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  • 1. Allen, Naomi E
    et al.
    Travis, Ruth C
    Appleby, Paul N
    Albanes, Demetrius
    Barnett, Matt J
    Black, Amanda
    Bueno-de-Mesquita, H Bas
    Deschasaux, Mélanie
    Galan, Pilar
    Goodman, Gary E
    Goodman, Phyllis J
    Gunter, Marc J
    Heliövaara, Markku
    Helzlsouer, Kathy J
    Henderson, Brian E
    Hercberg, Serge
    Knekt, Paul
    Kolonel, Laurence N
    Lasheras, Christina
    Linseisen, Jakob
    Metter, E Jeffrey
    Neuhouser, Marian L
    Olsen, Anja
    Pala, Valeria
    Platz, Elizabeth A
    Rissanen, Harri
    Reid, Mary E
    Schenk, Jeannette M
    Stampfer, Meir J
    Stattin, Pär
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Urology.
    Tangen, Catherine M
    Touvier, Mathilde
    Trichopoulou, Antonia
    van den Brandt, Piet A
    Key, Timothy J
    Selenium and Prostate Cancer: Analysis of Individual Participant Data From Fifteen Prospective Studies.2016In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 108, no 11Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Some observational studies suggest that a higher selenium status is associated with a lower risk of prostate cancer but have been generally too small to provide precise estimates of associations, particularly by disease stage and grade.

    METHODS: Collaborating investigators from 15 prospective studies provided individual-participant records (from predominantly men of white European ancestry) on blood or toenail selenium concentrations and prostate cancer risk. Odds ratios of prostate cancer by selenium concentration were estimated using multivariable-adjusted conditional logistic regression. All statistical tests were two-sided.

    RESULTS: Blood selenium was not associated with the risk of total prostate cancer (multivariable-adjusted odds ratio [OR] per 80 percentile increase = 1.01, 95% confidence interval [CI] = 0.83 to 1.23, based on 4527 case patients and 6021 control subjects). However, there was heterogeneity by disease aggressiveness (ie, advanced stage and/or prostate cancer death, Pheterogeneity = .01), with high blood selenium associated with a lower risk of aggressive disease (OR = 0.43, 95% CI = 0.21 to 0.87) but not with nonaggressive disease. Nail selenium was inversely associated with total prostate cancer (OR = 0.29, 95% CI = 0.22 to 0.40, Ptrend < .001, based on 1970 case patients and 2086 control subjects), including both nonaggressive (OR = 0.33, 95% CI = 0.22 to 0.50) and aggressive disease (OR = 0.18, 95% CI = 0.11 to 0.31, Pheterogeneity = .08).

    CONCLUSIONS: Nail, but not blood, selenium concentration is inversely associated with risk of total prostate cancer, possibly because nails are a more reliable marker of long-term selenium exposure. Both blood and nail selenium concentrations are associated with a reduced risk of aggressive disease, which warrants further investigation.

  • 2.
    Bill-Axelson, Anna
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Urology.
    Holmberg, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Endocrine Surgery.
    Filén, Frej
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Urology.
    Ruutu, Mirja
    Garmo, Hans
    Busch, Christer
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology.
    Nordling, Stig
    Häggman, Michael
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Urology.
    Andersson, Swen-Olof
    Bratell, Stefan
    Spångberg, Anders
    Palmgren, Juni
    Adami, Hans-Olov
    Johansson, Jan-Erik
    Lindeborg, T.
    Einarsson, G.
    Ekman, P.
    Wijkström, H.
    Karlberg, L.
    Hagberg, G.
    Busch, Christer
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology.
    de la Torre, Manuel
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology.
    Hamberg, Hans
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology.
    Lindgren, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology.
    Mavadati, E.
    Gobén, B.
    Pettersson, I.
    Damber, J.E.
    Lindgren, A.
    Varenhorst, E.
    Norlén, B.J.
    Radical prostatectomy versus watchful waiting in localized prostate cancer: the Scandinavian prostate cancer group-4 randomized trial2008In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 100, no 16, p. 1144-54Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The benefit of radical prostatectomy in patients with early prostate cancer has been assessed in only one randomized trial. In 2005, we reported that radical prostatectomy improved prostate cancer survival compared with watchful waiting after a median of 8.2 years of follow-up. We now report results after 3 more years of follow-up. METHODS: From October 1, 1989, through February 28, 1999, 695 men with clinically localized prostate cancer were randomly assigned to radical prostatectomy (n = 347) or watchful waiting (n = 348). Follow-up was complete through December 31, 2006, with histopathologic review and blinded evaluation of causes of death. Relative risks (RRs) were estimated using the Cox proportional hazards model. Statistical tests were two-sided. RESULTS: During a median of 10.8 years of follow-up (range = 3 weeks to 17.2 years), 137 men in the surgery group and 156 in the watchful waiting group died (P = .09). For 47 of the 347 men (13.5%) who were randomly assigned to surgery and 68 of the 348 men (19.5%) who were not, death was due to prostate cancer. The difference in cumulative incidence of death due to prostate cancer remained stable after about 10 years of follow-up. At 12 years, 12.5% of the surgery group and 17.9% of the watchful waiting group had died of prostate cancer (difference = 5.4%, 95% confidence interval [CI] = 0.2 to 11.1%), for a relative risk of 0.65 (95% CI = 0.45 to 0.94; P = .03). The difference in cumulative incidence of distant metastases did not increase beyond 10 years of follow-up. At 12 years, 19.3% of men in the surgery group and 26% of men in the watchful waiting group had been diagnosed with distant metastases (difference = 6.7%, 95% CI = 0.2 to 13.2%), for a relative risk of 0.65 (95% CI = 0.47 to 0.88; P = .006). Among men who underwent radical prostatectomy, those with extracapsular tumor growth had 14 times the risk of prostate cancer death as those without it (RR = 14.2, 95% CI = 3.3 to 61.8; P < .001). CONCLUSION: Radical prostatectomy reduces prostate cancer mortality and risk of metastases with little or no further increase in benefit 10 or more years after surgery.

  • 3.
    Bratt, Ola
    et al.
    Lund Univ, Div Urol Canc, Dept Translat Med Urol, Lund, Sweden.;Cambridge Univ Hosp, CamPARI Clin, Dept Urol, Cambridge, England..
    Drevin, Linda
    Univ Uppsala Hosp, Reg Canc Ctr, Uppsala, Sweden..
    Akre, Olof
    Karolinska Inst, Dept Urol, Stockholm, Sweden..
    Garmo, Hans
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Stattin, Pär
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Urology. Umea Univ, Dept Surg & Perioperat Sci Urol & Androl, Umea, Sweden..
    Family History and Probability of Prostate Cancer, Differentiated by Risk Category: A Nationwide Population-Based Study2016In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 108, no 10, article id djw110Article in journal (Refereed)
    Abstract [en]

    Background: Familial prostate cancer risk estimates are inflated by clinically insignificant low-risk cancer, diagnosed after prostate-specific antigen testing. We provide age-specific probabilities of non-low-and high-risk prostate cancer. Methods: Fifty-one thousand, eight hundred ninety-seven brothers of 32 807 men with prostate cancer were identified in Prostate Cancer data Base Sweden (PCBaSe). Nelson-Aalen estimates with 95% confidence intervals (CIs) were calculated for cumulative, family history-stratified probabilities of any, non-low-(any of Gleason score >= 7, prostate-specific antigen [PSA] >= 10 ng/mL, T3-4, N1, and/or M1) and high-risk prostate cancer (Gleason score >= 8 and/or T3-4 and/or PSA >= 20 ng/mL and/or N1 and/or M1). Results: The population probability of any prostate cancer was 4.8% (95% CI = 4.8% to 4.9%) at age 65 years and 12.9% (95% CI = 12.8% to 12.9%) at age 75 years, of non-low-risk prostate cancer 2.8% (95% CI = 2.7% to 2.8%) at age 65 years and 8.9% (95% CI = 8.8% to 8.9%) at age 75 years, and of high-risk prostate cancer 1.4% (95% CI = 1.3% to 1.4%) at age 65 years and 5.2% (95% CI = 5.1% to 5.2%) at age 75 years. For men with one affected brother, probabilities of any prostate cancer were 14.9% (95% CI = 14.1% to 15.8%) at age 65 years and 30.3% (95% CI = 29.3% to 31.3%) at age 75 years, of non-low-risk prostate cancer 7.3% (95% CI = 6.7% to 7.9%) at age 65 years and 18.8% (95% CI = 17.9% to 19.6%) at age 75 years, and of high-risk prostate cancer 3.0% (95% CI = 2.6% to 3.4%) at age 65 years and 8.9% (95% CI = 8.2% to 9.5%) at age 75 years. Probabilities were higher for men with a stronger family history. For example, men with two affected brothers had a 13.6% (95% CI = 9.9% to 17.6 %) probability of high-risk cancer at age 75 years. Conclusions: The age-specific probabilities of non-low-and high-risk cancer presented here are more informative than relative risks of any prostate cancer and more suitable to use for counseling men with a family history of prostate cancer.

  • 4. Bratt, Ola
    et al.
    Garmo, Hans
    Adolfsson, Jan
    Bill-Axelson, Anna
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Urology.
    Holmberg, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Endocrine Surgery.
    Lambe, Mats
    Stattin, Pär
    Effects of Prostate-Specific Antigen Testing on Familial Prostate Cancer Risk Estimates2010In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 102, no 17, p. 1336-1343Article in journal (Refereed)
    Abstract [en]

    Background Family history is a strong risk factor for prostate cancer. The aim of this study was to investigate whether increased diagnostic activity is related to the incidence of prostate cancer among brothers of men with prostate cancer. Methods Data were from the nationwide population-based Prostate Cancer Database Sweden (PCBaSe Sweden), which includes data from the National Prostate Cancer Register, the Swedish Cancer Register, the Register of the Total Population, the Multi-Generation Register, and the Census database. We investigated the relationship of tumor characteristics, time from diagnosis of the index patient (ie, prostate cancer patients in the National Prostate Cancer Register for whom at least one brother and their father could be identified), calendar period, geographic factors, and socioeconomic status to standardized incidence ratios (SIRs) for prostate cancer among 22 511 brothers of 13 975 index patients in PCBaSe Sweden. Results Brothers of index patients with prostate cancer were at increased risk for a diagnosis of prostate cancer (SIR = 3.1, 95% confidence interval [CI] = 2.9 to 3.3). Risk was higher for T1c tumors (SIR = 3.4, 95% CI = 3.2 to 3.8) than for metastatic tumors (SIR = 2.0, 95% CI = 1.5 to 2.6), and risk of T1c tumors was especially high during the first year after the diagnosis of the index patient (SIR = 4.3, 95% CI = 3.8 to 4.9), compared with the following years (SIR range = 2.8-3.3), and for brothers of index patients who had a higher socioeconomic status (SIR = 4.2, 95% CI = 3.7 to 4.7), compared with brothers of index patients with lower socioeconomic status (SIR = 2.8, 95% CI = 2.4 to 3.2). Conclusions Increased diagnostic activity among men with a family history of prostate cancer appears to contribute to their increased risk of prostate cancer and to lead to detection bias in epidemiological and genetic studies of familial prostate cancer.

  • 5. Chang, Ellen T.
    et al.
    Ekström Smedby, Karin
    Hjalgrim, Henrik
    Porwit-MacDonald, Anna
    Roos, Göran
    Glimelius, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology.
    Adami, Hans-Olov
    Family history of hematopoietic malignancy and risk of lymphoma2005In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 97, no 19, p. 1466-1474Article in journal (Other academic)
    Abstract [en]

    BACKGROUND: A family history of hematopoietic malignancy is associated with an increased risk of non-Hodgkin lymphoma (NHL) and Hodgkin lymphoma (HL), although the magnitude of the relative risk is unclear. We estimated the association between familial hematopoietic cancer and risk of lymphoma using validated, registry-based family data, and we also investigated whether associations between some environmental exposures and risk of lymphoma vary between individuals with and without such a family history. METHODS: In a population-based case-control study of malignant lymphoma, 1506 case patients and 1229 control subjects were linked to the Swedish Multi-Generation Register and then to the Swedish Cancer Register to ascertain history of cancer in first-degree relatives of patients with malignant lymphoma. Multiple logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for associations with the risk of lymphoma. RESULTS: A history of hematopoietic malignancy in any first-degree relative was associated with an increased risk of all NHL (OR = 1.8, 95% CI = 1.2 to 2.5), common B-cell NHL subtypes, and HL. Relative risks were generally stronger in association with sibling hematopoietic cancer (OR for all NHL = 3.2, 95% CI = 1.3 to 7.6) than with parental hematopoietic cancer (OR = 1.6, 95% CI = 1.1 to 2.3). A family history of NHL or chronic lymphocytic leukemia (CLL) was associated with an increased risk of several NHL subtypes and HL, whereas familial multiple myeloma was associated with a higher risk of follicular lymphoma. There was no statistically significant heterogeneity in NHL risk associations with environmental factors between individuals with and without familial hematopoietic malignancy. CONCLUSIONS: The increased risk of NHL and HL among individuals with a family history of hematopoietic malignancy was approximately twofold for both lymphoma types. There was no evidence that etiologic associations varied between familial NHL and nonfamilial NHL.

  • 6. Chang, Ellen T.
    et al.
    Hjalgrim, Henrik
    Ekström Smedby, Karin
    Åkerman, Måns
    Tani, Edneia
    Johnsen, Hans E.
    Glimelius, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology.
    Adami, Hans-Olov
    Melbye, Mads
    Body mass index and risk of malignant lymphoma in Scandinavian men and women2005In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 97, no 3, p. 210-218Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The incidence of non-Hodgkin lymphoma and prevalence of obesity are increasing globally. A suggested positive association between obesity and risk of non-Hodgkin lymphoma has prompted us to investigate the relationship between body mass index (BMI) and risk of malignant lymphoma subtypes in a population-based case-control study. METHODS: Telephone interviews were conducted with 3055 case patients with non-Hodgkin lymphoma and 618 case patients with Hodgkin lymphoma diagnosed between October 1, 1999, and August 30, 2002, and 3187 population-based control subjects. The interviews assessed current height, normal adult weight, and other possible risk factors. Multivariable odds ratios (ORs) and corresponding 95% confidence intervals (CIs) for risk of lymphoma were estimated by unconditional logistic regression. All statistical tests were two-sided. RESULTS: BMI was not associated with risk of overall non-Hodgkin lymphoma or of Hodgkin lymphoma (for example, comparing the highly obese group [BMI > or =35.0 kg/m2] with the normal-weight group [BMI = 18.5-24.9 kg/m2], OR for risk of non-Hodgkin lymphoma = 0.9, 95% CI = 0.6 to 1.3; P(trend) across all categories of BMI = .27). BMI was also not associated with risk of any non-Hodgkin lymphoma subtype evaluated, although there was some evidence of a positive association with risk of diffuse large B-cell lymphoma (for example, comparing the highly obese group with the normal-weight group, OR for diffuse large B-cell lymphoma = 1.5, 95% CI = 0.9 to 2.4; P(trend) =.05). CONCLUSIONS: Excess weight does not appear to be associated with an increased risk of malignant lymphoma in general, or with a risk of most major lymphoma subtypes. Hence, the growing incidence of obesity is unlikely to be an important contributor to the increasing incidence of non-Hodgkin lymphoma worldwide.

  • 7. Chang, Ellen T.
    et al.
    Smedby, Karin Ekström
    Hjalgrim, Henrik
    Glimelius, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology.
    Adami, Hans-Olov
    Reliability of self-reported family history of cancer in a large case-control study of lymphoma2006In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 98, no 1, p. 61-68Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Case-control studies of familial cancer risk traditionally rely on self-reported family history of cancer, which may bias results due to differential recall between case patients and control subjects. To evaluate the reliability of self-reported data, we analyzed questionnaire and registry-based data on familial cancer from a population-based case-control study of malignant lymphoma. METHODS: All 1508 lymphoma case patients and 1229 control subjects completed a telephone interview assessing cancer in family members. Participants were linked to the Swedish Multi-Generation Register and Cancer Register to identify confirmed cancer diagnoses in first-degree relatives. The sensitivity and specificity of self-reported familial cancer were calculated among case patients and control subjects and were compared using logistic regression. All statistical tests were two-sided. RESULTS: Lymphoma case patients reported a family history of any cancer with statistically significantly higher sensitivity than control subjects (0.85, 95% confidence interval [CI] = 0.83 to 0.87 and 0.80, 95% CI = 0.77 to 0.82, respectively) but with marginally lower specificity (0.89, 95% CI = 0.87 to 0.91 and 0.92, 95% CI = 0.90 to 0.94, respectively). The sensitivity of self-reporting familial cancers by site ranged from less than 0.20 for rare malignancies to nearly 0.75 for more common types, whereas specificity was generally 0.98 or greater. For most sites, the reliability of self-report was similar in patients and control subjects. However, patients reported familial hematopoietic cancer with statistically significantly higher sensitivity (0.60, 95% CI = 0.57 to 0.62) than control subjects (0.38, 95% CI = 0.35 to 0.40). Odds ratios for the association between familial cancer and risk of non-Hodgkin lymphoma were consistently higher when based on self-reported, compared with registry data-based, family history of any cancer or of hematopoietic cancer. CONCLUSIONS: Reliability of self-reported family history of cancer varies between case patients and control subjects. Recall bias may thus produce biased results in case-control studies of familial cancer risk.

