examined leisure time inactivity directly. We investigated the association of total physical activity and different types of physical activity with risk of endometrial cancer in the Swedish Mammography Cohort, a population-based prospective cohort, including 33,723 women and 199 endometrial cancer cases. After adjustments for potential confounders (age, body mass index, parity, history of diabetes, total fruit and vegetable intake, and education), the relative risks for endometrial cancer for the second to fourth quartile of total physical activity compared with the lowest one were 0.80 [95% confidence interval (95% CI), 0.54-1.18], 0.87 (95% CI, 0.59-1.28), and 0.79 (95% CI, 0.53-1.17). High leisure time inactivity (watching TV/sitting >= 5 hours daily) compared with low was associated with increased risk of endometrial cancer (relative risk, 1.66; 95% CI, 1.05-2.61). The associations were not modified by body mass index. Findings from this study suggest that total physical activity is weakly inversely associated with endometrial cancer risk and that leisure time inactivity is statistically significantly associated with increased risk for endometrial cancer.

  • 21.
    Friberg, Emilie
    et al.
    Karolinska Inst, Div Insurance Med, Dept Clin Neurosci, SE-17177 Stockholm, Sweden.;Natl Inst Environm Med, Div Nutr Epidemiol, Stockholm, Sweden..
    Wallin, Alice
    Natl Inst Environm Med, Div Nutr Epidemiol, Stockholm, Sweden..
    Wolk, Alicja
    Natl Inst Environm Med, Div Nutr Epidemiol, Stockholm, Sweden..
    Sucrose, High-Sugar Foods, and Risk of Endometrial Cancer-a Population-Based Cohort Study2011In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 20, no 9, p. 1831-1837Article in journal (Refereed)
    Abstract [en]

    Background: Consumption of high-sugar foods stimulates insulin production, which has been associated with endometrial cancer. Although a relationship between sucrose, high-sugar food consumption, and endometrial cancer risk is biologically plausible, this hypothesis has previously been explored in very few studies. Methods: We used data from the Swedish Mammography Cohort, including 61,226 women aged 40 to 74 years. We examined the association between consumption of total sucrose, high-sugar foods (at baseline 1987-1990 and 1997) and endometrial cancer risk by using Cox proportional hazards models to estimate incidence rate ratios (RR) with 95% CI. Results: During 18.4 years of follow-up, 729 participants were diagnosed with incident endometrial cancer. Total sucrose intake and consumption of sweet buns and cookies was associated with increased risk of endometrial cancer. RRs (with 95% CIs) for consuming more than 35 grams of sucrose per day and consuming sweet buns and cookies more than 3 times per week were 1.36 (1.04-1.77) and 1.42 (1.15-1.75) as compared with less than 15 grams of sucrose per day and consuming sweet buns and cookies less than 0.5 times per week, respectively. RRs for consuming more than 15 grams of sucrose per day as compared with 15 grams or less were 1.97 (1.27-3.04) among obese women and 1.56 (1.20-2.04) among women with low fat intake. Conclusions: These data indicate that sucrose intake and consumption of sweet buns and cookies may be associated with increased risk of endometrial cancer. Impact: Given the high intake of sweetened foods, these results have public health implications in terms of prevention of endometrial cancer. Cancer Epidemiol Biomarkers Prev; 20(9); 1831-7. (C)2011 AACR.

  • 22.
    Friberg, Emilie
    et al.
    Karolinska Inst, Natl Inst Environm Med, Div Nutr Epidemiol, SE-17177 Stockholm, Sweden..
    Wolk, Alicja
    Karolinska Inst, Natl Inst Environm Med, Div Nutr Epidemiol, SE-17177 Stockholm, Sweden..
    Long-term Alcohol Consumption and Risk of Endometrial Cancer Incidence: A Prospective Cohort Study2009In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 18, no 1, p. 355-358Article in journal (Refereed)
    Abstract [en]

    Alcohol consumption has been hypothesized to increase the risk of endometrial cancer. We used data from the prospective population-based Swedish Mammography Cohort including 61,226 women to examine the association between alcohol and endometrial cancer incidence. Alcohol consumption was assessed with validated food frequency questionnaires at baseline 1.987 to 1.990 and at follow-up in 1997. During a mean follow-up of 17.6 years, 687 endometrial cancer cases were identified in the Swedish cancer registries. We found no association between alcohol consumption and endometrial cancer risk after adjustment for age, body mass index, and smoking, The multivariable rate ratios (95% confidence intervals) for the three upper categories of long-term alcohol consumption as compared with no consumption were 1.01 (0.84-1.22) for <3.4 g/d, 1.01 (0.80-1.27) for 3.4 to 9.9 g/d, and 1.09 (0.71-1.67) for >= 1.0 g/d, respectively. The association did not differ by age, body mass index, folic acid intake, or postmenopausal hormone use in stratified analysis. In conclusion, our results suggest that low alcohol consumption (up to one drink per day) is unlikely to substantially influence risk of endometrial cancer. (Cancer Epidemiol Biomarkers Prev 2009;18(1):355-8)

  • 23.
    Gabrielson, Marike
    et al.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
    Ubhayasekera, Kumari
    Uppsala University, Disciplinary Domain of Science and Technology, Chemistry, Department of Chemistry - BMC, Analytical Chemistry.
    Acharya, Santosh R.
    Uppsala University, Disciplinary Domain of Science and Technology, Chemistry, Department of Chemistry - BMC, Analytical Chemistry.
    Franko, Mikael Andersson
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
    Eriksson, Mikael
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
    Bergquist, Jonas
    Uppsala University, Disciplinary Domain of Science and Technology, Chemistry, Department of Chemistry - BMC, Analytical Chemistry.
    Czene, Kamila
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
    Hall, Per
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden;South Gen Hosp, Dept Oncol, Stockholm, Sweden.
    Inclusion of Endogenous Plasma Dehydroepiandrosterone Sulfate and Mammographic Density in Risk Prediction Models for Breast Cancer2020In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 29, no 3, p. 574-581Article in journal (Refereed)
    Abstract [en]

    Background: Endogenous hormones and mammographic density are risk factors for breast cancer. Joint analyses of the two may improve the ability to identify high-risk women.

    Methods: This study within the KARMA cohort included pre-diagnostic measures of plasma hormone levels of dehydroepiandrosterone (DHEA), its sulfate (DHEAS), and mammographic density in 629 cases and 1,223 controls, not using menopausal hormones. We evaluated the area under the receiver-operating curve (AUC) for risk of breast cancer by adding DHEA, DHEAS, and mammographic density to the Gail or Tyrer-Cuzick 5-year risk scores or the CAD2Y 2-year risk score.

    Results: DHEAS and percentage density were independently and positively associated with breast cancer risk (P = 0.007 and P < 0.001, respectively) for postmenopausal, but not premenopausal, women. No significant association was seen for DHEA. In postmenopausal women, those in the highest tertiles of both DHEAS and density were at greatest risk of breast cancer (OR, 3.5; 95% confidence interval, 1.9-6.3) compared with the lowest tertiles. Adding DHEAS significantly improved the AUC for the Gail (+2.1 units, P = 0.008) and Tyrer-Cuzick (+1.3 units, P = 0.007) risk models. Adding DHEAS to the Gail and Tyrer-Cuzick models already including mammographic density further increased the AUC by 1.2 units (P = 0.006) and 0.4 units (P = 0.007), respectively, compared with only including density.

    Conclusions: DHEAS and mammographic density are independent risk factors for breast cancer and improve risk discrimination for postmenopausal breast cancer.

    Impact: Combining DHEAS and mammographic density could help identify women at high risk who may benefit from individualized breast cancer screening and/or preventive measures among postmenopausal women.

  • 24. Genkinger, J M
    et al.
    Hunter, D J
    Spiegelman, D
    Anderson, K E
    Arslan, A
    Beeson, W L
    Buring, J E
    Fraser, G E
    Freudenheim, J L
    Goldbohm, R A
    Hankinson, S E
    Jacobs, D R
    Koushik, A
    Lacey, J V
    Larsson, S C
    Leitzmann, M
    McCullough, M L
    Miller, A B
    Rodriguez, C
    Rohan, T E
    Schouten, L J
    Shore, R
    Smit, E
    Wolk, A
    Zhang, S M
    Smith-Warner, S A
    Dairy products and ovarian cancer: A pooled analysis of 12 cohort studies2006In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 15, no 2, p. 364-372Article in journal (Refereed)
    Abstract [en]

    Background: Dairy foods and their constituents (lactose and calcium) have been hypothesized to promote ovarian carcinogenesis. Although case-control studies have reported conflicting results for dairy foods and lactose, several cohort studies have shown positive associations between skim milk, lactose, and ovarian cancer. Methods: A pooled analysis of the primary data from 12 prospective cohort studies was conducted. The study population consisted of 553,217 women among whom 2,132 epithelial ovarian cases were identified. Study-specific relative risks and 95% confidence intervals were calculated by Cox proportional hazards models and then pooled by a random-effects model. Results: No statistically significant associations were observed between intakes of milk, cheese, yogurt, ice cream, and dietary and total calcium intake and risk of ovarian cancer. Higher lactose intakes comparing >= 30 versus < 10 g/d were associated with a statistically significant higher risk of ovarian cancer, although the trend was not statistically significant (pooled multivariate relative risk, 1.19; 95% confidence interval, 1.01-1.40; P-trend = 0.19). Associations for endometrioid, mucinous, and serous ovarian cancer were similar to the overall findings. Discussion: Overall, no associations were observed for intakes of specific dairy foods or calcium and ovarian cancer risk. A modest elevation in the risk of ovarian cancer was seen for lactose intake at the level that was equivalent to three or more servings of milk per day. Because a new dietary guideline recommends two to three servings of dairy products per day, the relation between dairy product consumption and ovarian cancer risk at these consumption levels deserves further examination.

  • 25. Genkinger, Jeanine M.
    et al.
    Li, Ruifeng
    Spiegelman, Donna
    Anderson, Kristin E.
    Albanes, Demetrius
    Bergkvist, Leif
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Centre for Clinical Research, County of Västmanland.
    Bernstein, Leslie
    Black, Amanda
    van den Brandt, Piet A.
    English, Dallas R.
    Freudenheim, Jo L.
    Fuchs, Charles S.
    Giles, Graham G.
    Giovannucci, Edward
    Goldbohm, R. Alexandra
    Horn-Ross, Pamela L.
    Jacobs, Eric J.
    Koushik, Anita
    Mannisto, Satu
    Marshall, James R.
    Miller, Anthony B.
    Patel, Alpa V.
    Robien, Kim
    Rohan, Thomas E.
    Schairer, Catherine
    Stolzenberg-Solomon, Rachael
    Wolk, Alicja
    Ziegler, Regina G.
    Smith-Warner, Stephanie A.
    Coffee, Tea, and Sugar-Sweetened Carbonated Soft Drink Intake and Pancreatic Cancer Risk: A Pooled Analysis of 14 Cohort Studies2012In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 21, no 2, p. 305-318Article in journal (Refereed)
    Abstract [en]

    Background: Coffee has been hypothesized to have pro- and anticarcinogenic properties, whereas tea may contain anticarcinogenic compounds. Studies assessing coffee intake and pancreatic cancer risk have yielded mixed results, whereas findings for tea intake have mostly been null. Sugar-sweetened carbonated soft drink (SSB) intake has been associated with higher circulating levels of insulin, which may promote carcinogenesis. Few prospective studies have examined SSB intake and pancreatic cancer risk; results have been heterogeneous. Methods: In this pooled analysis from 14 prospective cohort studies, 2,185 incident pancreatic cancer cases were identified among 853,894 individuals during follow-up. Multivariate (MV) study-specific relative risks (RR) and 95% confidence intervals (CI) were calculated using Cox proportional hazards models and then pooled using a random-effects model. Results: No statistically significant associations were observed between pancreatic cancer risk and intake of coffee (MVRR = 1.10; 95% CI, 0.81-1.48 comparing >= 900 to <0 g/d; 237g approximate to 8oz), tea (MVRR = 0.96; 95% CI, 0.78-1.16 comparing >= 400 to 0 g/d; 237g approximate to 8oz), or SSB (MVRR = 1.19; 95% CI, 0.98-1.46 comparing >= 250 to 0 g/d; 355g approximate to 12oz; P value, test for between-studies heterogeneity > 0.05). These associations were consistent across levels of sex, smoking status, and body mass index. When modeled as a continuous variable, a positive association was evident for SSB (MVRR = 1.06; 95% CI, 1.02-1.12). Conclusion and Impact: Overall, no associations were observed for intakes of coffee or tea during adulthood and pancreatic cancer risk. Although we were only able to examine modest intake of SSB, there was a suggestive, modest positive association for risk of pancreatic cancer for intakes of SSB.

  • 26. Genkinger, Jeanine M.
    et al.
    Spiegelman, Donna
    Anderson, Kristin E.
    Bergkvist, Leif
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Centre for Clinical Research, County of Västmanland.
    Bernstein, Leslie
    van den Brandt, Piet A.
    English, Dallas R.
    Freudenheim, Jo L.
    Fuchs, Charles S.
    Giles, Graham G.
    Giovannucci, Edward
    Hankinson, Susan E.
    Horn-Ross, Pamela L.
    Leitzmann, Michael
    Mannisto, Satu
    Marshall, James R.
    McCullough, Marjorie L.
    Miller, Anthony B.
    Reding, Douglas J.
    Robien, Kim
    Rohan, Thomas E.
    Schatzkin, Arthur
    Stevens, Victoria L.
    Stolzenberg-Solomon, Rachael Z.
    Verhage, Bas A. J.
    Wolk, Alicja
    Ziegler, Regina G.
    Smith-Warner, Stephanie A.
    Alcohol Intake and Pancreatic Cancer Risk: A Pooled Analysis of Fourteen Cohort Studies2009In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 18, no 3, p. 765-776Article, review/survey (Refereed)
    Abstract [en]

    Background: Few risk factors have been implicated in pancreatic cancer etiology. Alcohol has been theorized to promote carcinogenesis. However, epidemiologic studies have reported inconsistent results relating alcohol intake to pancreatic cancer risk. Methods: We conducted a pooled analysis of the primary data from 14 prospective cohort studies. The study sample consisted of 862,664 individuals among whom 2,187 incident pancreatic cancer cases were identified. Study-specific relative risks and 95% confidence intervals were calculated using Cox proportional hazards models and then pooled using a random effects model. Results: A slight positive association with pancreatic cancer risk was observed for alcohol intake (pooled multivariate relative risk, 1.22; 95% confidence interval, 1.03-1.45 comparing >= 30 to 0 grams/day of alcohol; P value, test for between-studies heterogeneity = 0.80). For this comparison, the positive association was only statistically significant among women although the difference in the results by gender was not statistically significant (P value, test for interaction = 0.19). Slightly stronger results for alcohol intake were observed when we limited the analysis to cases with adenocarcinomas of the pancreas. No statistically significant associations were observed for alcohol from wine, beer, and spirits comparing intakes of >= 5 to 0 grams/day. A stronger positive association between alcohol consumption and pancreatic cancer risk was observed among normal weight individuals compared with overweight and obese individuals (P value, test for interaction = 0.01). Discussion: Our findings are consistent with a modest increase in risk of pancreatic cancer with consumption of 30 or more grams of alcohol per day. (Cancer Epidemiol Biomarkers Prev 2009;18(3):765-76)

  • 27.
    Ghanipour, Arezo
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Colorectal Surgery.
    Jirström, Karin
    Pontén, Fredrik
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology.
    Glimelius, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology, Oncology.
    Påhlman, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Colorectal Surgery.
    Birgisson, Helgi
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Colorectal Surgery.
    The prognostic significance of tryptophanyl-tRNA synthetase in colorectal cancer2009In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 18, no 11, p. 2949-2956Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Tryptophanyl-tRNA synthetase (TrpRS) is an aminoacyl-tRNA synthetase involved in protein synthesis and regulation of RNA transcription and translation and is an inhibitor of angiogenesis. TrpRS has been shown to be differentially expressed in colorectal cancer (CRC) and has thus been identified as a potential prognostic marker. The aim of this study was to analyze the correlation of TrpRS to the prognosis of patients diagnosed and treated for CRC within a defined population. METHODS: With a polyclonal, monospecific IgG antibody, TrpRS expression was assessed by immunohistochemistry on tissue microarrays with tumors from a population-based CRC cohort (n = 320). Staining intensity and fraction of positive tumor cells were recorded. A Cox multivariate model including TrpRS expression, carcinoembryonic antigen, age, stage, tumor differentiation, and lymphatic and vascular vessel invasion was used to calculate the hazard ratio and 95% confidence interval (95% CI) for time to recurrence, disease-free survival, and overall survival. RESULTS: Low expression of TrpRS correlated to increased risk for lymph node metastasis (P = 0.025) and a more advanced tumor stage (P = 0.001). Patients with tumors and increased levels of TrpRS expression had better survival than patients with low expression levels. Multivariate analyses revealed significantly better disease-free survival (relative risk, 0.59; 95% CI, 0.38-0.95) for patients with high expression than for patients with low expression of TrpRS. For colon cancer patients, a reduced risk for recurrence was seen in patients with increased TrpRS expression (relative risk, 0.23; 95% CI, 0.07-0.80). CONCLUSION: Low expression of TrpRS in tumor tissue correlates with increased risk for recurrence and worse survival in patients with CRC. This can be related to its antiangiogenic properties and could aid in the future selection of new drugs in the treatment of CRC.