  • 8.
    Chen, Dan
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Genomics.
    Juko-Pecirep, Ivana
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Genomics.
    Hammer, Joanna
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Genomics.
    Ivansson, Emma
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Biochemistry and Microbiology. Uppsala University, Science for Life Laboratory, SciLifeLab.
    Enroth, Stefan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Genomics.
    Gustavsson, Inger
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Genomics.
    Feuk, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Genomics.
    Magnusson, Patrik K. E.
    McKay, James D.
    Wilander, Erik
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology.
    Gyllensten, Ulf
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Genomics.
    Genome-wide Association Study of Susceptibility Loci for Cervical Cancer2013In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 105, no 9, p. 624-633Article in journal (Refereed)
    Abstract [en]

    Background Cervical carcinoma has a heritable genetic component, but the genetic basis of cervical cancer is still not well understood. Methods We performed a genome-wide association study of 731 422 single nucleotide polymorphisms (SNPs) in 1075 cervical cancer case subjects and 4014 control subjects and replicated it in 1140 case subjects and 1058 control subjects. The association between top SNPs and cervical cancer was estimated by odds ratios (ORs) and 95% confidence intervals (CIs) with unconditional logistic regression. All statistical tests were two-sided. Results Three independent loci in the major histocompatibility complex (MHC) region at 6p21.3 were associated with cervical cancer: the first is adjacent to the MHC class I polypeptide-related sequence A gene (MICA) (rs2516448; OR = 1.42, 95% CI = 1.31 to 1.54; P = 1.6 x 10(-18)); the second is between HLA-DRB1 and HLA-DQA1 (rs9272143; OR = 0.67, 95% CI = 0.62 to 0.72; P = 9.3 x 10(-24)); and the third is at HLA-DPB2 (rs3117027; OR=1.25, 95% CI = 1.15 to 1.35; P = 4.9 x 10(-8)). We also confirmed previously reported associations of B*0702 and DRB1*1501-DQB1*0602 with susceptibility to and DRB1*1301-DQA1*0103-DQB1*0603 with protection against cervical cancer. The three new loci are statistically independent of these specific human leukocyte antigen alleles/haplotypes. MICA encodes a membrane-bound protein that acts as a ligand for NKG2D to activate antitumor effects. The risk allele of rs2516448 is in perfect linkage disequilibrium with a frameshift mutation (A5.1) of MICA, which results in a truncated protein. Functional analysis shows that women carrying this mutation have lower levels of membrane-bound MICA. Conclusions Three novel loci in the MHC may affect susceptibility to cervical cancer in situ, including the MICA-A5.1 allele that may cause impaired immune activation and increased risk of tumor development.

  • 9.
    Cnattingius, Sven
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences.
    Zack, M.M.
    Ekbom, A.
    Gunnarskog, J.
    Kreuger, A.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health.
    Linet, M.
    Adami, Hans-Olov
    Prenatal and neonatal risk factors for childhood lymphatic leukemia1995In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 87, no 12, p. 908-914Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Because the incidence of childhood acute lymphatic leukemia peaks between 2 and 4 years of age, the risk factors may exert their influence during the prenatal and/or the neonatal periods. Results of previous studies of perinatal risk factors have been contradictory, perhaps because most studies either have been hospital based or have been restricted to limited geographical areas. PURPOSE: A nationwide case-control study was carried out to identify maternal and perinatal risk factors for this disease. METHODS: The case-control study was nested in cohorts defined by all live births in Sweden recorded in the nationwide Medical Birth Register. Since 1973, this register has routinely collected information on all hospital births in regard to maternal demographic data, reproductive history, pregnancy, delivery, and the neonatal period. From the Swedish National Cancer Register, 613 case subjects were identified in successive birth cohorts from 1973 through 1989. Five control subjects per case subject were randomly selected from the pool of children matched by sex and month and year of birth. Conditional logistic regression was used to calculate the odds ratios (ORs) and 95% confidence intervals (CIs) for potential risk factors and to estimate their effects after adjustment for possible confounders. RESULTS: Risk of childhood lymphatic leukemia at all ages increased with Down's syndrome (OR = 20.0; 95% CI = 4.2-94.2), maternal renal disease (OR = 4.4; 95% CI = 1.6-12.1), use of supplementary oxygen (OR = 2.3; 95% CI = 1.5-3.6), postpartum asphyxia (OR = 1.8; 95% CI = 1.2-2.6), birth weight of more than 4500 g (OR = 1.7; 95% CI = 1.1-2.7), and hypertensive disease during pregnancy (OR = 1.4; 95% CI = 1.0-1.9). Down's syndrome affected risk mostly in children younger than 5 years, whereas other factors affected those children 5 years old or older. Being one of a multiple birth also increased risk among older children (OR = 2.5; 95% CI = 1.0-6.0). Use of supplementary oxygen may act as a causal intermediate (surrogate) for postpartum asphyxia and its causes, as would high birth weight for its causes. CONCLUSIONS: Several maternal and perinatal risk factors were found to be associated with childhood lymphatic leukemia, but they showed age-specific differences. Overall, only a few risk factors were identified, and these accounted for a small proportion of cases. We concluded that most risk factors for childhood lymphatic leukemia remain unidentified in very young children.

  • 10. Ek, Weronica E
    et al.
    Levine, David M
    D'Amato, Mauro
    Pedersen, Nancy L
    Magnusson, Patrik K E
    Bresso, Francesca
    Onstad, Lynn E
    Schmidt, Peter T
    Törnblom, Hans
    Nordenstedt, Helena
    Romero, Yvonne
    Chow, Wong-Ho
    Murray, Liam J
    Gammon, Marilie D
    Liu, Geoffrey
    Bernstein, Leslie
    Casson, Alan G
    Risch, Harvey A
    Shaheen, Nicholas J
    Bird, Nigel C
    Reid, Brian J
    Corley, Douglas A
    Hardie, Laura J
    Ye, Weimin
    Wu, Anna H
    Zucchelli, Marco
    Spector, Tim D
    Hysi, Pirro
    Vaughan, Thomas L
    Whiteman, David C
    MacGregor, Stuart
    Germline genetic contributions to risk for esophageal adenocarcinoma, Barrett's esophagus, and gastroesophageal reflux2013In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 105, no 22, p. 1711-8Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Esophageal adenocarcinoma (EA) is an increasingly common cancer with poor survival. Barrett's esophagus (BE) is the main precursor to EA, and every year 0.12% to 0.5% of BE patients progress to EA. BE typically arises on a background of chronic gastroesophageal reflux (GERD), one of the risk factors for EA.

    METHODS: We used genome-wide association data to investigate the genetic architecture underlying GERD, BE, and EA. We applied a method to estimate the variance explained (array heritability, h(2)g) and the genetic correlation (rg) between GERD, BE, and EA by considering all single nucleotide polymorphisms (SNPs) simultaneously. We also estimated the polygenic overlap between GERD, BE, and EA using a prediction approach. All tests were two-sided, except in the case of variance-explained estimation where one-sided tests were used.

    RESULTS: We estimated a statistically significant genetic variance explained for BE (h(2)g = 35%; standard error [SE] = 6%; one-sided P = 1 × 10(-9)) and for EA (h(2)g = 25 %; SE = 5%; one-sided P = 2 × 10(-7)). The genetic correlation between BE and EA was found to be high (rg = 1.0; SE = 0.37). We also estimated a statistically significant polygenic overlap between BE and EA (one-sided P = 1 × 10(-6)), which suggests, together with the high genetic correlation, that shared genes underlie the development of BE and EA. Conversely, no statistically significant results were obtained for GERD.

    CONCLUSIONS: We have demonstrated that risk to BE and EA is influenced by many germline genetic variants of small effect and that shared polygenic effects contribute to risk of these two diseases.

  • 11. Fall, Katja
    et al.
    Garmo, Hans
    Regional Oncological Center, Uppsala University.
    Andrén, Ove
    Bill-Axelson, Anna
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Urology.
    Adolfsson, Jan
    Adami, Hans-Olov
    Johansson, Jan-Erik
    Holmberg, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Endocrine Surgery.
    Prostate-specific antigen levels as a predictor of lethal prostate cancer2007In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 99, no 7, p. 526-532Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Rates of long-term survival among patients with untreated localized prostate cancer are high. To avoid unnecessary treatment, tools are needed to identify the small proportion of patients who are destined to develop lethal prostate cancer. METHODS: To evaluate the accuracy of early changes in prostate-specific antigen (PSA) levels as predictors of prostate cancer outcome, we assessed serial measurements of PSA level among 267 men with localized prostate cancer in a Scandinavian cohort of men who were diagnosed between 1989 and 1999 and who were managed by watchful waiting. We then 1) fitted individual regression lines to the PSA values assessed for each patient during the first 2 years of follow-up by using three different models, 2) evaluated early PSA curve characteristics as determinants of the cumulative incidence of lethal prostate cancer and calculated hazard ratios for baseline PSA value and rate of change in PSA level to prostate cancer outcome, and 3) plotted time-dependent receiver operating characteristic (ROC) curves. All P values are two-sided. RESULTS: During complete follow-up for a mean of 8.5 years, 34 patients (13%) died from prostate cancer, and 18 (7%) developed metastases but were still alive at end of follow-up. In a log-linear model, both PSA value at baseline (P = .05) and the rate of PSA change (P<.001) were associated with the development of lethal prostate cancer. In the ROC analysis, however, the accuracy of classifying the disease as either indolent or destined to progress was low, regardless of the cut point chosen for initial PSA level or rate of change in PSA level. CONCLUSIONS: Although baseline PSA value and rate of PSA change are prognostic factors for lethal prostate cancer, they are poor predictors of lethal prostate cancer among patients with localized prostate cancer who are managed by watchful waiting.

  • 12. Frisch, Morten
    et al.
    Glimelius, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology.
    Wohlfahrt, J
    Adami, Hans-Olov
    Melbye, Mads
    Tobacco smoking as a risk factor in anal carcinoma: an antiestrogenic mechanism?1999In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 91, no 8, p. 708-715Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Human papillomavirus-associated anogenital carcinogenesis depends on poorly defined cofactors. Smoking was recently suggested to increase the risk of anal cancer more in premenopausal women than in postmenopausal women. Thus, we used our population-based anal cancer case-control study in Denmark and Sweden to test this hypothesis. METHODS: Our study included 417 patients (324 women and 93 men) who were diagnosed with anal cancer (84% invasive cancer) from 1991 through 1994; it also included five patients diagnosed in 1995. Two control groups were used: 1) 554 population control subjects (349 women and 205 men) and 2) 534 patients with rectal adenocarcinoma (343 women and 191 men). Odds ratios (ORs), calculated from logistic regression analyses, were used as measures of relative risk. All P values are two-sided. RESULTS: Compared with the risk for lifelong nonsmokers, the risk of anal cancer was high among premenopausal women who currently smoked tobacco (multivariate OR = 5.6; 95% confidence interval [CI] = 2.4-12.7) and increased linearly by 6.7% per pack-year smoked (one pack-year is equivalent to one pack of cigarettes smoked per day for 1 year) (P for trend <.001). Smoking was not statistically significantly associated with anal cancer risk in postmenopausal women or men. Women whose menstrual periods started late were at high risk (multivariate OR = 3.6; 95% CI = 1.8-7.3, for > or = 17 years of age versus < or = 12 years of age; P for trend <.001), and body mass index (weight in kg/[height in m]2) was inversely associated with risk among women (P<.001). CONCLUSIONS: Because the risk of anal cancer associated with smoking was restricted to premenopausal women and because higher risk was associated with late menarche and lean body composition, female sex hormones may be a factor in anal cancer development in women. Since the anal mucosa is an estrogen-sensitive area, we hypothesize an antiestrogenic mechanism of action for smoking in anal carcinogenesis.

  • 13. Greenhalf, William
    et al.
    Ghaneh, Paula
    Neoptolemos, John P.
    Palmer, Daniel H.
    Cox, Trevor F.
    Lamb, Richard F.
    Garner, Elizabeth
    Campbell, Fiona
    Mackey, John R.
    Costello, Eithne
    Moore, Malcolm J.
    Valle, Juan W.
    McDonald, Alexander C.
    Carter, Ross
    Tebbutt, Niall C.
    Goldstein, David
    Shannon, Jennifer
    Dervenis, Christos
    Glimelius, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Radiology, Oncology and Radiation Science, Oncology.
    Deakin, Mark
    Charnley, Richard M.
    Lacaine, Francois
    Scarfe, Andrew G.
    Middleton, Mark R.
    Anthoney, Alan
    Halloran, Christopher M.
    Mayerle, Julia
    Olah, Attila
    Jackson, Richard
    Rawcliffe, Charlotte L.
    Scarpa, Aldo
    Bassi, Claudio
    Buechler, Markus W.
    Pancreatic Cancer hENT1 Expression and Survival From Gemcitabine in Patients From the ESPAC-3 Trial2014In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 106, no 1, p. djt347-Article in journal (Refereed)
    Abstract [en]

    Background Human equilibrative nucleoside transporter 1 (hENT1) levels in pancreatic adenocarcinoma may predict survival in patients who receive adjuvant gemcitabine after resection. Methods Microarrays from 434 patients randomized to chemotherapy in the ESPAC-3 trial (plus controls from ESPAC-1/3) were stained with the 10D7G2 anti-hENT1 antibody. Patients were classified as having high hENT1 expression if the mean H score for their cores was above the overall median H score (48). High and low hENT1-expressing groups were compared using Kaplan-Meier curves, log-rank tests, and Cox proportional hazards models. All statistical tests were two-sided. Results Three hundred eighty patients (87.6%) and 1808 cores were suitable and included in the final analysis. Median overall survival for gemcitabine-treated patients (n = 176) was 23.4 (95% confidence interval [CI] = 18.3 to 26.0) months vs 23.5 (95% CI = 19.8 to 27.3) months for 176 patients treated with 5-fluorouracil/folinic acid (months vs 23.5 (95% CI = 19.8 to 27.3) months for 176 patients treated with 5-fluorouracil/folinic acid (chi(2)(1)=0.24; P = .62). Median survival for patients treated with gemcitabine was 17.1 (95% CI = 14.3 to 23.8) months for those with low hENT1 expression vs 26.2 (95% CI = 21.2 to 31.4) months for those with high hENT1 expression (chi(2)(1)=9.87; P = .002). For the 5-fluorouracil group, median survival was 25.6 (95% CI = 20.1 to 27.9) and 21.9 (95% CI = 16.0 to 28.3) months for those with low and high hENT1 expression, respectively (chi(2)(1) = 0.83; P = .36). hENT1 levels were not predictive of survival for the 28 patients of the observation group (chi(2)(1) = 0.37; P = .54). Multivariable analysis confirmed hENT1 expression as a predictive marker in gemcitabine-treated (Wald chi(2)(1) = 9.16; P = .003) but not 5-fluorouracil-treated (Wald chi(2)(1) = 1.22; P = .27) patients. Conclusions Subject to prospective validation, gemcitabine should not be used for patients with low tumor hENT1 expression.

  • 14. Helgesen, Fred
    et al.
    Holmberg, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences.
    Johansson, Jan-Erik
    Bergström, Reinhold
    Uppsala University, Disciplinary Domain of Humanities and Social Sciences, Faculty of Social Sciences, Department of Information Science.
    Adami, Hans-Olov
    Trends in prostate cancer survival in Sweden, 1960 through 1988: Evidence of increasing diagnosis of nonlethal tumors1996In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 88, no 17, p. 1216-1221Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The incidence of prostate cancer has increased during the past 30 years but has been paralleled by increases in survival rates from this disease, despite the absence of documented major improvement in curative treatment. Since a high prevalence of microscopic prostate cancer has been observed in autopsied men and because many prostate cancers may never surface clinically, increased diagnostic activities might have led to increased detection of less aggressive tumors. PURPOSE: This study was conducted to elucidate whether the trends in prostate cancer incidence and patient survival may be due to increasing diagnoses of nonlethal tumors. METHODS: We analyzed a population-based cohort comprising all cases of prostate cancer (n = 80,901) detected in Sweden during the period of 1960 through 1988. Five hundred eighteen patients (0.64% of the total number) who could not be followed because of emigration or an incomplete national registration number were excluded. Observed and relative survival rates were calculated for the entire cohort of 80,383 assessable patients per 5-year age group in 5-year periods of diagnosis and according to diagnostic method and were compared between geographic areas with differences in incidence rates. To estimate the independent effects of these determinants, multivariate analyses were performed. RESULTS: For the 80,383 patients with complete follow-up, the 10- and 20-year observed survival rates were 17.5% (95% confidence interval [CI] = 17.2%-17.9%) and 3.5% (95% CI = 3.2%-3.7%), and the relative survival rates were 41.1% (95% CI = 40.3%-41.9%) and 28.6% (95% CI = 26.5%-30.1%), respectively. Relative survival rates improved markedly over time; 10-year relative survival rates increased from 29% (95% CI = 27%-31%) among case patients diagnosed in 1960 through 1964 to 45% (95% CI = 43%-46%) among those diagnosed in 1975 through 1979. Relative survival rates leveled off after about 18 years at 18% (95% CI = 15%-20%) among patients diagnosed in 1960 through 1964 and at 31% (95% CI = 28%-34%) among those diagnosed in 1970 through 1974. An even more favorable outlook was observed in those case patients diagnosed later. In areas with a high or low incidence of prostate cancer, the 10-year relative survival rates were 45% (95% CI = 44%-47%) and 36% (95% CI = 34%-38%), respectively. In the early 1960s, the calculated loss of life expectancy after diagnosis varied from about 68% (95% CI = 61%-75%) of the expected length of life in the youngest age group to about 48% (95% CI = 46%-50%) in the oldest age group. From 1960 through 1964 to 1985 through 1988, the loss of life expectancy decreased by more than 50% in all age groups. The differences in relative survival rates between age groups were small, with a gradual decrease in age groups more than 60-64 years of age. CONCLUSIONS: Most of the great temporal improvement and geographic variation in survival rates are quantitatively consistent, with likely increases in the rate of detection of nonlethal tumors. IMPLICATIONS: The increase in relative survival rates must be taken into consideration when evaluating the outcome of treatment of prostate cancer, since nonrandomized comparisons may be confounded by time trends. Diagnosis of nonlethal tumors raises concerns because the individual would suffer from the psychologic burden of a cancer diagnosis without any therapeutic benefit.

  • 15.
    Holmberg, Lars
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Endocrine Surgery.
    Iversen, Ole-Erik
    Rudenstam, Carl Magnus
    Hammar, Mats
    Kumpulainen, Eero
    Jaskiewicz, Janusz
    Jassem, Jacek
    Dobaczewska, Daria
    Fjosne, Hans E.
    Peralta, Octavio
    Arriagada, Rodrigo
    Holmqvist, Marit
    Maenpa, Johanna
    Increased risk of recurrence after hormone replacement therapy in breast cancer survivors2008In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 100, no 7, p. 475-482Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Hormone replacement therapy (HT) is known to increase the risk of breast cancer in healthy women, but its effect on breast cancer risk in breast cancer survivors is less clear. The randomized HABITS study, which compared HT for menopausal symptoms with best management without hormones among women with previously treated breast cancer, was stopped early due to suspicions of an increased risk of new breast cancer events following HT. We present results after extended follow-up. METHODS: HABITS was a randomized, non-placebo-controlled noninferiority trial that aimed to be at a power of 80% to detect a 36% increase in the hazard ratio (HR) for a new breast cancer event following HT. Cox models were used to estimate relative risks of a breast cancer event, the maximum likelihood method was used to calculate 95% confidence intervals (CIs), and chi(2) tests were used to assess statistical significance, with all P values based on two-sided tests. The absolute risk of a new breast cancer event was estimated with the cumulative incidence function. Most patients who received HT were prescribed continuous combined or sequential estradiol hemihydrate and norethisterone. RESULTS: Of the 447 women randomly assigned, 442 could be followed for a median of 4 years. Thirty-nine of the 221 women in the HT arm and 17 of the 221 women in the control arm experienced a new breast cancer event (HR = 2.4, 95% CI = 1.3 to 4.2). Cumulative incidences at 5 years were 22.2% in the HT arm and 8.0% in the control arm. By the end of follow-up, six women in the HT arm had died of breast cancer and six were alive with distant metastases. In the control arm, five women had died of breast cancer and four had metastatic breast cancer (P = .51, log-rank test). CONCLUSION: After extended follow-up, there was a clinically and statistically significant increased risk of a new breast cancer event in survivors who took HT.

  • 16. Larsson, Susanna C
    et al.
    Giovannucci, Edward L
    Wolk, Alicja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Coffee Consumption and Risk of Gallbladder Cancer in a Prospective Study.2017In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 109, no 3, p. 1-3Article in journal (Refereed)
    Abstract [en]

    Evidence indicates that coffee consumption may reduce the risk of gallstone disease, which is strongly associated with increased risk of gallbladder cancer. The association between coffee consumption and gallbladder cancer incidence was examined in a prospective cohort study of 72 680 Swedish adults (aged 45 - 83 years) who were free of cancer and reported their coffee consumption at baseline. Gallbladder cancers were ascertained by linkage with the Swedish Cancer Register. The data were analyzed using Cox proportional hazards regression models. Statistical tests were two-sided. During 967 377 person-years of follow-up, 74 gallbladder cancer case patients were identified. Compared with consumption of one or less cups of coffee per day, the multivariable hazard ratios were 0.76 (95% confidence interval [CI] = 0.41 to 1.41) for two cups per day, 0.50 (95% CI = 0.24 to 1.06) for three cups per day, and 0.41 (95% CI = 0.20 to 0.83) for four or more cups per day. In conclusion, coffee consumption is associated with a reduced risk of gallbladder cancer.

  • 17. Li, Jing
    et al.
    Karlsson, Mats O.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences.
    Brahmer, Julie
    Spitz, Avery
    Zhao, Ming
    Hidalgo, Manuel
    Baker, Sharyn D.
    CYP3A phenotyping approach to predict systemic exposure to EGFR tyrosine kinase inhibitors2006In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 98, no 23, p. 1714-1723Article in journal (Refereed)
    Abstract [en]

    Background: Gefitinib is an orally active inhibitor of epidermal growth factor receptor (EGFR) tyrosine kinase (TK) with activity in non-small-cell lung cancer. The response to gefitinib is variable, possibly because of interindividual variation in the activity of cytochrome P450 3A (CYP3A), the principal enzyme that metabolizes gefitinib. We prospectively assessed the influence of CYP3A activity on gefitinib disposition and toxicity. Methods: Twenty-seven patients with advanced cancer were treated with daily oral gefitinib at 250 mg (n = 13) or 500 mg (n = 14) for 28 days. Concentration-time profiles of midazolam and geftinib were constructed based on measurement of their concentration in serial blood samples using high-performance liquid chromatography and mass spectroscopy. CYP3A activity was determined at baseline by assessment of midazolam apparent oral clearance. Pharmacokinetic studies were performed for a period of 28 days, and population modeling was performed using NONMEM software. A structural pharmacokinetic model was developed to describe the concentration-time profiles of unbound and total gefitinib plasma concentrations, and patient-specific covariates were added to the model to account for unexplained interindividual variability in pharmacokinetic parameters. Statistical tests were two-sided. Results: Gefitinib pharmacokinetics exhibited wide interindividual variability (interindividual variability on total and unbound gefitinib apparent oral clearance was 79% and 74%, respectively). Midazolam clearance (mean = 40 L/h, range = 10-111) was highly correlated with that of total and unbound gefitinib (R2 = .60 and R2 = .68, respectively) and with steady-state plasma through concentrations of gefitinib (R2 = .58 and R2 = .60, respectively), and it accounted for approximately 40% of interindividual variability in gefitinib clearance in the pharmacokinetic model. Both total and unbound gefitinib steady-state plasma trough concentrations were associated with the development of diarrhea (P <.05), but not skin rash. At a dose of 250 mg gefitinib, 11 of 13 patients achieved steady-state plasma trough concentrations above the IC 50 for inhibition of mutant EGFR in vitro (0.015 μM), but only one achieved a steady-state plasma trough concentration above the IC 50 for inhibition of wild-type EGFR (0.1 μM). Conclusions: As an in vivo phenotypic probe of CYP3A, midazolam oral clearance may have utility for prediction of gefitinib exposure and dose selection. A pharmacokinetic model incorporating this indicator of CYP3A activity has potential for optimization of treatment with gefitinib and other TK inhibitors that are metabolized in a similar manner.

  • 18.
    Loeb, Stacy
    et al.
    NYU, Dept Urol, New York, NY USA.;NYU, New York, NY USA.;Manhattan VA, New York, NY USA..
    Ventimiglia, Eugenio
    IRCCS Osped San Raffaele, Div Expt Oncol, Unit Urol, URI, Milan, Italy.;Univ Vita Salute San Raffaele, Milan, Italy.;Umea Univ Hosp, Dept Surg & Perioperat Sci Urol & Androl, Umea, Sweden..
    Salonia, Andrea
    IRCCS Osped San Raffaele, Div Expt Oncol, Unit Urol, URI, Milan, Italy.;Univ Vita Salute San Raffaele, Milan, Italy..
    Folkvaljon, Yasin
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences.
    Stattin, Pär
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Urology. Umea Univ Hosp, Dept Surg & Perioperat Sci Urol & Androl, Umea, Sweden..
    Meta-Analysis of the Association Between Phosphodiesterase Inhibitors (PDE5Is) and Risk of Melanoma2017In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 109, no 8, article id djx086Article in journal (Refereed)
    Abstract [en]

    The US Food and Drug Administration recently announced the need to evaluate the association between PDE5is and melanoma. We performed a meta-analysis on the association between PDE5i and melanoma using random effects models and examined whether it met Hill's criteria for causality. A systematic search of Medline, EMBASE, and the Cochrane Library from 1998 to 2016 identified three case-control studies and two cohort studies, including a total of 866 049 men, of whom 41 874 were diagnosed with melanoma. We found a summary estimate indicating an increased risk of melanoma in PDE5i users (relative risk = 1.12, 95% confidence interval = 1.02 to 1.23). However, there was no difference in risk between men with low and high exposure to PDE5i, and risk was higher for in situ melanoma than localized and high-risk melanoma, suggesting a lack of dose response and biological gradient. PDE5i use was also associated with basal cell cancer, suggesting a lack of specificity and likely confounding by ultraviolet exposure. Thus, although this meta-analysis found a statistically significant association between PDE5i and melanoma, it did not satisfy Hill's criteria for causality.

  • 19. Makarov, Danil V.
    et al.
    Loeb, Stacy
    Ulmert, David
    Drevin, Linda
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Lambe, Mats
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Stattin, Par
    Prostate Cancer Imaging Trends After a Nationwide Effort to Discourage Inappropriate Prostate Cancer Imaging2013In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 105, no 17, p. 1306-1313Article in journal (Refereed)
    Abstract [en]

    Background Reducing inappropriate use of imaging to stage incident prostate cancer is a challenging problem highlighted recently as a Physician Quality Reporting System quality measure and by the American Society of Clinical Oncology and the American Urological Association in the Choosing Wisely campaign. Since 2000, the National Prostate Cancer Register (NPCR) of Sweden has led an effort to decrease national rates of inappropriate prostate cancer imaging by disseminating utilization data along with the latest imaging guidelines to urologists in Sweden. We sought to determine the temporal and regional effects of this effort on prostate cancer imaging rates. Methods We performed a retrospective cohort study among men diagnosed with prostate cancer from the NPCR from 1998 to 2009 (n = 99 879). We analyzed imaging use over time stratified by clinical risk category (low, intermediate, high) and geographic region. Generalized linear models with a logit link were used to test for time trend. Results Thirty-six percent of men underwent imaging within 6 months of prostate cancer diagnosis. Overall, imaging use decreased over time, particularly in the low-risk category, among whom the imaging rate decreased from 45% to 3% (P < .001), but also in the high-risk category, among whom the rate decreased from 63% to 47% (P < .001). Despite substantial regional variation, all regions experienced clinically and statistically (P < .001) significant decreases in prostate cancer imaging. Conclusions A Swedish effort to provide data on prostate cancer imaging use and imaging guidelines to clinicians was associated with a reduction in inappropriate imaging over a 10-year period, as well as slightly decreased appropriate imaging in high-risk patients. These results may inform current efforts to promote guideline-concordant imaging in the United States and internationally.

  • 20. Melbye, Mads
    et al.
    Smedby, Karin Ekström
    Lehtinen, Tuula
    Rostgaard, Klaus
    Glimelius, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology.
    Munksgaard, Lars
    Schöllkopf, Claudia
    Sundström, Christer
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology.
    Chang, Ellen T.
    Koskela, Pentti
    Adami, Hans-Olov
    Hjalgrim, Henrik
    Atopy and risk of non-Hodgkin lymphoma2007In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 99, no 2, p. 158-166Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: A possible connection between allergy and cancer has been suspected, but allergy-related conditions or atopy have been inconsistently associated with reduced risks of non-Hodgkin lymphoma. We investigated this association in a population-based case-control study and in a prospective study with prediagnostic blood specimens. METHODS: We carried out a population-based study of 3055 case patients with non-Hodgkin lymphoma and 3187 control subjects in Denmark and Sweden, including questionnaire information on allergy and blood specimens, and a nested case-control study within a prospective cohort of more than 400,000 Finnish women. In the second study, serum specimens from the 198 case patients who developed non-Hodgkin lymphoma within a median of 8.9 years after the blood was drawn were matched with serum specimens from 594 control subjects. In both studies, laboratory-based evidence of allergy (atopy) was determined in serum on the basis of specific IgE reactivity to common inhalant allergens. Dissemination of disease was classified by the Ann Arbor system. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated by logistic regression. RESULTS: In the first study, ever having hay fever, but not other allergic conditions, was associated with a reduced risk of non-Hodgkin lymphoma. In particular, subjects with specific IgE reactivity in serum had a 32% (95% CI = 20% to 42%) lower risk of overall non-Hodgkin lymphoma than those without such reactivity. However, among case patients, dissemination of the disease was strongly inversely associated with specific IgE reactivity. In the second (i.e., prospective) study, no association was found between non-Hodgkin lymphoma and specific IgE reactivity, except possibly immediately before a diagnosis of non-Hodgkin lymphoma (> or = 10 years before diagnosis, OR = 1.00, 95% CI = 0.48 to 2.09; 5-9 years before, OR = 0.95, 95% CI = 0.50 to 1.84; 1-4 years before, OR = 0.33, 95% CI = 0.11 to 1.02; and < 1 year before, OR = 0.27, 95% CI = 0.03 to 2.31). CONCLUSION: Allergy may not be causally associated with the risk of non-Hodgkin lymphoma. The inverse association observed in some case-control studies may arise because non-Hodgkin lymphoma suppresses the immunologic response to allergens.

  • 21. Naucler, Pontus
    et al.
    Ryd, Walter
    Törnberg, Sven
    Strand, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Dermatology and Venereology.
    Wadell, Göran
    Elfgren, Kristina
    Rådberg, Thomas
    Strander, Björn
    Forslund, Ola
    Hansson, Bengt-Göran
    Hagmar, Björn
    Johansson, Bo
    Rylander, Eva
    Dillner, Joakim
    Efficacy of HPV DNA Testing With Cytology Triage and/or Repeat HPV DNA Testing in Primary Cervical Cancer Screening2009In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 101, no 2, p. 88-99Article in journal (Refereed)
    Abstract [en]

    Primary cervical screening with both human papillomavirus (HPV) DNA testing and cytological examination of cervical cells with a Pap test (cytology) has been evaluated in randomized clinical trials. Because the vast majority of women with positive cytology are also HPV DNA positive, screening strategies that use HPV DNA testing as the primary screening test may be more effective. We used the database from the intervention arm (n = 6257 women) of a population-based randomized trial of double screening with cytology and HPV DNA testing to evaluate the efficacy of 11 possible cervical screening strategies that are based on HPV DNA testing alone, cytology alone, and HPV DNA testing combined with cytology among women aged 32-38 years. The main outcome measures were sensitivity for detection of cervical intraepithelial neoplasia grade 3 or worse (CIN3+) within 6 months of enrollment or at colposcopy for women with a persistent type-specific HPV infection and the number of screening tests and positive predictive value (PPV) for each screening strategy. All statistical tests were two-sided. Compared with screening by cytology alone, double testing with cytology and for type-specific HPV persistence resulted in a 35% (95% confidence interval [CI] = 15% to 60%) increase in sensitivity to detect CIN3+, without a statistically significant reduction in the PPV (relative PPV = 0.76, 95% CI = 0.52 to 1.10), but with more than twice as many screening tests needed. Several strategies that incorporated screening for high-risk HPV subtypes were explored, but they resulted in reduced PPV compared with cytology. Compared with cytology, primary screening with HPV DNA testing followed by cytological triage and repeat HPV DNA testing of HPV DNA-positive women with normal cytology increased the CIN3+ sensitivity by 30% (95% CI = 9% to 54%), maintained a high PPV (relative PPV = 0.87, 95% CI = 0.60 to 1.26), and resulted in a mere 12% increase in the number of screening tests (from 6257 to 7019 tests). Primary HPV DNA-based screening with cytology triage and repeat HPV DNA testing of cytology-negative women appears to be the most feasible cervical screening strategy.