  • 28.
    Grundmark, Birgitta
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Endocrine Surgery.
    Garmo, Hans
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Loda, Massimo
    Busch, Christer
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology.
    Holmberg, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Endocrine Surgery.
    Zethelius, Björn
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Geriatrics.
    The Metabolic Syndrome and the Risk of Prostate Cancer under Competing Risks of Death from Other Causes2010In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 19, no 8, p. 2088-2096Article in journal (Refereed)
    Abstract [en]

    Background:

    Associations between metabolic syndrome (MetS) components and prostate cancer development have not been studied comprehensively; results have been divergent. Using the National Cholesterol Education Program Adult Treatment panel III (NCEP) and International Diabetes Federation (IDF) definitions of the MetS, we investigated such associations taking competing risks of death into consideration.

    Methods:

    In the prospective Uppsala Longitudinal Study of Adult Men of 2,322 Caucasian men with 34 years of follow-up baseline, MetS measurements at age 50 years were used. Cumulative incidence of prostate cancer and death with/without the MetS were calculated. Competing risk of dying was taken into account by calculating the conditional probability of prostate cancer with/without the MetS.

    Results:

    Two hundred and thirty-seven prostate cancers were identified. Prostate cancer probability by age 80 years with baseline MetS compared with without MetS was nonsignificantly higher [5.2 percent units (confidence interval (CI), -0.8% to 11.3%; NCEP); 2.7 percent units (CI, -2.7% to 8.0%; IDF)]; cumulative incidence proportions of death was significantly higher [19.3 percent units (CI, 13.4-25.3%; NCEP); 15.3 percent units (CI, 9.5-21.1%; IDF)]; and conditional probability of prostate cancer considering death from other causes was significantly higher [7.3 percent-units (CI, 0.2-14.5%); odds ratio of 1.64 (CI, 1.03-2.23; NCEP)] and nonsignificantly higher [5.0 percent-units (CI, -1.6% to 11.6%); odds ratio of 1.43 (CI, 0.89-1.90; IDF].

    Conclusions:

    The MetS by the NCEP definition is associated with prostate cancer, taking the competing risk of early death from other causes into account. Impact: The results further highlight the public health effect of the increasing prevalence of MetS and the importance of considering competing risks when studying risk factors for cancer.

  • 29.
    Hamfjord, Julian
    et al.
    Oslo Univ Hosp, Dept Oncol, POB 4956 Nydalen, N-0424 Oslo, Norway.;Oslo Univ Hosp, Inst Canc Res, Dept Canc Genet, Oslo, Norway.;Univ Oslo, Fac Med, Inst Clin Med, Oslo, Norway..
    Myklebust, Tor Age
    Canc Registry Norway, Dept Registrat, Oslo, Norway.;More & Romsdal Hosp Trust, Dept Res & Innovat, Alesund, Norway..
    Larsen, Inger Kristin
    Canc Registry Norway, Dept Registrat, Oslo, Norway..
    Kure, Elin H.
    Oslo Univ Hosp, Inst Canc Res, Dept Canc Genet, Oslo, Norway.;Univ South Eastern Norway, Fac Technol Nat Sci & Maritime Sci, Bo In Telemark, Norway..
    Glimelius, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Experimental and Clinical Oncology. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical and experimental pathology. Uppsala University, Science for Life Laboratory, SciLifeLab.
    Guren, Tormod K.
    Oslo Univ Hosp, Dept Oncol, POB 4956 Nydalen, N-0424 Oslo, Norway..
    Tveit, Kjell M.
    Univ Oslo, Fac Med, Inst Clin Med, Oslo, Norway..
    Guren, Marianne G.
    Oslo Univ Hosp, Dept Oncol, POB 4956 Nydalen, N-0424 Oslo, Norway..
    Survival Trends of Right- and Left-Sided Colon Cancer across Four Decades: A Norwegian Population-Based Study2022In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 31, no 2, p. 342-351Article in journal (Refereed)
    Abstract [en]

    Background: Patients with right-sided colon cancer (RCC) and left-sided colon cancer (LCC) differ clinically and molecularly. The main objective was to investigate stage-stratified survival and recurrence of RCC and LCC across four 10-year periods. Methods: Patients diagnosed from 1977 to 2016 with colon adenocarcinoma were included from the Cancer Registry of Norway. Primary tumor location (PTL) was defined as RCC if proximal and LCC if distal to the splenic flexure. Multivariable regressions were used to estimate HRs for overall survival (OS), recurrence-free survival (RFS), survival after recurrence (SAR), and excess HRs (eHR) for relative survival (RS). Results: 72,224 patients were eligible for analyses [55.1% (n = 39,769/72,224) had RCC]. In 1977 to 1986, there was no difference between LCC and RCC in OS [HR, 1.01; 95% confidence interval (CI), 0.97-1.06; P = 0.581] or RS (eHR, 0.96; 95% CI, 0.90-1.02; P = 0.179). In 2007 to 2016, LCC had significantly better OS (HR, 0.84; 95% CI, 0.80-0.87; P < 0.001) and RS (eHR, 0.76; 95% CI, 0.72-0.81; P < 0.001) compared with RCC. The gradually diverging and significantly favorable prognosis for LCC was evident for distant disease across all time periods and for regional disease from 2007 onward. There was no difference in RFS between LCC and RCC in patients less than 75 years during 2007 to 2016 (HR, 0.99; 95% CI, 0.91-1.08; P = 0.819); however, SAR was significantly better for LCC (HR, 0.61; 95% CI, 0.53-0.71; P < 0.001). Conclusions: A gradually diverging and increasingly favorable prognosis was observed for patients with LCC with advanced disease over the past four decades. Impact Current PTL survival disparities stress the need for further exploring targetable molecular subgroups across and within different PTLs to further improve patient outcomes.

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  • 30. Hjalgrim, Henrik
    et al.
    Ekström-Smedby, Karin
    Rostgaard, Klaus
    Amini, Rose-Marie
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology.
    Molin, Daniel
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology.
    Hamilton-Dutoit, Stephen
    Schöllkopf, Claudia
    Chang, Ellen T.
    Ralfkiaer, Elisabeth
    Adami, Hans-Olov
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology.
    Glimelius, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology.
    Melbye, Mads
    Cigarette smoking and risk of Hodgkin lymphoma: a population-based case-control study2007In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 16, no 8, p. 1561-1566Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Studies have inconsistently reported an association between tobacco smoking and Hodgkin lymphoma (HL) risk. The conflicting finding may reflect etiologic heterogeneity between HL subtypes, warranting further characterization of the relationship. METHODS: We collected information on tobacco-smoking habits in 586 classic HL cases and 3,187 population controls in a Danish-Swedish case-control study. HL EBV status was established for 499 cases by standard techniques. Odds ratios (OR) for an association with cigarette smoking were calculated by logistic regression for HL overall and stratified by age, sex, major histology subtypes, and tumor EBV status, adjusting for known confounders. RESULTS: Compared with never smokers, current cigarette smokers were at an increased overall HL risk [adjusted OR, 1.57; 95% confidence interval (95% CI), 1.22-2.03]. The association was strongest for EBV-positive HL (adjusted OR, 2.36; 95% CI, 1.51-3.71), but also applied to EBV-negative HL (adjusted OR, 1.43; 95% CI, 1.05-1.97; P(homogeneity EBV-pos) versus P(homogeneity EBV-neg) = 0.04). The association did not vary appreciably by age, sex, or histologic subtype, the apparent EBV-related difference present in all strata. There was no evidence of a dose-response pattern, whether by age at smoking initiation, daily cigarette consumption, number of years smoking, or cumulative number of cigarettes smoked. Similar results were obtained in analyses using non-HL patients (n = 3,055) participating in the founding study as comparison group. CONCLUSION: The observed association between cigarette smoking and HL risk is consistent with previous findings and biologically credible. Although not easily dismissed as an artifact, the limited evidence of a dose-response pattern renders the overall evidence of causality weak.

  • 31.
    Holmberg, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Endocrine Surgery.
    Reduction in breast cancer mortality from organized service screening with mammography: 1. Further confirmation with extended data2006In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 15, no 1, p. 45-51Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: In an earlier publication, our evaluation of data from breast cancer screening programs in seven Swedish counties suggested a 40% reduction in incidence-based breast cancer mortality among women actually screened. In the current study, we expand the previous analysis from seven counties to 13 large areas within nine counties, including six of the original counties and seven additional areas, examine a longer period of follow-up (20-44 years), apply new analytic methods for the evaluation of incidence-based breast cancer mortality, and estimate the number needed to screen to save one life.METHODS: Data from six of the original counties (one being excluded as it does not yet have 10 years of follow-up after the initiation of screening), with increased follow-up, and seven additional large areas, within three counties, representing approximately 45% of Swedish women, provide information about age at diagnosis, age at death, and screening history for 542,187 women in the prescreening and 566,423 women in the screening epochs. Regardless of year of diagnosis, there were a total of 6,231 deaths due to breast cancer in the period of study as a whole. Of these, 4,778 were incidence-based deaths in the two epochs, i.e., death among cases diagnosed within either the prescreening or screening period. Data were analyzed using Poisson regression and adjusted, when necessary, for self-selection bias, contemporaneous changes in incidence, and changes in mortality independent of screening.RESULTS: Attendance was uniformly high, averaging 75% in the screening epochs. Recall rates for assessment varied from 4% to 5% at the first round of screening and approximately 3% at later rounds. Detection rates averaged five breast cancers per 1,000 women screened in the first round, and four breast cancers per 1,000 women screened in subsequent rounds. There was a significant 45% reduction in incidence-based breast cancer mortality among screened women in the screening epoch relative to incidence-based breast cancer mortality in the prescreening epoch (relative risk, 0.55; 95% confidence intervals, 0.51-0.59). After adjusting for self-selection bias, there still was a significant 43% reduction in incidence-based breast cancer mortality associated with screening (relative risk, 0.57; 95% confidence intervals, 0.53-0.62).CONCLUSIONS: These results indicate a reduction in breast cancer mortality of between 40% and 45% in association with screening, after adjustment for self-selection bias. These results were obtained with modest human costs: the number needed to screen to save one life was estimated as 472.

  • 32.
    Holmberg, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Endocrine Surgery.
    Reduction in breast cancer mortality from the organised service screening with mammography: 2. Validation with alternative analytic methods2006In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 15, no 1, p. 52-6Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: In our companion article, incidence-based mortality analysis of data from breast cancer screening programs in 13 areas in Sweden indicated a 40% to 45% reduction in incidence-based breast cancer mortality among women actually screened. In this article, we apply new analytic methods for the evaluation of breast cancer mortality, using all breast cancer deaths in the period under study.METHODS: Data were available from 13 areas on breast cancer mortality by year of diagnosis, year of death, and screening exposure. The period of study varied by area, the overall range of year of diagnosis being 1968 to 2001. We had data on 6,231 deaths and an average population of 555,676 women ages 40 to 69 years. Analysis of the effect of being screened was conducted using an alternative statistical analysis applied to all breast cancer deaths in the period of study, in addition to the incidence-based mortality analysis in our companion article. Data were analyzed using Poisson regression and adjusted for self-selection bias, contemporaneous changes in incidence, and changes in mortality independent of screening.RESULTS: Using all deaths in the period of observation, a significant 42% reduction in breast cancer mortality was observed, adjusting for contemporaneous changes independent of screening [relative risk (RR), 0.58; 95% confidence interval (95% CI), 0.53-0.62]. After further adjustment for self-selection bias, the mortality reduction was 39% (RR, 0.61; 95% CI, 0.55-0.68), also highly significant.CONCLUSIONS: These results indicate a reduction in breast cancer mortality of 39% in association with screening, after adjustment for contemporaneous changes and self-selection bias. These results confirm previous conclusions arrived at using incidence-based mortality analyses.

  • 33.
    Holmberg, Lars
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences.
    Baron, John A.
    Byers, Tim
    Wolk, Alicja
    Ohlander, Eva-May
    Zack, Matthew
    Adami, Hans-Olov
    Alcohol intake and breast cancer risk: effect of exposure from 15 years of age1995In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 4, no 8, p. 843-847Article in journal (Refereed)
    Abstract [en]

    Research regarding the relationship between alcohol intake and breast cancer risk has suggested an association between the two, although the data are inconsistent regarding dose effects and susceptible populations. To clarify these issues, we investigated the association of breast cancer risk with alcohol intake at various ages in a population-based case-control study nested within a screening cohort in Sweden. Subjects were women 40-75 years old who participated in a screening program in central Sweden. Information about personal characteristics, diet, and alcohol intake was obtained by a questionnaire sent out at the invitation to the screening interview and at a supplementary interview conducted among a sample of women who did and did not develop breast cancer. Alcohol intake did not affect breast cancer risk among women under 50 years old. However, among those over 50 years of age, ever-drinking conferred a relative risk of 1.8 (95% confidence interval = 1.2-2.6). Current and former drinkers had similar increases in risk. No particular latent period of alcohol effect was identified, but drinking later in life to have a bigger effect than did drinking earlier in life.

  • 34.
    Huang, Tianyi
    et al.
    Harvard Med Sch, Brigham & Womens Hosp, Channing Div Network Med, Boston, MA 02115 USA.
    Townsend, Mary K.
    H Lee Moffitt Canc Ctr & Res Inst, Div Populat Sci, Tampa, FL USA.
    Wentzensen, Nicolas
    NCI, Div Canc Epidemiol & Genet, NIH, Washington, DC USA.
    Trabert, Britton
    NCI, Div Canc Epidemiol & Genet, NIH, Washington, DC USA.
    White, Emily
    Fred Hutchinson Canc Res Ctr, 1124 Columbia St, Seattle, WA 98104 USA.
    Arslan, Alan A.
    NYU, Sch Med, Dept Populat Hlth, New York, NY USA;NYU, Dept Environm Med, Sch Med, 550 1St Ave, New York, NY 10016 USA;NYU, Dept Obstet & Gynecol, Sch Med, New York, NY 10016 USA.
    Weiderpass, Elisabete
    WHO, Int Agcy Res Canc, Lyon, France.
    Buring, Julie E.
    Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA;Brigham & Womens Hosp, Div Prevent Med, 75 Francis St, Boston, MA 02115 USA;Harvard Med Sch, 181 Longwood Ave, Boston, MA 02115 USA.
    Clendenen, Tess V.
    NYU, Sch Med, Dept Populat Hlth, New York, NY USA.
    Giles, Graham G.
    Canc Council Victoria, Canc Epidemiol Div, Melbourne, Vic, Australia;Univ Melbourne, Sch Populat & Global Hlth, Ctr Epidemiol & Biostat, Melbourne, Vic, Australia;Monash Univ, Monash Hlth, Sch Clin Sci, Precis Med, Clayton, Vic, Australia.
    Lee, I-Min
    Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA;Brigham & Womens Hosp, Div Prevent Med, 75 Francis St, Boston, MA 02115 USA;Harvard Med Sch, 181 Longwood Ave, Boston, MA 02115 USA.
    Milne, Roger L.
    Canc Council Victoria, Canc Epidemiol Div, Melbourne, Vic, Australia;Univ Melbourne, Sch Populat & Global Hlth, Ctr Epidemiol & Biostat, Melbourne, Vic, Australia;Monash Univ, Monash Hlth, Sch Clin Sci, Precis Med, Clayton, Vic, Australia.
    Onland-Moret, N. Charlotte
    Univ Utrecht, Univ Med Ctr Utrecht, Julius Ctr Hlth Sci & Primary Care, Utrecht, Netherlands.
    Peters, Ulrike
    Fred Hutchinson Canc Res Ctr, 1124 Columbia St, Seattle, WA 98104 USA.
    Sandler, Dale P.
    NIEHS, Bethesda, MD USA.
    Schouten, Leo J.
    Maastricht Univ, GROW Sch Oncol & Dev Biol, Maastricht, Netherlands.
    van den Brandt, Piet A.
    Maastricht Univ, GROW Sch Oncol & Dev Biol, Maastricht, Netherlands.
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics. Karolinska Inst, Inst Environm Med, Stockholm, Sweden.
    Zeleniuch-Jacquotte, Anne
    NYU, Sch Med, Dept Populat Hlth, New York, NY USA;NYU, Dept Environm Med, Sch Med, 550 1St Ave, New York, NY 10016 USA.
    Tworoger, Shelley S.
    Harvard Med Sch, Brigham & Womens Hosp, Channing Div Network Med, Boston, MA 02115 USA;H Lee Moffitt Canc Ctr & Res Inst, Div Populat Sci, Tampa, FL USA;Harvard TH Chan Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
    Reproductive and Hormonal Factors and Risk of Ovarian Cancer by Tumor Dominance: Results from the Ovarian Cancer Cohort Consortium (OC3)2020In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 29, no 1, p. 200-207Article in journal (Refereed)
    Abstract [en]

    Background: Laterality of epithelial ovarian tumors may reflect the underlying carcinogenic pathways and origins of tumor cells.