  • 22.
    Padula, William V.
    et al.
    Johns Hopkins Univ, Dept Hlth Policy & Management, Baltimore, MD 21218 USA..
    Larson, Richard A.
    Univ Chicago, Dept Med, 5841 S Maryland Ave, Chicago, IL 60637 USA..
    Dusetzina, Stacie B.
    Univ N Carolina, Eshelman Sch Pharm, Chapel Hill, NC 27599 USA.;Univ N Carolina, Gillings Sch Global Publ Hlth, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA.;Univ N Carolina, Cecil G Sheps Ctr Hlth Serv Res, Chapel Hill, NC 27599 USA..
    Apperley, Jane F.
    Imperial Coll, Hammersmith Hosp, Dept Haematol, London, England..
    Hehlmann, Rudiger
    Heidelberg Univ, Dept Med, Mannheim, Germany..
    Baccarani, Michele
    S Orsola Malpighi Univ Hosp, Dept Haematol & Oncol, Bologna, Italy..
    Eigendorff, Ekkehard
    Univ Hosp, Dept Haematol & Oncol, Jena, Germany..
    Guilhot, Joelle
    CHU Poitiers, INSERM, CIC 1402, Poitiers, France..
    Guilhot, Francois
    CHU Poitiers, INSERM, CIC 1402, Poitiers, France..
    Mahon, Francois-Xavier
    Univ Victor Segalen, Lab Hematol, Pessac, France..
    Martinelli, Giovanni
    Univ Bologna, Dept Hematol, L & A Seragnoli, Bologna, Italy..
    Mayer, Jiri
    Univ Hosp Brno, Dept Internal Med Hematol & Oncol, Brno, Czech Republic..
    Müller, Martin C.
    Heidelberg Univ, Dept Hematol & Oncol, Mannheim, Germany..
    Niederwieser, Dietger
    Univ Hosp Leipzig, Dept Hematol & Oncol, Leipzig, Germany..
    Saussele, Susanne
    Heidelberg Univ, Dept Med, Mannheim, Germany..
    Schiffer, Charles A.
    Wayne State Univ, Barbara Ann Karmanos Canc Inst, Detroit, MI 48201 USA..
    Silver, Richard T.
    Weill Cornell Med Ctr, Dept Med, New York, NY 10065 USA..
    Simonsson, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Haematology.
    Conti, Rena M.
    Univ Chicago, Dept Pediat, Chicago, IL 60637 USA.;Univ Chicago, Dept Publ Hlth Sci, Chicago, IL 60637 USA..
    Cost-effectiveness of Tyrosine Kinase Inhibitor Treatment Strategies for Chronic Myeloid Leukemia in Chronic Phase After Generic Entry of Imatinib in the United States2016In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 108, no 7, article id djw003Article in journal (Refereed)
    Abstract [en]

    Background: We analyzed the cost-effectiveness of treating incident chronic myeloid leukemia in chronic phase (CML-CP) with generic imatinib when it becomes available in United States in 2016. In the year following generic entry, imatinib's price is expected to drop 70% to 90%. We hypothesized that initiating treatment with generic imatinib in these patients and then switching to the other tyrosine-kinase inhibitors (TKIs), dasatinib or nilotinib, because of intolerance or lack of effectiveness ("imatinib-first") would be cost-effective compared with the current standard of care: "physicians' choice" of initiating treatment with any one of the three TKIs. Methods: We constructed Markov models to compare the five-year cost-effectiveness of imatinib-first vs physician's choice from a US commercial payer perspective, assuming 3% annual discounting ($US 2013). The models' clinical endpoint was five-year overall survival taken from a systematic review of clinical trial results. Per-person spending on incident CML-CP treatment overall care components was estimated using Truven's MarketScan claims data. The main outcome of the models was cost per quality-adjusted life-year (QALY). We interpreted outcomes based on a willingness-to-pay threshold of $100 000/QALY. A panel of European LeukemiaNet experts oversaw the study's conduct. Results: Both strategies met the threshold. Imatinib-first ($277 401, 3.87 QALYs) offered patients a 0.10 decrement in QALYs at a savings of $88 343 over five years to payers compared with physician's choice ($365 744, 3.97 QALYs). The imatinibfirst incremental cost-effectiveness ratio was approximately $883 730/QALY. The results were robust to multiple sensitivity analyses. Conclusion: When imatinib loses patent protection and its price declines, its use will be the cost-effective initial treatment strategy for CML-CP.

  • 23. Punt, Cornelis J A
    et al.
    Buyse, Marc
    Köhne, Claus-Henning
    Hohenberger, Peter
    Labianca, Roberto
    Schmoll, Hans J
    Påhlman, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Colorectal Surgery.
    Sobrero, Alberto
    Douillard, Jean-Yves
    Endpoints in adjuvant treatment trials: a systematic review of the literature in colon cancer and proposed definitions for future trials.2007In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 99, no 13, p. 998-1003Article in journal (Refereed)
    Abstract [en]

    Disease-free survival is increasingly being used as the primary endpoint of most trials testing adjuvant treatments in cancer. Other frequently used endpoints include overall survival, recurrence-free survival, and time to recurrence. These endpoints are often defined differently in different trials in the same type of cancer, leading to a lack of comparability among trials. In this Commentary, we used adjuvant studies in colon cancer as a model to address this issue. In a systematic review of the literature, we identified 52 studies of adjuvant treatment in colon cancer published in 1997–2006 that used eight other endpoints in addition to overall survival. Both the definition of these endpoints and the starting point for measuring time to the events that constituted these endpoints varied widely. A panel of experts on clinical research on colorectal cancer then reached consensus on the definition of each endpoint. Disease-free survival—defined as the time from randomization to any event, irrespective of cause—was considered to be the most informative endpoint for assessing the effect of treatment and therefore the most relevant to clinical practice. The proposed guidelines may add to the quality and cross-comparability of future studies of adjuvant treatments for cancer.

  • 24.
    Riman, Tomas
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health.
    Dickman, Paul W.
    Nilsson, Staffan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health.
    Correia, Nestor
    Nordlinder, Hans
    Magnusson, Cecilia M.
    Weiderpass, Elisabete
    Persson, Ingemar R.
    Hormone replacement therapy and the risk of invasive epithelial ovarian cancer in Swedish women2002In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 94, no 7, p. 497-504Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Estrogen replacement therapy (ERT), which is mainly used to relieve climacteric symptoms, increases a woman's risk for uterine endometrial cancer and epithelial ovarian cancer (EOC). Estrogens are often combined with progestins in hormone replacement therapy (HRT) to reduce the risk of uterine endometrial cancer. Data on the association between HRT including progestins and EOC risk are limited. This nationwide case-control study examined EOC risk in relation to HRT regimens with sequentially added progestins (HRTsp) and continuously added progestins (HRTcp). METHODS: Between 1993 and 1995, we enrolled 655 histologically verified incident case patients with EOC and 3899 randomly selected population controls, all 50-74 years of age. Data on HRT use were collected through mailed questionnaires. Multivariate-adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were estimated by the use of unconditional logistic regression. RESULTS: Risks of EOC were elevated among ever users as compared with never users of both ERT (OR = 1.43, 95% CI = 1.02 to 2.00) and HRTsp (OR = 1.54, 95% CI = 1.15 to 2.05); risks were elevated for serous, mucinous, and endometrioid subtypes. For all EOC types combined, the greatest risk increases were seen with hormone use exceeding 10 years. Ever use of HRTcp was not associated with increased EOC risk relative to HRTcp never use (OR = 1.02, 95% CI = 0.73 to 1.43). The risk of EOC was elevated among HRTsp ever users as compared with HRTcp ever users (OR = 1.78, 95% CI = 1.05 to 3.01). ORs for EOC after ever use of low-potency estrogens were 1.18 (95% CI = 0.89 to 1.55) for oral and 1.33 (95% CI = 1.03 to 1.72) for vaginal applications, but no relationship was seen between EOC risk and duration of use. CONCLUSION: Ever users of ERT and HRTsp but not HRTcp may be at increased risk of EOC.