    Methods: We pooled data from 9 prospective studies participating in the Ovarian Cancer Cohort Consortium. Information on measures of tumor size or tumor dominance was extracted from surgical pathology reports or obtained through cancer registries. We defined dominant tumors as those restricted to one ovary or where the dimension of one ovary was at least twice as large as the other, and nondominant tumors as those with similar dimensions across the two ovaries or peritoneal tumors. Competing risks Cox models were used to examine whether associations with reproductive and hormonal risk factors differed by ovarian tumor dominance.

    Results: Of 1,058 ovarian cancer cases with tumor dominance information, 401 were left-dominant, 363 were right-dominant, and 294 were nondominant. Parity was more strongly inversely associated with risk of dominant than nondominant ovarian cancer (P-heterogeneity = 0.004). Ever use of oral contraceptives (OC) was associated with lower risk of dominant tumors, but was not associated with nondominant tumors (Pheterogeneity = 0.01). Higher body mass index was associated with higher risk of left-dominant tumors, but not significantly associated with risk of right-dominant or nondominant tumors (P-heterogeneity = 0.08).

    Conclusions: These data suggest that reproductive and hormonal risk factors appear to have a stronger impact on dominant tumors, which may have an ovarian or endometriosis origin.

    Impact: Examining the associations of ovarian cancer risk factors by tumor dominance may help elucidate the mechanisms through which these factors influence ovarian cancer risk.

  • 35.
    Jochems, Sylvia H. J.
    et al.
    Lund Univ, Dept Clin Sci Lund, Lund, Sweden..
    Häggström, Christel
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Endocrine Surgery. Umeå Univ, Northern Register Ctr, Dept Publ Hlth & Clin Med, Umeå, Sweden..
    Stattin, Pär
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Urology.
    Järvholm, Bengt
    Umeå Univ, Dept Publ Hlth & Clin Med, Umeå, Sweden..
    Stocks, Tanja
    Lund Univ, Dept Clin Sci Lund, Lund, Sweden.;Lund Univ, Dept Clin Sci Lund, Barngatan 4, SE-22185 Lund, Sweden..
    Association of Blood Pressure with Prostate Cancer Risk by Disease Severity and Prostate Cancer Death: A Pooled Cohort Study2022In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 31, no 7, p. 1483-1491Article in journal (Refereed)
    Abstract [en]

    Background: The association of blood pressure (BP) with prostate cancer risk after accounting for asymptomatic prostate-specific antigen (PSA) testing, and with prostate cancer death, is unclear.

    Methods: We investigated BP, measured at a mean age of 38 years among 430,472 men from five Swedish cohorts, in association with incident prostate cancer (n = 32,720) and prostate cancer death (n = 6718). HRs were calculated from multivariable Cox regression models.

    Results: Increasing systolic and diastolic BP levels combined were associated with a slightly lower prostate cancer risk, with a HR of 0.98 (95% CI, 0.97-0.99) per standard deviation (SD) of mid-BP (average of systolic and diastolic BP). The association was restricted to the PSA era (1997 onwards, HR, 0.96; 95% CI, 0.95-0.98), to diagnoses initiated by a PSA test in asymptomatic men (HR, 0.95; 95% CI, 0.93-0.97), and to low-risk prostate cancer (HR, 0.95; 95% CI, 0.92-0.97). There was no clear association with more advanced disease at diagnosis. In cases, a slightly higher risk of prostate cancer death was observed for higher BP levels (HR, 1.05; 95% CI, 1.01-1.08) per SD of mid-BP; however, the association was restricted to distant metastatic disease (Pheterogeneity between case groups = 0.01), and there was no association for BP measured less than 10 years prior to diagnosis.

    Conclusions: Prediagnostic BP is unlikely an important risk factor for prostate cancer development and death. Less asymptomatic PSA testing among men with higher BP levels may explain their lower risk of prostate cancer.

    Impact: Elevated BP is unlikely to be an important risk factor for prostate cancer.

  • 36. Khankari, Nikhil K
    et al.
    Banbury, Barbara L
    Borges, Maria C
    Haycock, Philip
    Albanes, Demetrius
    Arndt, Volker
    Berndt, Sonja I
    Bézieau, Stéphane
    Brenner, Hermann
    Campbell, Peter T
    Casey, Graham
    Chan, Andrew T
    Chang-Claude, Jenny
    Conti, David V
    Cotterchio, Michelle
    English, Dallas R
    Figueiredo, Jane C
    Giles, Graham G
    Giovannucci, Edward L
    Gunter, Marc J
    Hampe, Jochen
    Hoffmeister, Michael
    Hopper, John L
    Jenkins, Mark A
    Joshi, Amit D
    Marchand, Loic Le
    Lemire, Mathieu
    Li, Christopher I
    Li, Li
    Lindblom, Annika
    Martín, Vicente
    Moreno, Victor
    Newcomb, Polly A
    Offit, Kenneth
    Pharoah, Paul D P
    Rennert, Gad
    Sakoda, Lori C
    Schafmayer, Clemens
    Schmit, Stephanie L
    Slattery, Martha L
    Song, Mingyang
    Thibodeau, Stephen N
    Ulrich, Cornelia M
    Weinstein, Stephanie J
    White, Emily
    Win, Aung Ko
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Woods, Michael O
    Wu, Anna H
    Cai, Qiuyin
    Denny, Joshua C
    Edwards, Todd L
    Murff, Harvey J
    Gruber, Stephen B
    Peters, Ulrike
    Zheng, Wei
    Mendelian Randomization of Circulating Polyunsaturated Fatty Acids and Colorectal Cancer Risk.2020In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 29, no 4, p. 860-870Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Results from epidemiologic studies examining polyunsaturated fatty acids (PUFA) and colorectal cancer risk are inconsistent. Mendelian randomization may strengthen causal inference from observational studies. Given their shared metabolic pathway, examining the combined effects of aspirin/NSAID use with PUFAs could help elucidate an association between PUFAs and colorectal cancer risk.

    METHODS: Information was leveraged from genome-wide association studies (GWAS) regarding PUFA-associated SNPs to create weighted genetic scores (wGS) representing genetically predicted circulating blood PUFAs for 11,016 non-Hispanic white colorectal cancer cases and 13,732 controls in the Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO). Associations per SD increase in the wGS were estimated using unconditional logistic regression. Interactions between PUFA wGSs and aspirin/NSAID use on colorectal cancer risk were also examined.

    RESULTS: Modest colorectal cancer risk reductions were observed per SD increase in circulating linoleic acid [ORLA = 0.96; 95% confidence interval (CI) = 0.93-0.98; P = 5.2 × 10-4] and α-linolenic acid (ORALA = 0.95; 95% CI = 0.92-0.97; P = 5.4 × 10-5), whereas modest increased risks were observed for arachidonic (ORAA = 1.06; 95% CI = 1.03-1.08; P = 3.3 × 10-5), eicosapentaenoic (OREPA = 1.04; 95% CI = 1.01-1.07; P = 2.5 × 10-3), and docosapentaenoic acids (ORDPA = 1.03; 95% CI = 1.01-1.06; P = 1.2 × 10-2). Each of these effects was stronger among aspirin/NSAID nonusers in the stratified analyses.

    CONCLUSIONS: Our study suggests that higher circulating shorter-chain PUFAs (i.e., LA and ALA) were associated with reduced colorectal cancer risk, whereas longer-chain PUFAs (i.e., AA, EPA, and DPA) were associated with an increased colorectal cancer risk.