  • 25.
    Sampson, Joshua N.
    et al.
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Wheeler, William A.
    Informat Management Serv Inc, Silver Spring, MD USA..
    Yeager, Meredith
    Natl Canc Inst, Div Canc Epidemiol & Genet, Canc Genom Res Lab, Gaithersburg, MD USA..
    Panagiotou, Orestis
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Wang, Zhaoming
    Natl Canc Inst, Div Canc Epidemiol & Genet, Canc Genom Res Lab, Gaithersburg, MD USA..
    Berndt, Sonja I.
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Lan, Qing
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Abnet, Christian C.
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Amundadottir, Laufey T.
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Figueroa, Jonine D.
    Landi, Maria Teresa
    Mirabello, Lisa
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA.;Canc Prevent & Res Inst ISPO, Environm & Occupat Epidemiol Unit, Florence, Italy..
    Savage, Sharon A.
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Taylor, Philip R.
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    De Vivo, Immaculata
    Brigham & Womens Hosp, Dept Med, Channing Div Network Med, Boston, MA 02115 USA.;Harvard Univ, Sch Med, Boston, MA 02115 USA.;Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA..
    McGlynn, Katherine A.
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Purdue, Mark P.
    Ontario Hlth Study, Toronto, ON, Canada..
    Rajaraman, Preetha
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Adami, Hans-Olov
    Karolinska Inst, Dept Med Epidemiol & Biostatist, Stockholm, Sweden..
    Ahlbom, Anders
    Karolinska Inst, Inst Environm Med, Dept Epidemiol, S-10401 Stockholm, Sweden..
    Albanes, Demetrius
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Amary, Maria Fernanda
    UCL Canc Inst, London, England.;Royal Natl Orthopaed Hosp NHS Trust, Middlesbrough, Cleveland, England..
    An, She-Juan
    Guangdong Acad Med Sci, Guangdong Gen Hosp, Guangdong Prov Key Lab Translat Med Lung Canc, Guangdong Lung Canc Inst, Guangzhou, Guangdong, Peoples R China..
    Andersson, Ulrika
    Umea Univ, Dept Radiat Sci Oncol, Umea, Sweden..
    Andriole, Gerald, Jr.
    Washington Univ, Sch Med, Div Urol Surg, St Louis, MO 63110 USA..
    Andrulis, Irene L.
    Univ Toronto, Litwin Ctr Canc Genet, Toronto, ON, Canada.;Mt Sinai Hosp, Lunenfeld Tanenbaum Res Inst, Toronto, ON M5G 1X5, Canada..
    Angelucci, Emanuele
    Osped Oncol Riferimento Regionale Businco, Hematol Unit, Cagliari, Italy..
    Ansell, Stephen M.
    Mayo Clin, Dept Med, Rochester, MN USA..
    Arici, Cecilia
    Univ Brescia, Dept Med & Surg Specialties, Radiol Sci & Publ Hlth, Brescia, Italy..
    Armstrong, Bruce K.
    Univ Sydney, Sydney Sch Publ Hlth, Sydney, NSW 2006, Australia..
    Arslan, Alan A.
    NYU, Sch Med, Dept Obstet & Gynecol, New York, NY USA.;NYU, Sch Med, Dept Environm Med, New York, NY USA.;NYU, Sch Med, Dept Populat Hlth, New York, NY USA.;NYU Langone, Med Ctr, Perlmutter Canc Ctr, New York, NY USA..
    Austin, Melissa A.
    Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA..
    Baris, Dalsu
    Barkauskas, Donald A.
    Univ So Calif, Dept Prevent Med, USC Keck Sch Med, Los Angeles, CA 90089 USA..
    Bassig, Bryan A.
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA.;Yale Sch Publ Hlth, Dept Environm Hlth Sci, New Haven, CT USA. German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Baden Wurttembe, Germany..
    Becker, Nikolaus
    Benavente, Yolanda
    Inst Catala Oncol, IDIBELL, Unit Infect & Canc UNIC, Canc Epidemiol Res Programme, Barcelona, Spain.;Ctr Invest Biomed Red Epidemiol Salud Publ CIBERE, Madrid, Spain..
    Benhamou, Simone
    Fdn Jean Dausset Ctr Etude Polymorphisme Humain C, Inst Natl sante & Rech med, U946, Paris, France.;Ctr Natl Receherche Sci, Inst Gustave Roussy, UMR8200, Villejuif, France..
    Berg, Christine
    Natl Canc Inst, Canc Prevent Div, Early Detect Res Grp, Bethesda, MD USA..
    Van Den Berg, David
    Univ So Calif, Dept Prevent Med, USC Keck Sch Med, Los Angeles, CA 90089 USA.;Univ So Calif, Norris Comprehens Canc Ctr, USC Keck Sch Med, Los Angeles, CA USA..
    Bernstein, Leslie
    Beckman Res Inst City Hope, Dept Canc Etiol, Duarte, CA USA..
    Bertrand, Kimberly A.
    Brigham & Womens Hosp, Dept Med, Channing Div Network Med, Boston, MA 02115 USA.;Harvard Univ, Sch Med, Boston, MA 02115 USA.;Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA..
    Birmann, Brenda M.
    Brigham & Womens Hosp, Dept Med, Channing Div Network Med, Boston, MA 02115 USA.;Harvard Univ, Sch Med, Boston, MA 02115 USA..
    Black, Amanda
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Boeing, Heiner
    German Inst Human Nutr, Dept Epidemiol, Potsdam, Germany..
    Boffetta, Paolo
    Tisch Canc Inst, Icahn Sch Med Mt Sinai, New York, NY USA..
    Boutron-Ruault, Marie-Christine
    Univ Paris 11, F-94805 Villejuif, France.;Inst Gustave Roussy, F-94805 Villejuif, France..
    Bracci, Paige M.
    Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA..
    Brinton, Louise
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Brooks-Wilson, Angela R.
    BC Canc Agcy, Genome Sci Ctr, Vancouver, BC, Canada.;Simon Fraser Univ, Dept Biomed Physiol & Kinesiol, Burnaby, BC V5A 1S6, Canada..
    Bueno-de-Mesquita, H. Bas
    Natl Inst Publ Hlth & Environm RIVM, Bilthoven, Netherlands.;Univ Med Ctr Utrecht, Dept Gastroenterol & Hepatol, Utrecht, Netherlands..
    Burdett, Laurie
    Natl Canc Inst, Div Canc Epidemiol & Genet, Canc Genom Res Lab, Gaithersburg, MD USA..
    Buring, Julie
    Brigham & Womens Hosp, Dept Med, Div Prevent Med, Boston, MA 02115 USA.;Harvard Univ, Sch Med, Boston, MA USA.;Brigham & Womens Hosp, Dept Med, Div Aging, Boston, MD 02115 USA.;Harvard Univ, Sch Med, Boston, MD USA..
    Butler, Mary Ann
    NIOSH, Ctr Dis Control & Prevent, Cincinnati, OH 45226 USA..
    Cai, Qiuyin
    Vanderbilt Univ, Ctr Med, Dept Med, Nashville, TN 37232 USA.;Vanderbilt Univ, Med Ctr, Vanderbilt Ingram Canc Ctr, Nashville, TN USA..
    Cancel-Tassin, Geraldine
    Ctr Rech Pathol Prostat, Paris, France.;Univ Paris 06, ONCOTYPE URO, GRC 5, Paris, France..
    Canzian, Federico
    German Canc Res Ctr, Genom Epidemiol Grp, Heidelberg, Germany..
    Carrato, Alfredo
    Ramon y Cajal Univ Hosp, Madrid, Spain..
    Carreon, Tania
    NIOSH, Ctr Dis Control & Prevent, Cincinnati, OH 45226 USA..
    Carta, Angela
    Univ Brescia, Dept Med & Surg Specialties, Radiol Sci & Publ Hlth, Brescia, Italy..
    Chan, John K. C.
    Queen Elizabeth Hosp, Dept Pathol, Hong Kong, Hong Kong, Peoples R China..
    Chang, Ellen T.
    Stanford Univ, Sch Med, Div Epidemiol, Dept Hlth Res & Policy, Stanford, CA 94305 USA.;Exponent Inc, Ctr Epidemiol & Computat Biol, Hlth Sci, Menlo Pk, CA USA..
    Chang, Gee-Chen
    Natl Yang Ming Univ, Sch Med, Dept Med, Taipei 112, Taiwan.;Taichung Vet Gen Hosp, Div Chest Med, Dept Internal Med, Taichung, Taiwan..
    Chang, I-Shou
    Natl Hlth Res Inst, Natl Inst Canc Res, Zhunan, Taiwan..
    Chang, Jiang
    Chinese Acad Med Sci, Canc Inst & Hosp, Dept Etiol & Carcinogenesis, Beijing 100730, Peoples R China.;Peking Union Med Coll, Beijing 100021, Peoples R China..
    Chang-Claude, Jenny
    Chen, Chien-Jen
    Genom Res Ctr, Taipei, Taiwan..
    Chen, Chih-Yi
    Chung Shan Med Univ, Chung Shan Med Univ Hosp, Dept Surg, Div Thorac Surg,Inst Med, Taichung, Taiwan..
    Chen, Chu
    Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98104 USA.;Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA..
    Chen, Chung-Hsing
    Natl Hlth Res Inst, Natl Inst Canc Res, Zhunan, Taiwan..
    Chen, Constance
    Brigham & Womens Hosp, Dept Med, Channing Div Network Med, Boston, MA 02115 USA.;Harvard Univ, Sch Med, Boston, MA 02115 USA.;Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA..
    Chen, Hongyan
    Fudan Univ, Sch Life Sci, Minist Educ, Key Lab Contemporary Anthropol, Shanghai 200433, Peoples R China..
    Chen, Kexin
    Med Univ, Canc Inst & Hosp, Natl Clin Res Ctr Canc, Key Lab Canc Prevent & Therapy,Dept Epidemiol & B, Tianjin, Peoples R China..
    Chen, Kuan-Yu
    Natl Taiwan Univ Hosp, Dept Internal Med, Taipei 100, Taiwan..
    Chen, Kun-Chieh
    Taichung Vet Gen Hosp, Div Chest Med, Dept Internal Med, Taichung, Taiwan..
    Chen, Ying
    Natl Univ Singapore, Saw Swee Hock Sch Publ Hlth, Singapore 117548, Singapore..
    Chen, Ying-Hsiang
    Natl Hlth Res Inst, Inst Populat Hlth Sci, Zhunan, Taiwan..
    Chen, Yi-Song
    Natl Hlth Res Inst, Inst Populat Hlth Sci, Zhunan, Taiwan..
    Chen, Yuh-Min
    Taipei Vet Gen Hosp, Dept Chest Med, Taipei, Taiwan.;Taipei Med Univ, Taipei Canc Ctr, Taipei, Taiwan..
    Chien, Li-Hsin
    Natl Hlth Res Inst, Inst Populat Hlth Sci, Zhunan, Taiwan..
    Chirlaque, Maria-Dolores
    Ctr Invest Biomed Red Epidemiol Salud Publ CIBERE, Madrid, Spain.;IMIB Arrixaca, Dept Epidemiol, Murcia Reg Hlth Author, Murcia, Spain..
    Choi, Jin Eun
    Kyungpook Natl Univ, Med Ctr, Canc Res Ctr, Daegu, South Korea..
    Choi, Yi Young
    Kyungpook Natl Univ, Med Ctr, Canc Res Ctr, Daegu, South Korea..
    Chow, Wong-Ho
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Chung, Charles C.
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Clavel, Jacqueline
    Univ Paris 11, F-94805 Villejuif, France.;INSERM, Ctr Res Epidemiol & Populat Hlth CESP, U1018, Environm Epidemiol Canc Grp, Villejuif, France..
    Clavel-Chapelon, Franoise
    Ctr Res Epidemiol & Populat Hlth CESP, INSERM, Nutr,Hormones & Womens Hlth team, U1018, F-94805 Villejuif, France.;Univ Paris 11, F-94805 Villejuif, France.;Inst Gustave Roussy, F-94805 Villejuif, France..
    Cocco, Pierluigi
    Univ Cagliari, Dept Publ Hlth Clin & Mol Med, Cagliari, Italy..
    Colt, Joanne S.
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Comperat, Eva
    Ctr Rech Pathol Prostat, Paris, France.;Univ Paris 06, ONCOTYPE URO, GRC 5, Paris, France.;AP HP, Pitie Salpetriere, Dept Urol, Paris, France.;AP HP, Pitie Salpetriere, Dept Pathol, Paris, France..
    Conde, Lucia
    Univ Alabama Birmingham, Sch Publ Hlth, Dept Epidemiol, Birmingham, AL 35294 USA.;Univ Alabama Birmingham, Ctr Comprehens Canc, Birmingham, AL 35294 USA.;Univ Calif Berkeley, Sch Publ Hlth, Div Environm Hlth Sci, Berkeley, CA 94720 USA.;BC Canc Agcy, Ctr Lymphoid Canc, Vancouver, BC, Canada..
    Connors, Joseph M.
    Univ British Columbia, Dept Med, Vancouver, BC, Canada..
    Conti, David
    Univ So Calif, Dept Prevent Med, USC Keck Sch Med, Los Angeles, CA 90089 USA.;Univ So Calif, Norris Comprehens Canc Ctr, USC Keck Sch Med, Los Angeles, CA USA..
    Cortessis, Victoria K.
    Univ So Calif, Dept Prevent Med, USC Keck Sch Med, Los Angeles, CA 90089 USA.;Univ So Calif, Norris Comprehens Canc Ctr, USC Keck Sch Med, Los Angeles, CA USA.;Univ So Calif, Dept Obstet & Gynecol, Los Angeles, CA 90089 USA..
    Cotterchio, Michelle
    Canc Care Ontario, Toronto, ON, Canada.;Univ Toronto, Dalla Lana Sch Publ Hlth, Toronto, ON, Canada..
    Cozen, Wendy
    Univ So Calif, Dept Prevent Med, USC Keck Sch Med, Los Angeles, CA 90089 USA.;Univ So Calif, Norris Comprehens Canc Ctr, USC Keck Sch Med, Los Angeles, CA USA..
    Crouch, Simon
    Univ York, Dept Hlth Sci, York YO10 5DD, N Yorkshire, England..
    Crous-Bou, Marta
    Brigham & Womens Hosp, Dept Med, Channing Div Network Med, Boston, MA 02115 USA.;Harvard Univ, Sch Med, Boston, MA 02115 USA.;Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA..
    Cussenot, Olivier
    Ctr Rech Pathol Prostat, Paris, France.;Univ Paris 06, ONCOTYPE URO, GRC 5, Paris, France.;Hop Tenon, AP HP, Dept Urol, F-75970 Paris, France..
    Davis, Faith G.
    Univ Alberta, Sch Publ Hlth, Edmonton, AB, Canada..
    Ding, Ti
    Shanxi Canc Hosp, Taiyuan, Shanxi, Peoples R China..
    Diver, W. Ryan
    Amer Canc Soc, Epidemiol Res Program, Atlanta, GA 30329 USA..
    Dorronsoro, Miren
    Ctr Invest Biomed Red Epidemiol Salud Publ CIBERE, Madrid, Spain.;BioDonostia Res Inst, Dept Hlth, Basque Region, Spain..
    Dossus, Laure
    Ctr Res Epidemiol & Populat Hlth CESP, INSERM, Nutr,Hormones & Womens Hlth team, U1018, F-94805 Villejuif, France.;Univ Paris 11, F-94805 Villejuif, France.;Inst Gustave Roussy, F-94805 Villejuif, France..
    Duell, Eric J.
    Bellvitge Biomed Res Inst IDIBELL, Catalan Inst Oncol ICO, Canc Epidemiol Res Program, Unit Nutr Environm & Canc, Barcelona, Spain..
    Ennas, Maria Grazia
    Univ Cagliari, Dept Biomed Sci, Cagliari, Italy..
    Erickson, Ralph L.
    Walter Reed Army Inst Res, Silver Spring, MD USA..
    Feychting, Maria
    Karolinska Inst, Inst Environm Med, Dept Epidemiol, S-10401 Stockholm, Sweden..
    Flanagan, Adrienne M.
    UCL Canc Inst, London, England.;Royal Natl Orthopaed Hosp NHS Trust, Middlesbrough, Cleveland, England..
    Foretova, Lenka
    Masaryk Mem Canc Inst, Dept Canc Epidemiol & Genet, Brno, Czech Republic.;MF MU, Brno, Czech Republic..
    Fraumeni, Joseph F., Jr.
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Freedman, Neal D.
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Freeman, Laura E. Beane
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Fuchs, Charles
    Brigham & Womens Hosp, Dept Med, Channing Div Network Med, Boston, MA 02115 USA.;Harvard Univ, Sch Med, Boston, MA 02115 USA.;Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA..
    Gago-Dominguez, Manuela
    Inst Invest Sanitaria de Santiago, Serv Galego Saude SERGAS, Galician Fdn Genom Med, Genom Med Grp, Santiago De Compostela, Spain..
    Gallinger, Steven
    Mt Sinai Hosp, Lunenfeld Tanenbaum Res Inst, Toronto, ON M5G 1X5, Canada..
    Gao, Yu-Tang
    Shanghai Canc Inst, Dept Epidemiol, Shanghai, Peoples R China..
    Gapstur, Susan M.
    Amer Canc Soc, Epidemiol Res Program, Atlanta, GA 30329 USA..
    Garcia-Closas, Montserrat
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA.;Inst Canc Res, Div Genet & Epidemiol, London, England..
    Garcia-Closas, Reina
    Hosp Univ Canarias, Unidad Invest, San Cristobal la Laguna, Spain..
    Gascoyne, Randy D.
    Univ British Columbia, Dept Pathol, Vancouver, BC, Canada..
    Gastier-Foster, Julie
    Nationwide Childrens Hosp, Columbus, OH USA.;Ohio State Univ, Dept Pathol & Pediat, Columbus, OH 43210 USA..
    Gaudet, Mia M.
    Amer Canc Soc, Epidemiol Res Program, Atlanta, GA 30329 USA..
    Gaziano, J. Michael
    Brigham & Womens Hosp, Dept Med, Div Prevent Med, Boston, MA 02115 USA.;Harvard Univ, Sch Med, Boston, MA USA.;Brigham & Womens Hosp, Dept Med, Div Aging, Boston, MD 02115 USA.;Harvard Univ, Sch Med, Boston, MD USA.;Vet Affairs Boston Healthcare Syst, Geriatr Res Educ & Clin Ctr, Massachusetts Vet Epidemiol Res & Informat Ctr, Boston, MA USA..
    Giffen, Carol
    Informat Management Serv Inc, Silver Spring, MD USA..
    Giles, Graham G.
    Canc Council Victoria, Canc Epidemiol Ctr, Melbourne, Vic, Australia.;Univ Melbourne, Melbourne Sch Populat & Global Hlth, Ctr Biostat & Epidemiol, Carlton, Vic 3053, Australia..
    Giovannucci, Edward
    Brigham & Womens Hosp, Dept Med, Channing Div Network Med, Boston, MA 02115 USA.;Harvard Univ, Sch Med, Boston, MA 02115 USA.;Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.;Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA..
    Glimelius, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Experimental and Clinical Oncology. Karolinska Inst, Dept Pathol & Oncol, Stockholm, Sweden..
    Goggins, Michael
    Sidney Kimmel Canc Ctr, Dept Oncol, Baltimore, MD USA.;Johns Hopkins Univ, Baltimore, MD USA.;Sidney Kimmel Canc Ctr, Dept Pathol, Baltimore, MD USA.;Sidney Kimmel Canc Ctr, Dept Med, Baltimore, MD USA..
    Gokgoz, Nalan
    Univ Toronto, Litwin Ctr Canc Genet, Toronto, ON, Canada.;Mt Sinai Hosp, Lunenfeld Tanenbaum Res Inst, Toronto, ON M5G 1X5, Canada..
    Goldstein, Alisa M.
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Gorlick, Richard
    Childrens Hosp Montefiore, Albert Einstein Coll Med, Bronx, NY USA..
    Gross, Myron
    Univ Minnesota, Lab Med & Pathol, Minneapolis, MN USA..
    Grubb, Robert, III
    Washington Univ, Sch Med, Div Urol Surg, St Louis, MO 63110 USA..
    Gu, Jian
    Univ Texas MD Anderson Canc Ctr, Dept Epidemiol, Houston, TX 77030 USA..
    Guan, Peng
    China Med Univ, Sch Publ Hlth, Dept Epidemiol, Shenyang 110001, Peoples R China..
    Gunter, Marc
    Univ London Imperial Coll Sci Technol & Med, Sch Publ Hlth, Dept Epidemiol & Biostat, London, England..
    Guo, Huan
    Huazhong Univ Sci & Technol, Sch Publ Hlth, Inst Occupat Med, Wuhan 430074, Peoples R China.;Huazhong Univ Sci & Technol, Sch Publ Hlth, Minist Educ, Key Lab Environm & Hlth, Wuhan 430074, Peoples R China..
    Habermann, Thomas M.
    Mayo Clin, Dept Med, Rochester, MN USA..
    Haiman, Christopher A.
    Halai, Dina
    UCL Canc Inst, London, England.;Royal Natl Orthopaed Hosp NHS Trust, Middlesbrough, Cleveland, England..
    Hallmans, Goran
    Umea Univ, Dept Publ Hlth & Clin Med, Nutr Res, Umea, Sweden..
    Hassan, Manal
    Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, Houston, TX USA..
    Hattinger, Claudia
    He, Qincheng
    China Med Univ, Sch Publ Hlth, Dept Epidemiol, Shenyang 110001, Peoples R China..
    He, Xingzhou
    Chinese Ctr Dis Control & Prevent, Beijing, Peoples R China..
    Helzlsouer, Kathy
    Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA..
    Henderson, Brian
    Univ So Calif, Dept Prevent Med, USC Keck Sch Med, Los Angeles, CA 90089 USA..
    Henriksson, Roger
    Umea Univ, Dept Radiat Sci Oncol, Umea, Sweden..
    Hjalgrim, Henrik
    Statens Serum Inst, Dept Epidemiol Res, Div Hlth Surveillance & Res, DK-2300 Copenhagen, Denmark..
    Hoffman-Bolton, Judith
    Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA..
    Hohensee, Chancellor
    Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98104 USA..
    Holford, Theodore R.
    Yale Univ, Sch Publ Hlth, Dept Biostat, New Haven, CT USA..
    Holly, Elizabeth A.
    Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA..
    Hong, Yun-Chul
    Seoul Natl Univ, Coll Med, Dept Prevent Med, Seoul, South Korea..
    Hoover, Robert N.
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Horn-Ross, Pamela L.
    Canc Prevent Inst Calif, Fremont, CA USA..
    Hosain, G. M. Monawar
    New Hampshire State Canc Registry, Concord, NH USA..
    Hosgood, H. Dean, III
    Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10467 USA..
    Hsiao, Chin-Fu
    Natl Hlth Res Inst, Inst Populat Hlth Sci, Zhunan, Taiwan.;Natl Hlth Res Inst, Taiwan Lung Canc Tissue Specimen Informat Resourc, Zhunan, Taiwan..
    Hu, Nan
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Hu, Wei
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Hu, Zhibin
    Nanjing Med Univ, Jiangsu Collaborat Innovat Ctr Canc Personalized, Nanjing, Jiangsu, Peoples R China.;Nanjing Med Univ, Sch Publ Hlth, Ctr Canc, Jiangsu Key Lab Canc Biomarkers Prevent & Treatme, Nanjing, Jiangsu, Peoples R China..
    Huang, Ming-Shyan
    Kaohsiung Med Univ, Sch Med, Kaohsiung Med Univ Hosp, Dept Internal Med, Kaohsiung, Taiwan..
    Huerta, Jose-Maria
    IMIB Arrixaca, Dept Epidemiol, Murcia Reg Hlth Author, Murcia, Spain..
    Hung, Jen-Yu
    Kaohsiung Med Univ, Sch Med, Kaohsiung Med Univ Hosp, Dept Internal Med, Kaohsiung, Taiwan..
    Hutchinson, Amy
    Natl Canc Inst, Div Canc Epidemiol & Genet, Canc Genom Res Lab, Gaithersburg, MD USA..
    Inskip, Peter D.
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Jackson, Rebecca D.
    Ohio State Univ, Div Endocrinol Diabet & Metab, Columbus, OH 43210 USA..
    Jacobs, Eric J.
    Amer Canc Soc, Epidemiol Res Program, Atlanta, GA 30329 USA..
    Jenab, Mazda
    Int Agcy Res Canc, F-69372 Lyon, France..
    Jeon, Hyo-Sung
    Kyungpook Natl Univ, Mol Diagnost & Imaging Ctr, Daegu, South Korea..
    Ji, Bu-Tian
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Jin, Guangfu
    Nanjing Med Univ, Jiangsu Collaborat Innovat Ctr Canc Personalized, Nanjing, Jiangsu, Peoples R China.;Nanjing Med Univ, Sch Publ Hlth, Ctr Canc, Jiangsu Key Lab Canc Biomarkers Prevent & Treatme, Nanjing, Jiangsu, Peoples R China..
    Jin, Li
    Fudan Univ, Sch Life Sci, Minist Educ, Key Lab Contemporary Anthropol, Shanghai 200433, Peoples R China..
    Johansen, Christoffer
    Danish Canc Soc Res Ctr, Unit Survivorship, Copenhagen, Denmark..
    Johnson, Alison
    Vermont Canc Registry, Burlington, VT USA..
    Jung, Yoo Jin
    Seoul Natl Univ, Coll Med, Canc Res Inst, Dept Thorac & Cardiovasc Surg, Seoul, South Korea..
    Kaaks, Rudolph
    Kamineni, Aruna
    Grp Hlth Res Inst, Seattle, WA USA..
    Kane, Eleanor
    Univ York, Dept Hlth Sci, York YO10 5DD, N Yorkshire, England..
    Kang, Chang Hyun
    Seoul Natl Univ, Coll Med, Canc Res Inst, Dept Thorac & Cardiovasc Surg, Seoul, South Korea..
    Karagas, Margaret R.
    Dartmouth Coll, Geisel Sch Med, Hanover, NH 03755 USA..
    Kelly, Rachel S.
    Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.;Univ London Imperial Coll Sci Technol & Med, Sch Publ Hlth, MRC PHE Ctr Environm & Hlth, London, England..
    Khaw, Kay-Tee
    Univ Cambridge, Cambridge CB2 1TN, England..
    Kim, Christopher
    Kim, Hee Nam
    Chonnam Natl Univ, Ctr Creat Biomed Scientists, Gwangju, South Korea..
    Kim, Jin Hee
    Seoul Natl Univ, Grad Sch Publ Hlth, Dept Environm Hlth, Seoul, South Korea..
    Kim, Jun Suk
    Korea Univ, Guro Hosp, Coll Med, Dept Internal Med,Div Med Oncol, Seoul, South Korea..
    Kim, Yeul Hong
    Korea Univ, Coll Med, Anam Hosp, Div Hematol Oncol,Dept Internal Med, Seoul 136705, South Korea..
    Kim, Young Tae
    Seoul Natl Univ, Coll Med, Canc Res Inst, Dept Thorac & Cardiovasc Surg, Seoul, South Korea..
    Kim, Young-Chul
    Chonnam Natl Univ, Hwasun Hosp, Lung & Esophageal Canc Clin, Hwasun Eup, South Korea.;Chonnam Natl Univ, Sch Med, Dept Internal Med, Gwangju, South Korea..
    Kitahara, Cari M.
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Klein, Alison P.
    Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.;Johns Hopkins Univ, Sch Med, Dept Oncol, Baltimore, MD 21205 USA..
    Klein, Robert J.
    Icahn Sch Med Mt Sinai, Dept Genet & Genom Sci, Icahn Inst Genom & Multiscale Biol, New York, NY 10029 USA..
    Kogevinas, Manolis
    Ctr Res Environm Epidemiol CREAL, Barcelona, Spain.;Hosp del Mar, Municipal Inst Med Res IMIM, Barcelona, Spain.;Natl Sch Publ Hlth, Athens, Greece..
    Kohno, Takashi
    Natl Canc Ctr, Res Inst, Div Genome Biol, Tokyo 104, Japan..
    Kolonel, Laurence N.
    Canc Res Ctr Hawaii, Honolulu, HI USA..
    Kooperberg, Charles
    Kricker, Anne
    Univ Sydney, Sydney Sch Publ Hlth, Sydney, NSW 2006, Australia..
    Krogh, Vittorio
    Fdn IRCCS Ist Nazl Tumori, Epidemiol & Prevent Unit, Milan, Italy..
    Kunitoh, Hideo
    Japanese Red Cross Med Ctr, Dept Med Oncol, Tokyo, Japan..
    Kurtz, Robert C.
    Mem Sloan Kettering Canc Ctr, Dept Med, New York, NY 10021 USA..
    Kweon, Sun-Seog
    Chonnam Natl Univ, Hwasun Hosp, Jeonnam Reg Canc Ctr, Hwasun Eup, South Korea.;Chonnam Natl Univ, Sch Med, Dept Prevent Med, Gwangju, South Korea..
    LaCroix, Andrea
    Lawrence, Charles
    Westat Corp, Rockville, MD USA..
    Lecanda, Fernando
    Univ Navarra, Univ Navarra Clin, Dept Pediat, Pamplona, Spain..
    Lee, Victor Ho Fun
    Univ Hong Kong, Dept Clin Oncol, Hong Kong, Hong Kong, Peoples R China..
    Li, Donghui
    Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, Houston, TX USA..
    Li, Haixin
    Med Univ, Canc Inst & Hosp, Natl Clin Res Ctr Canc, Key Lab Canc Prevent & Therapy,Dept Epidemiol & B, Tianjin, Peoples R China..
    Li, Jihua
    Li, Yao-Jen
    Genom Res Ctr, Taipei, Taiwan..
    Li, Yuqing
    Canc Prevent Inst Calif, Fremont, CA USA..
    Liao, Linda M.
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Liebow, Mark
    Mayo Clin, Dept Med, Rochester, MN USA..
    Lightfoot, Tracy
    Univ York, Dept Hlth Sci, York YO10 5DD, N Yorkshire, England..
    Lim, Wei-Yen
    Natl Univ Singapore, Saw Swee Hock Sch Publ Hlth, Singapore 117548, Singapore..
    Lin, Chien-Chung
    Natl Cheng Kung Univ, Cheng Kung Univ Med Coll & Hosp, Dept Internal Med, Tainan 701, Taiwan..
    Lin, Dongxin
    Chinese Acad Med Sci, Canc Inst & Hosp, Dept Etiol & Carcinogenesis, Beijing 100730, Peoples R China.;Peking Union Med Coll, Beijing 100021, Peoples R China..
    Lindstrom, Sara
    Brigham & Womens Hosp, Dept Med, Channing Div Network Med, Boston, MA 02115 USA.;Harvard Univ, Sch Med, Boston, MA 02115 USA.;Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA..
    Linet, Martha S.
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Link, Brian K.
    Liu, Chenwei
    Natl Canc Inst, Div Canc Epidemiol & Genet, Canc Genom Res Lab, Gaithersburg, MD USA..
    Liu, Jianjun
    Qujing Ctr Dis Control & Prevent, Sanjiangdadao, Qujing, Peoples R China.;Genome Inst Singapore, Human Genet, Singapore, Singapore..
    Liu, Li
    Huazhong Univ Sci & Technol, Ctr Canc, Union Hosp, Wuhan 430074, Peoples R China. Umea Univ, Dept Surg & Perioperat Sci Urol & Androl, Umea, Sweden. Univ Florence, Dept Surg & Translat Med, Sect Anatomopathol, Florence, Italy..
    Ljungberg, Boerje
    Lloreta, Josep
    Ctr Invest Biomed Red Epidemiol Salud Publ CIBERE, Madrid, Spain..
    Di Lollo, Simonetta
    Lu, Daru
    Fudan Univ, Sch Life Sci, Minist Educ, Key Lab Contemporary Anthropol, Shanghai 200433, Peoples R China..
    Lund, Eiluv
    Univ Tromso, Arctic Univ Norway, Fac Hlth Sci, Dept Community Med, Tromso, Norway. Spanish Natl Canc Res Ctr CNIO, Genet & Mol Epidemiol Grp, Madrid, Spain..
    Malats, Nuria
    Mannisto, Satu
    Natl Inst Hlth & Welf, Dept Chron Dis Prevent, Helsinki, Finland..
    Le Marchand, Loic
    Univ Hawaii, Ctr Canc, Canc Epidemiol Program, Honolulu, HI 96822 USA. Stanford Univ, Lucile Packard Childrens Hosp, Palo Alto, CA 94304 USA..
    Marina, Neyssa
    Masala, Giovanna
    Canc Res & Prevent Inst ISPO, Mol & Nutr Epidemiol Unit, Florence, Italy..
    Mastrangelo, Giuseppe
    Univ Padua, Dept Cardiac Thorac & Vasc Sci, Padua, Italy..
    Matsuo, Keitaro
    Aichi Canc Res Inst, Div Mol Med, Nagoya, Aichi, Japan..
    Maynadie, Marc
    Univ Burgundy, Registre Hemopathies Malignes Cote dOr, EA 4184, Dijon, France.;Dijon Univ Hosp, Dijon, France..
    Mckay, James
    Int Agcy Res Canc, F-69372 Lyon, France..
    McKean-Cowdin, Roberta
    Univ So Calif, Dept Prevent Med, USC Keck Sch Med, Los Angeles, CA 90089 USA..
    Melbye, Mads
    Statens Serum Inst, Dept Epidemiol Res, Div Hlth Surveillance & Res, DK-2300 Copenhagen, Denmark.;Stanford Univ, Dept Med, Sch Med, Stanford, CA 94305 USA. Brown Univ, Dept Epidemiol, Div Biol & Med, Providence, RI 02912 USA..
    Melin, Beatrice S.
    Umea Univ, Dept Radiat Sci Oncol, Umea, Sweden..
    Michaud, Dominique S.
    Mitsudomi, Tetsuya
    Kinki Univ, Sch Med, Div Thorac Surg, Sayama, Osaka 589, Japan..
    Monnereau, Alain
    Univ Paris 11, F-94805 Villejuif, France.;INSERM, Ctr Res Epidemiol & Populat Hlth CESP, U1018, Environm Epidemiol Canc Grp, Villejuif, France.;Inst Bergonie, Registre Hemopathies Malignes Gironde, Bordeaux, France. Aarhus Univ, Epidemiol Sect, DK-8000 Aarhus C, Denmark. Aalborg Univ Hosp, Dept Cardiol, Aalborg, Denmark..
    Montalvan, Rebecca
    Westat Corp, Rockville, MD USA..
    Moore, Lee E.
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Mortensen, Lotte Maxild
    Nieters, Alexandra
    Univ Med Ctr Freiburg, Ctr Chron Immunodeficiency, Freiburg, Baden Wurttembe, Germany..
    North, Kari E.
    Univ N Carolina, Dept Epidemiol, Chapel Hill, NC USA.;Univ N Carolina, Carolina Ctr Genome Sci, Chapel Hill, NC USA..
    Novak, Anne J.
    Mayo Clin, Dept Med, Rochester, MN USA..
    Oberg, Ann L.
    Mayo Clin, Dept Hlth Sci Res, Div Biomed Stat & Informat, Rochester, MN USA..
    Offit, Kenneth
    Mem Sloan Kettering Canc Ctr, Dept Med, New York, NY 10021 USA..
    Oh, In-Jae
    Chonnam Natl Univ, Hwasun Hosp, Lung & Esophageal Canc Clin, Hwasun Eup, South Korea.;Chonnam Natl Univ, Sch Med, Dept Internal Med, Gwangju, South Korea..
    Olson, Sara H.
    Mem Sloan Kettering Canc Ctr, Dept Epidemiol & Biostat, New York, NY 10021 USA..
    Palli, Domenico
    Canc Res & Prevent Inst ISPO, Mol & Nutr Epidemiol Unit, Florence, Italy..
    Pao, William
    Vanderbilt Univ, Med Ctr, Div Hematol & Oncol, Nashville, TN 37235 USA..
    Park, In Kyu
    Seoul Natl Univ, Coll Med, Canc Res Inst, Dept Thorac & Cardiovasc Surg, Seoul, South Korea..
    Park, Jae Yong
    Kyungpook Natl Univ, Med Ctr, Lung Canc Ctr, Daegu, South Korea..
    Park, Kyong Hwa
    Korea Univ, Coll Med, Anam Hosp, Div Hematol Oncol,Dept Internal Med, Seoul 136705, South Korea..
    Patino-Garcia, Ana
    Univ Navarra, Univ Navarra Clin, Dept Pediat, Pamplona, Spain..
    Pavanello, Sofia
    Univ Padua, Dept Cardiac Thorac & Vasc Sci, Padua, Italy..
    Peeters, Petra H. M.
    Univ London Imperial Coll Sci Technol & Med, Sch Publ Hlth, Dept Epidemiol & Biostat, London, England.;Univ Med Ctr Utrecht, Julius Ctr Hlth Sci & Primary Care 194, Utrecht, Netherlands.;Univ London Imperial Coll Sci Technol & Med, Sch Publ Hlth, Dept Primary Care & Publ Hlth, London, England..
    Perng, Reury-Perng
    Taipei Vet Gen Hosp, Dept Chest Med, Taipei, Taiwan..
    Peters, Ulrike
    Petersen, Gloria M.
    Mayo Clin, Div Epidemiol, Dept Hlth Sci Res, Rochester, MN USA..
    Picci, Piero
    Orthopaed Rizzoli Inst, Expt Oncol Lab, Bologna, Italy..
    Pike, Malcolm C.
    Mem Sloan Kettering Canc Ctr, Dept Epidemiol & Biostat, New York, NY 10021 USA..
    Porru, Stefano
    Univ Brescia, Dept Med & Surg Specialties, Radiol Sci & Publ Hlth, Brescia, Italy..
    Prescott, Jennifer
    Brigham & Womens Hosp, Dept Med, Channing Div Network Med, Boston, MA 02115 USA.;Harvard Univ, Sch Med, Boston, MA 02115 USA.;Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA..
    Prokunina-Olsson, Ludmila
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Qian, Biyun
    Acad Sinica, Genom Res Ctr, Taipei 115, Taiwan..
    Qiao, You-Lin
    Chinese Acad Med Sci, Canc Inst & Hosp, Dept Epidemiol, Beijing 100730, Peoples R China..
    Rais, Marco
    Univ Cagliari, Dept Publ Hlth Clin & Mol Med, Cagliari, Italy..
    Riboli, Elio
    Univ York, Dept Hlth Sci, York YO10 5DD, N Yorkshire, England.;Univ London Imperial Coll Sci Technol & Med, Sch Publ Hlth, London, England..
    Riby, Jacques
    Univ Alabama Birmingham, Sch Publ Hlth, Dept Epidemiol, Birmingham, AL 35294 USA.;Univ Alabama Birmingham, Ctr Comprehens Canc, Birmingham, AL 35294 USA.;Univ Calif Berkeley, Sch Publ Hlth, Div Environm Hlth Sci, Berkeley, CA 94720 USA.;BC Canc Agcy, Ctr Lymphoid Canc, Vancouver, BC, Canada..
    Risch, Harvey A.
    Yale Univ, Sch Publ Hlth, Dept Chron Dis Epidemiol, New Haven, CT USA..
    Rizzato, Cosmeri
    German Canc Res Ctr, Genom Epidemiol Grp, Heidelberg, Germany..
    Rodabough, Rebecca
    Roman, Eve
    Roupret, Morgan
    Ctr Rech Pathol Prostat, Paris, France.;Univ Paris 06, ONCOTYPE URO, GRC 5, Paris, France.;AP HP, Pitie Salpetriere, Dept Urol, Paris, France..
    Ruder, Avima M.
    NIOSH, Ctr Dis Control & Prevent, Cincinnati, OH 45226 USA..
    de Sanjose, Silvia
    Inst Catala Oncol, IDIBELL, Unit Infect & Canc UNIC, Canc Epidemiol Res Programme, Barcelona, Spain..
    Scelo, Ghislaine
    Int Agcy Res Canc, F-69372 Lyon, France..
    Schned, Alan
    Dartmouth Coll, Geisel Sch Med, Hanover, NH 03755 USA..
    Schumacher, Fredrick
    Univ So Calif, Dept Prevent Med, USC Keck Sch Med, Los Angeles, CA 90089 USA..
    Schwartz, Kendra
    Orthopaed Rizzoli Inst, Expt Oncol Lab, Bologna, Italy..
    Schwenn, Molly
    Maine Canc Registry, Augusta, ME USA..
    Scotlandi, Katia
    Seow, Adeline
    Natl Univ Singapore, Saw Swee Hock Sch Publ Hlth, Singapore 117548, Singapore..
    Serra, Consol
    Univ Pompeu Fabra, Dept Ciencies Experimentals & Salut, Barcelona, Spain..
    Serra, Massimo
    Orthopaed Rizzoli Inst, Expt Oncol Lab, Bologna, Italy..
    Sesso, Howard D.
    Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.;Brigham & Womens Hosp, Dept Med, Div Prevent Med, Boston, MA 02115 USA.;Harvard Univ, Sch Med, Boston, MA USA.;Brigham & Womens Hosp, Dept Med, Div Aging, Boston, MD 02115 USA.;Harvard Univ, Sch Med, Boston, MD USA..
    Setiawan, Veronica Wendy
    Univ So Calif, Dept Prevent Med, USC Keck Sch Med, Los Angeles, CA 90089 USA..
    Severi, Gianluca
    Canc Council Victoria, Canc Epidemiol Ctr, Melbourne, Vic, Australia.;Univ Melbourne, Melbourne Sch Populat & Global Hlth, Ctr Biostat & Epidemiol, Carlton, Vic 3053, Australia.;Human Genet Fdn, Turin, Italy..
    Severson, Richard K.
    Wayne State Univ, Dept Family Med & Publ Hlth Sci, Detroit, MI USA. Karmanos Canc Inst, Detroit, MI USA..
    Shanafelt, Tait D.
    Mayo Clin, Dept Med, Rochester, MN USA..
    Shen, Hongbing
    Nanjing Med Univ, Jiangsu Collaborat Innovat Ctr Canc Personalized, Nanjing, Jiangsu, Peoples R China.;Nanjing Med Univ, Sch Publ Hlth, Ctr Canc, Jiangsu Key Lab Canc Biomarkers Prevent & Treatme, Nanjing, Jiangsu, Peoples R China..
    Shen, Wei
    Nanjing Med Univ, Jiangsu Collaborat Innovat Ctr Canc Personalized, Nanjing, Jiangsu, Peoples R China.;Nanjing Med Univ, Sch Publ Hlth, Ctr Canc, Jiangsu Key Lab Canc Biomarkers Prevent & Treatme, Nanjing, Jiangsu, Peoples R China..
    Shin, Min-Ho
    Chonnam Natl Univ, Sch Med, Dept Prevent Med, Gwangju, South Korea..
    Shiraishi, Kouya
    Shu, Xiao-Ou
    Vanderbilt Univ, Ctr Med, Dept Med, Nashville, TN 37232 USA.;Vanderbilt Univ, Med Ctr, Vanderbilt Ingram Canc Ctr, Nashville, TN USA..
    Siddiq, Afshan
    Univ London Imperial Coll Sci Technol & Med, Sch Publ Hlth, London, England..
    Sierrasesumaga, Luis
    Univ Navarra, Univ Navarra Clin, Dept Pediat, Pamplona, Spain..
    Sihoe, Alan Dart Loon
    Queen Mary Hosp, Div Cardiothorac Surg, Dept Surg, Hong Kong, Hong Kong, Peoples R China. Univ Melbourne, Dept Pathol, Parkville, Vic 3052, Australia..
    Skibola, Christine F.
    Univ Alabama Birmingham, Sch Publ Hlth, Dept Epidemiol, Birmingham, AL 35294 USA.;Univ Alabama Birmingham, Ctr Comprehens Canc, Birmingham, AL 35294 USA.;Univ Calif Berkeley, Sch Publ Hlth, Div Environm Hlth Sci, Berkeley, CA 94720 USA.;BC Canc Agcy, Ctr Lymphoid Canc, Vancouver, BC, Canada..
    Smith, Alex
    Univ York, Dept Hlth Sci, York YO10 5DD, N Yorkshire, England..
    Smith, Martyn T.
    Univ Calif Berkeley, Sch Publ Hlth, Div Environm Hlth Sci, Berkeley, CA 94720 USA.;BC Canc Agcy, Ctr Lymphoid Canc, Vancouver, BC, Canada..
    Southey, Melissa C.
    Spinelli, John J.
    BC Canc Agcy, Canc Control Res, Vancouver, BC, Canada.;Univ British Columbia, Sch Populat & Publ Hlth, Vancouver, BC V5Z 1M9, Canada..
    Staines, Anthony
    Dublin City Univ, Sch Nursing & Human Sci, Dublin 9, Ireland..
    Stampfer, Meir
    Brigham & Womens Hosp, Dept Med, Channing Div Network Med, Boston, MA 02115 USA.;Harvard Univ, Sch Med, Boston, MA 02115 USA.;Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.;Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA..
    Stern, Marianna C.
    Stevens, Victoria L.
    Amer Canc Soc, Epidemiol Res Program, Atlanta, GA 30329 USA..
    Stolzenberg-Solomon, Rachael S.
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Su, Jian
    Guangdong Acad Med Sci, Guangdong Gen Hosp, Guangdong Prov Key Lab Translat Med Lung Canc, Guangdong Lung Canc Inst, Guangzhou, Guangdong, Peoples R China..
    Su, Wu-Chou
    Natl Cheng Kung Univ, Med Coll & Hosp, Tainan 701, Taiwan..
    Sund, Malin
    Umea Univ, Dept Surg & Perioperat Sci, Surg, Umea, Sweden..
    Sung, Jae Sook
    Korea Univ, Canc Res Inst, Seoul, South Korea..
    Sung, Sook Whan
    Seoul St Marys Hosp, Dept Thorac & Cardiovasc Surg, Seoul, South Korea..
    Tan, Wen
    Chinese Acad Med Sci, Canc Inst & Hosp, Dept Etiol & Carcinogenesis, Beijing 100730, Peoples R China.;Peking Union Med Coll, Beijing 100021, Peoples R China..
    Tang, Wei
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Tardon, Adonina
    Ctr Invest Biomed Red Epidemiol Salud Publ CIBERE, Madrid, Spain.;Univ Oviedo, Inst Univ Oncol, Oviedo, Spain..
    Thomas, David
    St Vincents Hosp, Garvan Inst Med Res, Kinghorn Canc Ctr, Darlinghurst, NSW 2010, Australia..
    Thompson, Carrie A.
    Mayo Clin, Dept Med, Rochester, MN USA..
    Tinker, Lesley F.
    Tirabosco, Roberto
    Royal Natl Orthopaed Hosp NHS Trust, Middlesbrough, Cleveland, England..
    Tjonneland, Anne
    Danish Canc Soc, Res Ctr, Copenhagen, Denmark..
    Travis, Ruth C.
    Univ Oxford, Canc Epidemiol Unit, Oxford, England..
    Trichopoulos, Dimitrios
    Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.;Acad Athens, Bur Epidemiol Res, Athens, Greece.;Hellen Hlth Fdn, Athens, Greece..
    Tsai, Fang-Yu
    Natl Hlth Res Inst, Natl Inst Canc Res, Zhunan, Taiwan..
    Tsai, Ying-Huang
    Chang Gung Mem Hosp, Dept Resp Thearpy, Chiayi, Taiwan..
    Tucker, Margaret
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Turner, Jenny
    Macquarie Univ, Australian Sch Adv Med, Sydney, NSW 2109, Australia.;Douglass Hanly Moir Pathol, Dept Histopathol, Macquarie Pk, NSW, Australia..
    Vajdic, Claire M.
    Univ New S Wales, Prince Wales Clin Sch, Sydney, NSW, Australia..
    Vermeulen, Roel C. H.
    Univ Med Ctr Utrecht, Julius Ctr Hlth Sci & Primary Care 194, Utrecht, Netherlands.;Univ Utrecht, Inst Risk Assessment Sci, Utrecht, Netherlands..
    Villano, Danylo J.
    Mem Sloan Kettering Canc Ctr, Dept Med, New York, NY 10021 USA..
    Vineis, Paolo
    Univ London Imperial Coll Sci Technol & Med, Sch Publ Hlth, MRC PHE Ctr Environm & Hlth, London, England.;Human Genet Fdn, Turin, Italy..
    Virtamo, Jarmo
    Mem Sloan Kettering Canc Ctr, Dept Med, New York, NY 10021 USA.;Natl Inst Hlth & Welf, Dept Chron Dis Prevent, Helsinki, Finland..
    Visvanathan, Kala
    Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA..
    Wactawski-Wende, Jean
    China Med Univ, Sch Publ Hlth, Dept Epidemiol, Shenyang 110001, Peoples R China.;SUNY Buffalo, Dept Social & Prevent Med, Buffalo, NY 14260 USA..
    Wang, Chaoyu
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Wang, Chih-Liang
    Chang Gung Mem Hosp, Dept Pulm & Crit Care, Taoyuan, Taiwan..
    Wang, Jiu-Cun
    Fudan Univ, Sch Life Sci, Minist Educ, Key Lab Contemporary Anthropol, Shanghai 200433, Peoples R China.;Fudan Univ, Sch Life Sci, State Key Lab Genet Engn, Shanghai, Peoples R China..
    Wang, Junwen
    Univ Hong Kong, Li Ka Shing Fac Med, Ctr Genom Sci, Hong Kong, Peoples R China.;Univ Hong Kong, Li Ka Shing Fac Med, Dept Biochem, Hong Kong, Hong Kong, Peoples R China..
    Wei, Fusheng
    China Natl Environm Monitoring Ctr, Beijing, Peoples R China..
    Weiderpass, Elisabete
    Karolinska Inst, Dept Med Epidemiol & Biostatist, Stockholm, Sweden.;Univ Tromso, Arctic Univ Norway, Fac Hlth Sci, Dept Community Med, Tromso, Norway. Spanish Natl Canc Res Ctr CNIO, Genet & Mol Epidemiol Grp, Madrid, Spain.;Canc Registry Norway, Oslo, Norway.;Folkhalsan Res Ctr, Dept Genet Epidemiol, Helsinki, Finland..
    Weiner, George J.
    Univ Iowa, Carver Coll Med, Dept Internal Med, Iowa City, IA USA..
    Weinstein, Stephanie
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Wentzensen, Nicolas
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    White, Emily
    Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA..
    Witzig, Thomas E.
    Mayo Clin, Dept Med, Rochester, MN USA..
    Wolpin, Brian M.
    Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.;Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.;Harvard Univ, Sch Med, Boston, MA USA..
    Wong, Maria Pik
    Univ Hong Kong, Li Ka Shing Fac Med, Dept Pathol, Hong Kong, Hong Kong, Peoples R China..
    Wu, Chen
    Chinese Acad Med Sci, Canc Inst & Hosp, Dept Etiol & Carcinogenesis, Beijing 100730, Peoples R China.;Peking Union Med Coll, Beijing 100021, Peoples R China.;Chinese Acad Med Sci, Canc Inst & Hosp, State Key Lab Mol Oncol, Beijing 100730, Peoples R China.;Peking Union Med Coll, Beijing 100021, Peoples R China..
    Wu, Guoping
    China Natl Environm Monitoring Ctr, Beijing, Peoples R China..
    Wu, Junjie
    Fudan Univ, Sch Life Sci, Minist Educ, Key Lab Contemporary Anthropol, Shanghai 200433, Peoples R China..
    Wu, Tangchun
    Huazhong Univ Sci & Technol, Sch Publ Hlth, Inst Occupat Med, Wuhan 430074, Peoples R China.;Huazhong Univ Sci & Technol, Sch Publ Hlth, Minist Educ, Key Lab Environm & Hlth, Wuhan 430074, Peoples R China..
    Wu, Wei
    Wu, Xifeng
    Univ Texas MD Anderson Canc Ctr, Dept Epidemiol, Houston, TX 77030 USA..
    Wu, Yi-Long
    Guangdong Acad Med Sci, Guangdong Gen Hosp, Guangdong Prov Key Lab Translat Med Lung Canc, Guangdong Lung Canc Inst, Guangzhou, Guangdong, Peoples R China..
    Wunder, Jay S.
    Univ Toronto, Litwin Ctr Canc Genet, Toronto, ON, Canada.;Mt Sinai Hosp, Lunenfeld Tanenbaum Res Inst, Toronto, ON M5G 1X5, Canada..
    Xiang, Yong-Bing
    Shanghai Jiao Tong Univ, Sch Med, Renji Hosp, Shanghai Canc Inst, Shanghai 200030, Peoples R China..
    Xu, Jun
    Univ Hong Kong, Sch Publ Hlth, Hong Kong, Hong Kong, Peoples R China..
    Xu, Ping
    Wuhan Iron & Steel Corp Staff Worker Hosp, Dept Oncol, Wuhan, Peoples R China..
    Yang, Pan-Chyr
    Natl Taiwan Univ, Coll Med, Dept Internal Med, Taipei, Taiwan..
    Yang, Tsung-Ying
    Taichung Vet Gen Hosp, Div Chest Med, Dept Internal Med, Taichung, Taiwan..
    Ye, Yuanqing
    Univ Texas MD Anderson Canc Ctr, Dept Epidemiol, Houston, TX 77030 USA..
    Yin, Zhihua
    China Med Univ, Sch Publ Hlth, Dept Epidemiol, Shenyang 110001, Peoples R China..
    Yokota, Jun
    Inst Predict & Personalized Med Canc IMPPC, Barcelona, Spain..
    Yoon, Ho-Il
    Seoul Natl Univ, Bundang Hosp, Dept Internal Med, Songnam, South Korea..
    Yu, Chong-Jen
    Natl Taiwan Univ Hosp, Dept Internal Med, Taipei 100, Taiwan..
    Yu, Herbert
    Univ Hawaii, Ctr Canc, Canc Epidemiol Program, Honolulu, HI 96822 USA. Stanford Univ, Lucile Packard Childrens Hosp, Palo Alto, CA 94304 USA..
    Yu, Kai
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Yuan, Jian-Min
    Univ Pittsburgh, Inst Canc, Pittsburgh, PA USA. Georgetown Univ, Med Ctr, Innovat Ctr Biomed Informat, Washington, DC USA. Georgetown Univ, Med Ctr, Dept Oncol, Washington, DC 20007 USA..
    Zelenetz, Andrew
    NYU, Sch Med, Dept Environm Med, New York, NY USA.;NYU, Sch Med, Dept Populat Hlth, New York, NY USA.;NYU Langone, Med Ctr, Perlmutter Canc Ctr, New York, NY USA.;Mem Sloan Kettering Canc Ctr, Dept Med, New York, NY 10021 USA..
    Zeleniuch-Jacquotte, Anne
    Zhang, Xu-Chao
    Guangdong Acad Med Sci, Guangdong Gen Hosp, Guangdong Prov Key Lab Translat Med Lung Canc, Guangdong Lung Canc Inst, Guangzhou, Guangdong, Peoples R China..
    Zhang, Yawei
    Yale Sch Publ Hlth, Dept Environm Hlth Sci, New Haven, CT USA. German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Baden Wurttembe, Germany..
    Zhao, Xueying
    Fudan Univ, Sch Life Sci, Minist Educ, Key Lab Contemporary Anthropol, Shanghai 200433, Peoples R China..
    Zhao, Zhenhong
    Fudan Univ, Sch Life Sci, Minist Educ, Key Lab Contemporary Anthropol, Shanghai 200433, Peoples R China..
    Zheng, Hong
    Med Univ, Canc Inst & Hosp, Natl Clin Res Ctr Canc, Key Lab Canc Prevent & Therapy,Dept Epidemiol & B, Tianjin, Peoples R China..
    Zheng, Tongzhang
    Yale Sch Publ Hlth, Dept Environm Hlth Sci, New Haven, CT USA. German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Baden Wurttembe, Germany..
    Zheng, Wei
    Vanderbilt Univ, Ctr Med, Dept Med, Nashville, TN 37232 USA.;Vanderbilt Univ, Med Ctr, Vanderbilt Ingram Canc Ctr, Nashville, TN USA..
    Zhou, Baosen
    China Med Univ, Sch Publ Hlth, Dept Epidemiol, Shenyang 110001, Peoples R China..
    Zhu, Meng
    Zucca, Mariagrazia
    Boca, Simina M.
    Cerhan, James R.
    Mayo Clin, Dept Hlth Sci Res, Rochester, MN USA..
    Ferri, Giovanni M.
    Univ Bari, Interdisciplinary Dept Med, Bari, Italy..
    Hartge, Patricia
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Hsiung, Chao Agnes
    Magnani, Corrado
    Univ Piemonte Orientale, Dept Translat Med, CPO Piemonte & Unit Med Stat & Epidemiol, Novara, Italy..
    Miligi, Lucia
    Morton, Lindsay M.
    Smedby, Karin E.
    Karolinska Univ Hosp, Karolinska Inst, Dept Med, Stockholm, Sweden..
    Teras, Lauren R.
    Vijai, Joseph
    Wang, Sophia S.
    Beckman Res Inst City Hope, Dept Canc Etiol, Duarte, CA USA..
    Brennan, Paul
    Int Agcy Res Canc, F-69372 Lyon, France..
    Caporaso, Neil E.
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Hunter, David J.
    Brigham & Womens Hosp, Dept Med, Channing Div Network Med, Boston, MA 02115 USA.;Harvard Univ, Sch Med, Boston, MA 02115 USA.;Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.;Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.;Broad Inst Harvard, Cambridge, MA USA.;MIT, Cambridge, MA 02139 USA..
    Kraft, Peter
    Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.;Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA..
    Rothman, Nathaniel
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Silverman, Debra T.
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Slager, Susan L.
    Mayo Clin, Dept Hlth Sci Res, Rochester, MN USA..
    Chanock, Stephen J.
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Chatterjee, Nilanjan
    NCI, Div Canc Epidemiol & Genet, Bethesda, MD USA..
    Analysis of Heritability and Shared Heritability Based on Genome-Wide Association Studies for 13 Cancer Types2015In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 107, no 12, article id djv279Article in journal (Refereed)
    Abstract [en]