    IMPACT: The interaction of PUFAs with aspirin/NSAID use indicates a shared colorectal cancer inflammatory pathway. Future research should continue to improve PUFA genetic instruments to elucidate the independent effects of PUFAs on colorectal cancer.

  • 37. Koushik, A
    et al.
    Hunter, D J
    Spiegelman, D
    Anderson, K E
    Arslan, A A
    Beeson, W L
    van den Brandt, P A
    Buring, J E
    Cerhan, J R
    Colditz, G A
    Fraser, G E
    Freudenheim, J L
    Genkinger, J M
    Goldbohm, R A
    Hankinson, S E
    Koenig, K L
    Larsson, S C
    Leitzmann, M
    McCullough, M L
    Miller, A B
    Patel, A
    Rohan, T E
    Schatzkin, A
    Smit, E
    Willett, W C
    Wolk, A
    Zhang, S M M
    Smith-Warner, S A
    Fruits and vegetables and ovarian cancer risk in a pooled analysis of 12 cohort studies2005In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 14, no 9, p. 2160-2167Article in journal (Refereed)
    Abstract [en]

    Because fruits and vegetables are rich in bioactive compounds with potential cancer-preventive actions, increased consumption may reduce the risk of ovarian cancer. Evidence on the association between fruit and vegetable intake and ovarian cancer risk has not been consistent. We analyzed and pooled the primary data from 12 prospective studies in North America and Europe. Fruit and vegetable intake was measured at baseline in each study using a validated food frequency questionnaire. To summarize the association between fruit and vegetable intake and ovarian cancer, study-specific relative risks (RR) were estimated using the Cox proportional hazards model, and then combined using a random-effects model. Among 560,441 women, 2,130 cases of invasive epithelial ovarian cancer occurred during a maximum follow-up of 7 to 22 years across studies. Total fruit intake was not associated with ovarian cancer risk-the pooled multivariate RR for the highest versus the lowest quartile of intake was 1.06 [95% confidence interval (95% CI), 0.92-1.21; P value, test for trend = 0.73; P value, test for between-studies heterogeneity = 0.741. Similarly, results for total vegetable intake indicated no significant association (pooled multivariate RR, 0.90; 95% Cl, 0.78-1.04, for the highest versus the lowest quartile; P value, test for trend = 0.06; P value, test for between-studies heterogeneity = 0.31). Intakes of botanically defined fruit and vegetable groups and individual fruits and vegetables were also not associated with ovarian cancer risk. Associations for total fruits and vegetables were similar for different histologic types. These results suggest that fruit and vegetable consumption in adulthood has no important association with the risk of ovarian cancer.

  • 38. Kulmala, Satu-Maria A.
    et al.
    Shabalova, Irena P.
    Petrovitchev, Nikolay
    Syrjänen, Kari J.
    Gyllensten, Ulf B.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology.
    Johansson, Bo C.
    Syrjänen, Stina M.
    Tosi, P.
    Type-specific persistence of high-risk human papillomavirus infections in the New Independent States of the former Soviet Union Cohort Study2007In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 16, no 1, p. 17-22Article in journal (Refereed)
    Abstract [en]

    Background: Prospective follow-up studies have recently suggested that persistent high-risk human papillomavirus (HPV) infections play a key role in the progression of CIN lesions and in the development of cervical cancer. However, data on type-specific persistence, viral integration, and the role of multiple infections are scanty.

    Materials and Methods: A cross-sectional/cohort study was conducted between 1998 and 2002 in three New Independent States of the former Soviet Union comprising a cohort of 3,187 women, of whom 854 women were followed up for a mean of 17 months (SD, 11.6). HPV genotyping was done with real-time PCR, detecting HPV types 16, 18/45, 31, 33/52/58, 35, and 39. The integration status of HPV16 was examined by using a novel Taqman-based PCR method.

    Results: The mean clearance time for the individual high– risk–type infection was 16.5 months (range = 0.9-34.9 months). HPV16 and HPV31 were the most persistent infections (clearance times = 18.1 and 16.2 months, respectively), whereas HPV39 infections cleared most rapidly. The mean copies per cell in HPV18/45, HPV31, HPV33/52/58, and HPV39 infections were higher in persisting HPV infections than in HPV infections that cleared, but the difference was not significant. Integration of HPV16 was not found to correlate with HPV persistence.

    Conclusions: A large proportion of women remained high-risk HPV positive after 18 months. Coinfection with multiple HPV types, viral load, or integration status did not correlate with persistence of high-risk HPV infections.

  • 39. Lambe, Mats
    et al.
    Hsieh, Chung-Cheng
    Tsaih, Shirng-wern
    Adami, Johanna
    Glimelius, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology.
    Adami, Hans-Olov
    Childbearing and the risk of Hodgkin's disease1998In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 7, no 9, p. 831-834Article in journal (Refereed)
    Abstract [en]

    The causes of Hodgkin's disease remain incompletely known, but a higher incidence in men than in women has prompted an interest in the role of female sex hormones and reproductive history. Available epidemiological data are, however, contradictory. We analyzed possible associations between parity, age at first birth, and the risk of developing Hodgkin's disease by a linkage between the Swedish Cancer Register and a nationwide Fertility Register. Among women born between 1925 and 1972, 917 cases with Hodgkin's disease and concomitant fertility information were identified. For each case patient, five age-matched controls were randomly selected among women in the Fertility Register. Conditional logistic regression was used to estimate odds ratios of Hodgkin's disease associated with a birth. We found a slightly and nonsignificantly reduced risk of Hodgkin's disease in ever-parous compared with nulliparous women. Among parous women, the number of children was unrelated to risk, whereas there was some evidence of an increased risk with late age at first birth in women under age 45 at diagnosis. No clear temporal relations between childbearing and subsequent risk were discernible in any parity or age group. Although uncontrolled confounding might have affected our results, they do not indicate that hormonal or immunological changes associated with childbearing play a role in the development of Hodgkin's disease.

  • 40.
    Larfors, Gunnar
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Haematology.
    Hallböök, Helene
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Haematology.
    Simonsson, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Haematology.
    Parental Age, Family Size, and Offspring's Risk of Childhood and Adult Acute Leukemia2012In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 21, no 7, p. 1185-1190Article in journal (Refereed)
    Abstract [en]

    Background: An association between childhood acute leukemia and advanced parental age was observed more than 50 years ago, and the association has been repeated in several, but not all, subsequent studies. In contrast to the many studies addressing childhood leukemia, few have included adult patients.

    Methods: In this register-based case control study, we examined the association between parental age and incidence of acute leukemia in 2,660 childhood cases and 4,412 adult cases of acute leukemia, compared with 28,288 age-matched controls selected from a population-based register. Relative risks were estimated with conditional logistic regression.

    Results: We found a small increased risk of childhood acute lymphoblastic leukemia with increasing paternal age (adjusted OR, 1.05 per 5-year increase in age). Risk estimates were similar for childhood acute myeloid leukemia (AML), whereas no association was found with adult leukemia. Meanwhile, we observed a decreased risk of adult AML with increasing number of siblings, both older and younger.

    Conclusions: The results support the idea of a prenatal etiology of leukemia but indicate that parental age effects are limited to childhood cases. Impact: This is the first large study on parental age and leukemia risk, which includes adult cases. The finding on family size and risk of adult AM L needs to be validated in future studies.

  • 41.
    Larfors, Gunnar
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Haematology.
    Lambert, Paul C.
    Lambe, Mats
    Ekbom, Anders
    Cnattingiusi, Sven
    Placental Weight and Breast Cancer Survival in Young Women2009In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 18, no 3, p. 777-783Article in journal (Refereed)
    Abstract [en]

    A growing body of evidence indicates that reproductive history influences survival in breast cancer, especially among women diagnosed during or shortly after a pregnancy. However, little is known about the underlying mechanisms. We hypothesized that increasing placental weight, as an indirect marker of exposure to elevated hormone levels during pregnancy, would be associated with reduced survival in breast cancer. A cohort of 1873 women with at least one pregnancy after January 1st, 1973, and a subsequent breast cancer diagnosis before the end of 1991 were followed up for death or emigration through 2006. Information on placental weight and potential confounding factors were collected from medical records and from nationwide registers, which resulted in data on placental weight in the most recent pregnancy before diagnosis for 1,057 cases. For each 100-gram increase in placental weight, the adjusted hazard ratio of death was 1.09 [95% confidence interval (CI), 0.99-1.19]. The association was stronger among primiparous women (adjusted hazard ratio, 1.26; 95% CI, 1.09-1.47), and among women diagnosed during pregnancy or within 2 years from last birth (adjusted hazard ratio, 1.30; 95% CI, 1.06-1.59). Increasing placental weight is associated with reduced breast cancer survival. These findings are consistent with the hypothesis that the reduced survival in breast cancer among women with a recent childbirth is linked to pregnancy hormone exposure.