    Background: Studies of related individuals have consistently demonstrated notable familial aggregation of cancer. We aim to estimate the heritability and genetic correlation attributable to the additive effects of common single-nucleotide polymorphisms (SNPs) for cancer at 13 anatomical sites. Methods: Between 2007 and 2014, the US National Cancer Institute has generated data from genome-wide association studies (GWAS) for 49 492 cancer case patients and 34 131 control patients. We apply novel mixed model methodology (GCTA) to this GWAS data to estimate the heritability of individual cancers, as well as the proportion of heritability attributable to cigarette smoking in smoking-related cancers, and the genetic correlation between pairs of cancers. Results: GWAS heritability was statistically significant at nearly all sites, with the estimates of array-based heritability, h(l)(2), on the liability threshold (LT) scale ranging from 0.05 to 0.38. Estimating the combined heritability of multiple smoking characteristics, we calculate that at least 24% (95% confidence interval [CI] = 14% to 37%) and 7% (95% CI = 4% to 11%) of the heritability for lung and bladder cancer, respectively, can be attributed to genetic determinants of smoking. Most pairs of cancers studied did not show evidence of strong genetic correlation. We found only four pairs of cancers with marginally statistically significant correlations, specifically kidney and testes (rho = 0.73, SE = 0.28), diffuse large B-cell lymphoma (DLBCL) and pediatric osteosarcoma (rho = 0.53, SE = 0.21), DLBCL and chronic lymphocytic leukemia (CLL) (rho = 0.51, SE = 0.18), and bladder and lung (rho = 0.35, SE = 0.14). Correlation analysis also indicates that the genetic architecture of lung cancer differs between a smoking population of European ancestry and a nonsmoking Asian population, allowing for the possibility that the genetic etiology for the same disease can vary by population and environmental exposures. Conclusion: Our results provide important insights into the genetic architecture of cancers and suggest new avenues for investigation.