  • 42.
    Larfors, Gunnar
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Haematology.
    Richter, Johan
    Skane Univ Hosp, Dept Hematol Oncol & Radiat Phys, Lund, Sweden.
    Själander, Anders
    Umea Univ, Dept Publ Hlth & Clin Med, Umea, Sweden.
    Stenke, Leif
    Karolinska Univ Hosp Solna, Div Hematol, Dept Med, Stockholm, Sweden;Karolinska Inst, Stockholm, Sweden.
    Höglund, Martin
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Haematology.
    Increased Risk of Chronic Myeloid Leukemia Following Gastric Conditions Indicating Helicobacter pylori Infection: A Case-Control Study2020In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 29, no 1, p. 151-156Article in journal (Refereed)
    Abstract [en]

    Background: On the basis of a previous report of increased chronic myeloid leukemia (CML) risk following peptic ulcer, we hypothesized that chronic Helicobacter pylori infection could serve as a risk factor for CML.

    Methods: In a population-based, retrospective case-control study, we used Swedish registry data on 980 patients with CML and 4,960 age- and sex-matched controls to investigate associations between markers of previous infection with Helicobacter pylori and CML incidence.

    Results: Previous diagnoses of dyspepsia, gastritis or peptic ulcers, as well as previous proton pump inhibitor (PPI) medication, were all associated with a significantly increased risk of CML (RRs, 1.5-2.0; P = 0.0005-0.05). Meanwhile, neither inflammatory bowel disease nor intake of NSAIDs were associated with CML, indicating that it is not gastrointestinal ulcer or inflammation per se that influences risk.

    Conclusions: The consistent associations suggest a shared background between gastric conditions and CML, and strengthen the case that Helicobacter pylori could constitute this common risk factor.

    Impact: As the etiology of CML is practically unknown, and Helicobacter pylori could potentially be a therapeutic target, even this indirect evidence encourages further studies on the potential involvement of Helicobacter pylori in CML etiology.

  • 43. Larsson, S C
    et al.
    Giovannucci, E
    Wolk, A
    A prospective study of dietary folate intake and risk of colorectal cancer: Modification by caffeine intake and cigarette smoking2005In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 14, no 3, p. 740-743Article in journal (Refereed)
    Abstract [en]

    Epidemiologic evidence indicates an inverse association of folate intake with risk of colorectal cancer, but whether this association is modified by intake of caffeine (in coffee and tea) or cigarette smoking-factors that possibly interfere with folate-has not been studied. Thus, we examined whether the association between dietary folate intake and incidence of colorectal cancer is modified by caffeine intake and smoking. Cox proportional hazards modeling was used to estimate rate ratios relating dietary folate intake to colorectal cancer incidence among 61,433 women ages 40 to 75 years at recruitment into the Swedish Mammography Cohort in 1987 to 1990. From March 1987 through June 2004, a total of 805 incident cases of colorectal cancer were diagnosed. After controlling for age and other potential confounders, we observed an inverse association between dietary folate intake and risk of colon cancer (rate ratio for the highest versus the lowest quintile, 0.61; 95% confidence interval, 0.41-0.91; P-trend = 0.02), but not of rectal cancer (rate ratio, 0.93; 95% confidence interval, 0.55-1.56; P-trend = 0.97). The inverse association between dietary folate intake and colon cancer risk was most pronounced among smokers (P-interaction = 0.03). We found no apparent modification of risk by caffeine intake. Findings from this population-based cohort study support an inverse association between dietary folate intake and risk of colon cancer and suggest that smokers might benefit most from a high dietary folate intake.

  • 44.
    Larsson, Susanna C.
    et al.
    Karolinska Inst, Natl Inst Environm Med, Div Nutr Epidemiol, SE-17177 Stockholm, Sweden..
    Akesson, Agneta
    Karolinska Inst, Natl Inst Environm Med, Div Nutr Epidemiol, SE-17177 Stockholm, Sweden..
    Wolk, Alicja
    Karolinska Inst, Natl Inst Environm Med, Div Nutr Epidemiol, SE-17177 Stockholm, Sweden..
    Dietary Acrylamide Intake and Prostate Cancer Risk in a Prospective Cohort of Swedish Men2009In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 18, no 6, p. 1939-1941Article in journal (Refereed)
    Abstract [en]

    Background: Acrylamide is a probable human carcinogen that can be formed in foods prepared at high temperatures. Whereas evidence indicates that acrylamide causes cancer in laboratory animals, epidemiologic data on dietary acrylamide intake in relation to cancer risk are limited and mainly null. We examined the association between dietary acrylamide intake and risk of prostate cancer in a cohort of men. Methods: The Cohort of Swedish Men is a population-based prospective study of 45,306 men who were cancer-free and completed a food frequency questionnaire at enrollment in 1997. Cox proportional hazards models were used to estimate relative risks adjusted for potential confounders. Results: During a mean follow-up of 9.1 years, we ascertained 2,696 incident cases of prostate cancer. We observed no association between acrylamide intake and risk of prostate cancer. Compared with the lowest quintile of acrylamide intake (mean, 23.7 mu g/d), the multivariable relative risks (95% confidence interval) for the highest quintile (mean, 49.8 mu g/d) were 0.88 (0.70-1.09) for total prostate cancer, 1.07 (0.87-1.32) for localized prostate cancer (n = 1,088), and 0.98 (0.78-1.22) for advanced prostate cancer (n = 951). Conclusions: Results from this prospective study provide no evidence that dietary acrylamide in amounts typically consumed by Swedish men is associated with risk of prostate cancer. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1939-41)

  • 45.
    Larsson, Susanna C.
    et al.
    Karolinska Inst, Natl Inst Environm Med, Div Nutr Epidemiol, SE-17177 Stockholm, Sweden..
    Akesson, Agneta
    Karolinska Inst, Natl Inst Environm Med, Div Nutr Epidemiol, SE-17177 Stockholm, Sweden..
    Wolk, Alicja
    Karolinska Inst, Natl Inst Environm Med, Div Nutr Epidemiol, SE-17177 Stockholm, Sweden..
    Long-Term Dietary Acrylamide Intake and Risk of Epithelial Ovarian Cancer in a Prospective Cohort of Swedish Women2009In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 18, no 3, p. 994-997Article in journal (Refereed)
    Abstract [en]

    Background: Acrylamide, a probable human carcinogen, can be formed in carbohydrate-rich foods cooked at high temperatures. Whether dietary acrylamide intake is associated with the risk of cancer in humans is uncertain. We aimed to assess the relation between dietary acrylamide intake and the incidence of epithelial ovarian cancer. Methods: The Swedish Mammography Cohort is a population-based prospective study of 61,057 Swedish women. Diet was assessed with a food-frequency questionnaire at baseline in 1987-1990 and again in 1997. Results: During a mean follow-up of 17.5 years, we ascertained 368 incident cases of ovarian cancer. We observed no association between acrylamide intake and the risk of ovarian cancer. Compared with the lowest quartile of acrylamide intake (mean intake, 16.9 mu g/day), the multivariable rate ratios for the highest quartile (mean intake, 32.5 mu g/day) were 0.86 (95% confidence interval, 0.63-1.16) for total ovarian cancer and 1.05 (95% confidence interval, 0.68-1.63) for serous ovarian cancer (n = 182 cases). Conclusions: The results from this prospective study provide no evidence that dietary acrylamide in amounts typically consumed by Swedish women is associated with the risk of ovarian cancer. (Cancer Epidemiol Biomarkers Prev 2009;18(3):994-7)

  • 46.
    Larsson, Susanna C.
    et al.
    Karolinska Inst, Div Nutr Epidemiol, Natl Inst Environm Med, SE-17177 Stockholm, Sweden..
    Andersson, Swen-Olf
    Orebro Univ Hosp, Dept Urol, Orebro, Sweden.;Orebro Univ Hosp, Ctr Assessment Med Technol, Orebro, Sweden..
    Johansson, Jan-Erik
    Orebro Univ Hosp, Dept Urol, Orebro, Sweden.;Orebro Univ Hosp, Ctr Assessment Med Technol, Orebro, Sweden..
    Wolk, Alicja
    Karolinska Inst, Div Nutr Epidemiol, Natl Inst Environm Med, SE-17177 Stockholm, Sweden..
    Fruit and vegetable consumption and risk of bladder cancer: A prospective cohort study2008In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 17, no 9, p. 2519-2522Article in journal (Refereed)
    Abstract [en]

    Fruit and vegetable consumption has been inconsistently associated with risk of bladder cancer. We used data from a prospective population-based cohort study of 82,002 Swedish women and men to examine the association between fruit and vegetable consumption and bladder cancer incidence. Diet was assessed with a validated food frequency questionnaire. During a mean follow-up of 9.4 years, 485 incident cases of bladder cancer were identified in the Swedish cancer registries. We found no statistically significant association between intakes of total fruits and vegetables, total fruits, or total vegetables and bladder cancer risk after adjustment for age, sex, education, and cigarette smoking. The multivariate rate ratios (95% confidence intervals) comparing the highest with the lowest quartile of intake were 0.80 (0.60-1.05) for total fruits and vegetables, 0.93 (0.69-1.25) for fruits, and 0.89 (0.67-1.19) for vegetables. Likewise, no associations were observed for citrus fruits, cruciferous vegetables, or green leafy vegetables. The associations did not differ by sex or smoking status. In conclusion, findings from this prospective study suggest that fruit and vegetable intakes are not likely to be appreciably associated with the risk of bladder cancer.

  • 47. Larsson, Susanna C.
    et al.
    Bergkvist, Leif
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Centre for Clinical Research, County of Västmanland.
    Wolk, Alicja
    Folate Intake and Risk of Breast Cancer by Estrogen and Progesterone Receptor Status in a Swedish Cohort2008In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 17, no 12, p. 3444-3449Article in journal (Refereed)
    Abstract [en]

    Background: Folate is a B vitamin involved in one-carbon metabolism and has been postulated to influence the risk of breast cancer. However, epidemiologic studies of folate intake in relation to breast cancer risk are inconclusive. We examined the association between dietary folate intake and the risk of breast cancer by estrogen receptor (ER) and progesterone receptor (PR) status of the breast tumor in the Swedish Mammography Cohort. Methods: Our study population consisted of 61,433 women who completed a food frequency questionnaire at baseline (1987-1990) and again in 1997. Cox proportional hazards models were used to estimate rate ratios (RR) with 95% confidence intervals (95% CI). Results: During an average of 17.4 years of follow-up, 2,952 incident cases of invasive breast cancer were ascertained. We observed no association between dietary folate intake and risk of total breast cancer or ER+/PR+ or ER-/PR- tumors. The multivariate RR of total breast cancer comparing extreme quintiles of folate intake was 1.01 (95%a CI, 0.90-1.13; P-trend = 0.84). However, folate intake was inversely associated with risk of ER+/PR- breast cancer (n = 417 cases; RR for highest versus lowest quintile, 0.79; 95% CI, 0.59-1.07; Ptrend = 0.01). Results did not vary by alcohol intake or menopausal status. Conclusions: These findings do not support an overall association between folate intake and risk of breast cancer but suggest that folate intake may be inversely associated with ER+/PR- tumors.

  • 48.
    Larsson, Susanna C.
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Bergkvist, Leif
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Centre for Clinical Research, County of Västmanland.
    Wolk, Alicja
    Fruit and vegetable consumption and incidence of gastric cancer: a prospective study2006In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 15, no 10, p. 1998-2001Article in journal (Refereed)
    Abstract [en]

    Background: Whether fruit and vegetable consumption may confer protection from gastric cancer remains controversial.

    Methods: We prospectively investigated the association between consumption of fruits and vegetables and the incidence of gastric cancer among participants from two population-based cohort studies: 36,664 women in the Swedish Mammography Cohort and 45,338 men in the Cohort of Swedish Men. Participants completed a food-frequency questionnaire in 1997 and were followed up for cancer incidence through June 2005. Cox proportional hazards models were used to estimate multivariate hazard ratios (HR) and 95% confidence intervals (95% CI).

    Results: During a mean follow-up of 7.2 years, we ascertained 139 incident cases of gastric cancer. Vegetable consumption was inversely associated with risk of gastric cancer, whereas no significant association was observed for fruit consumption. After controlling for age and other risk factors, women and men who consumed >= 2.5 servings/d of vegetables had a HR of 0.56 (95% CI, 0.34-0.93) for developing gastric cancer compared with those who consumed < 1 serving/d. The respective HR for fruit consumption was 0.86 (95% CI, 0.52-1.43). Among specific subgroups of vegetables, consumption of green leafy vegetables and root vegetables was inversely associated with risk of gastric cancer, the multivariate HRs comparing >= 3 servings/wk with < 0.5 serving/wk were 0.64 (95% CI, 0.42-0.99) for green leafy vegetables and 0.43 (95% CI, 0.27-0.69) for root vegetables.

    Conclusions: Frequent consumption of vegetables may reduce the risk of gastric cancer.

  • 49. Larsson, Susanna C.
    et al.
    Giovannucci, Edward
    Wolk, Alicja
    Folate intake and stomach cancer incidence in a prospective cohort of Swedish women2006In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 15, no 7, p. 1409-1412Article in journal (Refereed)
    Abstract [en]

    Background: Experimental and epidemiologic evidence suggests that folate may play a role in the development of some cancers. Case-control studies and one prospective cohort study on folate intake in relation to stomach cancer risk have yielded inconsistent results. Methods: We prospectively investigated the relation between folate intake and the incidence of stomach cancer among 61,433 women in the Swedish Mammography Cohort. Participants completed a food frequency questionnaire at baseline (1987-1990) and again in 1997. During follow-up through December 2004, 156 incident stomach cancer cases were diagnosed. Cox proportional hazards models were used to calculate multivariate-adjusted hazard ratios. Results: There was no association between dietary folate intake (i.e., folate from food sources) and the risk of stomach cancer. The multivariate hazard ratio for the highest compared with the lowest category of updated average dietary folate intake was 1.04 (95% confidence interval, 0.61-1.86; P-trend = 0.91). The relation between dietary folate intake and stomach cancer did not vary significantly by intake of alcohol, methionine, or caffeine. Conclusion: Results from this prospective study do not support an association between dietary folate intake and risk of stomach cancer.

  • 50.
    Larsson, Susanna C.
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Medical epidemiology. Unit of Cardiovascular and Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Höijer, Jonas
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Medical epidemiology.
    Sun, Jing
    Li, Xue
    Burgess, Stephen
    Michaëlsson, Karl
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Medical epidemiology.
    Genome-Wide Association and Two-Sample Mendelian Randomization Analyses of Plasma Ghrelin and Gastrointestinal Cancer Risk2023In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 32, no 12, p. 1771-1776Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Observational studies have suggested that the gut hormone ghrelin is an early marker of future risk of developing gastrointestinal cancer. However, whether ghrelin is a causal risk factor remains unclear. We conducted a genome-wide association study (GWAS) of plasma ghrelin and used Mendelian randomization (MR) to investigate the possible causal association between ghrelin and gastrointestinal cancer risk.

    METHODS: Genetic variants associated with plasma ghrelin were identified in a GWAS comprising 10 742 Swedish adults in the discovery (N=6259) and replication (N=4483) cohorts. The association between ghrelin and gastrointestinal cancer was examined through a two-sample MR analysis using the identified genetic variants as instruments and GWAS data from the UK Biobank, FinnGen, and a colorectal cancer consortium.

    RESULTS: GWAS found associations between multiple genetic variants within ±200 kb of the GHRL gene and plasma ghrelin. A two-sample MR analysis revealed that genetically predicted higher plasma ghrelin levels were associated with a lower risk of gastrointestinal cancer in UK Biobank and in a meta-analysis of the two studies. The combined odds ratio per approximate doubling of genetically predicted plasma ghrelin was 0.91 (95% confidence interval, 0.85-0.99; P=0.02). Colocalization analysis revealed limited evidence of shared causal variants for plasma ghrelin and gastrointestinal cancer at the GHRL locus (posterior probability H4=24.5%); however, this analysis was likely underpowered.

    CONCLUSIONS: Our study provides evidence in support of a possible causal association between higher plasma ghrelin levels and a reduced risk of gastrointestinal cancer.

    IMPACT: Elevated plasma ghrelin levels might reduce the risk of gastrointestinal cancer.

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