  • 26. Sclafani, Francesco
    et al.
    Gonzalez, David
    Cunningham, David
    Wilson, Sanna Hulkki
    Peckitt, Clare
    Tabernero, Josep
    Glimelius, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Radiology, Oncology and Radiation Science, Oncology.
    Cervantes, Andres
    Dewdney, Alice
    Wotherspoon, Andrew
    Brown, Gina
    Tait, Diana
    Oates, Jacqueline
    Chau, Ian
    TP53 Mutational Status and Cetuximab Benefit in Rectal Cancer: 5-Year Results of the EXPERT-C Trial2014In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 106, no 7, p. dju121-Article in journal (Refereed)
    Abstract [en]

    In this updated analysis of the EXPERT-C trial we show that, in magnetic resonance imaging-defined, high-risk, locally advanced rectal cancer, adding cetuximab to a treatment strategy with neoadjuvant CAPOX followed by chemoradiotherapy, surgery, and adjuvant CAPOX is not associated with a statistically significant improvement in progression-free survival (PFS) and overall survival (OS) in both KRAS/BRAF wild-type and unselected patients. In a retrospective biomarker analysis, TP53 was not prognostic but emerged as an independent predictive biomarker for cetuximab benefit. After a median follow-up of 65.0 months, TP53 wild-type patients (n = 69) who received cetuximab had a statistically significant better PFS (89.3% vs 65.0% at 5 years; hazard ratio [HR] = 0.23; 95% confidence interval [CI] = 0.07 to 0.78; two-sided P = .02 by Cox regression) and OS (92.7% vs 67.5% at 5 years; HR = 0.16; 95% CI = 0.04 to 0.70; two-sided P = .02 by Cox regression) than TP53 wild-type patients who were treated in the control arm. An interaction between TP53 status and cetuximab effect was found (P < .05) and remained statistically significant after adjusting for statistically significant prognostic factors and KRAS.

  • 27. Smedby, Karin Ekström
    et al.
    Hjalgrim, Henrik
    Askling, Johan
    Chang, Ellen T.
    Gregersen, Henrik
    Porwit-MacDonald, Anna
    Sundström, Christer
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology.
    Åkerman, Måns
    Melbye, Mads
    Glimelius, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology.
    Adami, Hans-Olov
    Autoimmune and chronic inflammatory disorders and risk of non-Hodgkin lymphoma by subtype2006In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 98, no 1, p. 51-60Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Some autoimmune and chronic inflammatory disorders are associated with increased risks of non-Hodgkin lymphoma (NHL). Because different NHL subtypes develop at different stages of lymphocyte differentiation, associations of autoimmune and inflammatory disorders with specific NHL subtypes could lead to a better understanding of lymphomagenic mechanisms. METHODS: In a population-based case-control study in Denmark and Sweden, 3055 NHL patients and 3187 matched control subjects were asked about their history of autoimmune and chronic inflammatory disorders, markers of severity, and treatment. Logistic regression with adjustment for study matching factors was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs) for NHL overall and for NHL subtypes. RESULTS: Risks of all NHL were increased in association with rheumatoid arthritis (OR = 1.5, 95% CI = 1.1 to 1.9), primary Sjögren syndrome (OR = 6.1, 95% CI = 1.4 to 27), systemic lupus erythematosus (OR = 4.6, 95% CI = 1.0 to 22), and celiac disease (OR = 2.1, 95% CI = 1.0 to 4.8). All of these conditions were also associated with diffuse large B-cell lymphoma, and some were associated with marginal zone, lymphoplasmacytic, or T-cell lymphoma. Ever use of nonsteroidal anti-inflammatory drugs, systemic corticosteroids, and selected immunosuppressants was associated with risk of NHL in rheumatoid arthritis patients but not in subjects without rheumatoid arthritis. Also, multivariable adjustment for treatment had little impact on risk estimates. Psoriasis, sarcoidosis, and inflammatory bowel disorders were not associated with increased risk of NHL overall or of any NHL subtype. CONCLUSIONS: Our results confirm the associations between certain autoimmune disorders and risk of NHL and suggest that the associations may not be general but rather mediated through specific NHL subtypes. These NHL subtypes develop during postantigen exposure stages of lymphocyte differentiation, consistent with a role of antigenic drive in autoimmunity-related lymphomagenesis.

  • 28. Smedby, Karin Ekström
    et al.
    Hjalgrim, Henrik
    Melbye, Mads
    Torrång, Anna
    Rostgaard, Klaus
    Munksgaard, Lars
    Adami, Johanna
    Hansen, Mads
    Porwit-MacDonald, Anna
    Jensen, Bjarne Anker
    Roos, Göran
    Pedersen, Bjarne Bach
    Sundström, Christer
    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.
    Adami, Hans-Olov
    Ultraviolet radiation exposure and risk of malignant lymphomas2005In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 97, no 3, p. 199-209Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The incidence of malignant lymphomas has been increasing rapidly, but the causes of these malignancies remain poorly understood. One hypothesis holds that exposure to ultraviolet (UV) radiation increases lymphoma risk. We tested this hypothesis in a population-based case-control study in Denmark and Sweden. METHODS: A total of 3740 patients diagnosed between October 1, 1999, and August 30, 2002, with incident malignant lymphomas, including non-Hodgkin lymphoma, chronic lymphocytic leukemia, and Hodgkin lymphoma, and 3187 population controls provided detailed information on history of UV exposure and skin cancer and information on other possible risk factors for lymphomas. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated by logistic regression. Statistical tests were two-sided. RESULTS: Multivariable-adjusted analyses revealed consistent, statistically significant negative associations between various measures of UV light exposure and risk of non-Hodgkin lymphoma. A high frequency of sun bathing and sunburns at age 20 years and 5-10 years before the interview and sun vacations abroad were associated with 30%-40% reduced risks of non-Hodgkin lymphoma (e.g., for sunbathing four times a week or more at age 20 versus never sunbathing, OR = 0.7, 95% CI = 0.6 to 0.9; for two or more sunburns a year at age 20 versus no sunburns, OR = 0.6, 95% CI = 0.5 to 0.8). These inverse associations increased in strength with increasing levels of exposure (all P(trend)< or =.01). Similar, albeit weaker, associations were observed for Hodgkin lymphoma. There were no clear differences among non-Hodgkin lymphoma subtypes, although associations were stronger for B-cell than for T-cell lymphomas. A history of skin cancer was associated with a doubling in risks of both non-Hodgkin and Hodgkin lymphoma. CONCLUSIONS: A history of high UV exposure was associated with reduced risk of non-Hodgkin lymphoma. The positive association between skin cancer and malignant lymphomas is, therefore, unlikely to be mediated by UV exposure.

  • 29. Stattin, P.
    et al.
    Garmo, H.
    Steineck, G.
    Bill-Axelson, Anna
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Urology.
    Re: Immediate Risk of Suicide and Cardiovascular Death After a Prostate Cancer Diagnosis: Cohort Study in the United States2010In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 102, no 18, p. 1447-1448Article in journal (Refereed)
  • 30. Stattin, Pär
    et al.
    Carlsson, Sigrid
    Holmström, Benny
    Vickers, Andrew
    Hugosson, Jonas
    Lilja, Hans
    Jonsson, Håkan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Orthopaedics.
    Prostate cancer mortality in areas with high and low prostate cancer incidence.2014In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 106, no 3, p. dju007-Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The effect of prostate-specific antigen (PSA) screening on prostate cancer mortality remains debated, despite evidence from randomized trials. We investigated the association between prostate cancer incidence, reflecting uptake of PSA testing, and prostate cancer mortality.

    METHODS: The study population consisted of all men aged 50 to 74 years residing in eight counties in Sweden with an early increase in prostate cancer incidence and six counties with a late increase during two time periods. Incidence of metastatic prostate cancer was investigated in the period from 2000 to 2009, and prostate cancer-specific mortality and excess mortality were investigated in the period from 1990 to 1999 and the period from 2000 to 2009 by calculating rate ratios for high- vs low-incidence counties and rate ratios for the period from 2000 to 2009 vs the period from 1990 to 1999 within these two groups. All statistical tests were two-sided.

    RESULTS: There were 4528134 person-years at risk, 1577 deaths from prostate cancer, and 1210 excess deaths in men with prostate cancer in high-incidence counties and 2471373 person-years at risk, 985 prostate cancer deaths, and 878 excess deaths in low-incidence counties in the period from 2000 to 2009. Rate ratios in counties with high vs low incidence adjusted for time period were 0.81 (95% confidence interval [CI] = 0.73 to 0.90) for prostate cancer- specific mortality and 0.74 (95% CI = 0.64 to 0.86) for excess mortality, and the rate ratio of metastatic prostate cancer was 0.85 (95% CI = 0.79 to 0.92).

    CONCLUSIONS: The lower prostate cancer mortality in high-incidence counties reflecting a high PSA uptake suggests that more-intense as compared with less-intense opportunistic PSA screening reduces prostate cancer mortality.

  • 31. Stattin, Pär
    et al.
    Holmberg, Erik
    Johansson, Jan-Erik
    Holmberg, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Endocrine Surgery.
    Adolfsson, Jan
    Hugosson, Jonas
    Outcomes in localized prostate cancer: National Prostate Cancer Register of Sweden follow-up study2010In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 102, no 13, p. 950-958Article in journal (Refereed)
    Abstract [en]

    BACKGROUND:

    Treatment for localized prostate cancer remains controversial. To our knowledge, there are no outcome studies from contemporary population-based cohorts that include data on stage, Gleason score, and serum levels of prostate-specific antigen (PSA).

    METHODS:

    In the National Prostate Cancer Register of Sweden Follow-up Study, a nationwide cohort, we identified 6849 patients aged 70 years or younger. Inclusion criteria were diagnosis with local clinical stage T1-2 prostate cancer from January 1, 1997, through December 31, 2002, a Gleason score of 7 or less, a serum PSA level of less than 20 ng/mL, and treatment with surveillance (including active surveillance and watchful waiting, n = 2021) or curative intent (including radical prostatectomy, n = 3399, and radiation therapy, n = 1429). Among the 6849 patients, 2686 had low-risk prostate cancer (ie, clinical stage T1, Gleason score 2-6, and serum PSA level of <10 ng/mL). The study cohort was linked to the Cause of Death Register, and cumulative incidence of death from prostate cancer and competing causes was calculated.

    RESULTS:

    For the combination of low- and intermediate-risk prostate cancers, calculated cumulative 10-year prostate cancer-specific mortality was 3.6% (95% confidence interval [CI] = 2.7% to 4.8%) in the surveillance group and 2.7% (95% CI = 2.1% to 3.45) in the curative intent group. For those with low-risk disease, the corresponding values were 2.4% (95% CI = 1.2% to 4.1%) among the 1085 patients in the surveillance group and 0.7% (95% CI = 0.3% to 1.4%) among the 1601 patients in the curative intent group. The 10-year risk of dying from competing causes was 19.2% (95% CI = 17.2% to 21.3%) in the surveillance group and 10.2% (95% CI = 9.0% to 11.4%) in the curative intent group.

    CONCLUSION:

    A 10-year prostate cancer-specific mortality of 2.4% among patients with low-risk prostate cancer in the surveillance group indicates that surveillance may be a suitable treatment option for many patients with low-risk disease.

  • 32. Terry, Paul
    et al.
    Giovannucci, Edward
    Michels, Karin B.
    Bergkvist, Leif
    Hansen, Holger
    Holmberg, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences.
    Wolk, Alicja
    Fruit, vegetables, dietary fiber, and risk of colorectal cancer2001In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 93, no 7, p. 525-533Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Several recent large prospective cohort studies have failed to demonstrate the presumed protective effect of fruit, vegetable, and dietary fiber consumption on colorectal cancer risk. To further explore this issue, we have examined these associations in a population that consumes relatively low amounts of fruit and vegetables and high amounts of cereals. METHODS: We examined data obtained from a food-frequency questionnaire used in a population-based prospective mammography screening study of women in central Sweden. Women with colorectal cancer diagnosed through December 31, 1998, were identified by linkage to regional cancer registries. Cox proportional hazards models were used to estimate relative risks. All statistical tests were two-sided. RESULTS: During an average 9.6 years of follow-up of 61 463 women, we observed 460 incident cases of colorectal cancer (291 colon cancers, 159 rectal cancers, and 10 cancers at both sites). In the entire study population, total fruit and vegetable consumption was inversely associated with colorectal cancer risk. Subanalyses showed that this association was due largely to fruit consumption. The association was stronger, however, and the dose-response effect was more evident among individuals who consumed the lowest amounts of fruit and vegetables. Individuals who consumed less than 1.5 servings of fruit and vegetables per day had a relative risk for developing colorectal cancer of 1.65 (95% confidence interval = 1.23 to 2.20; P(trend) =.001) compared with individuals who consumed more than 2.5 servings. We observed no association between colorectal cancer risk and the consumption of cereal fiber, even at amounts substantially greater than previously examined, or of non-cereal fiber. CONCLUSIONS: Individuals who consume very low amounts of fruit and vegetables have the greatest risk of colorectal cancer. Relatively high consumption of cereal fiber does not appear to lower the risk of colorectal cancer.

  • 33. Thrift, Aaron P
    et al.
    Shaheen, Nicholas J
    Gammon, Marilie D
    Bernstein, Leslie
    Reid, Brian J
    Onstad, Lynn
    Risch, Harvey A
    Liu, Geoffrey
    Bird, Nigel C
    Wu, Anna H
    Corley, Douglas A
    Romero, Yvonne
    Chanock, Stephen J
    Chow, Wong-Ho
    Casson, Alan G
    Levine, David M
    Zhang, Rui
    Ek, Weronica E
    MacGregor, Stuart
    Ye, Weimin
    Hardie, Laura J
    Vaughan, Thomas L
    Whiteman, David C
    Obesity and risk of esophageal adenocarcinoma and Barrett's esophagus: a Mendelian randomization study.2014In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 106, no 11Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Data from observational studies suggest that body mass index (BMI) is causally related to esophageal adenocarcinoma (EAC) and its precursor, Barrett's esophagus (BE). However, the relationships may be affected by bias and confounding.

    METHODS: We used data from the Barrett's and Esophageal Adenocarcinoma Genetic Susceptibility Study: 999 patients with EAC, 2061 patients with BE, and 2169 population controls. We applied the two-stage control function instrumental variable method of the Mendelian randomization approach to estimate the unbiased, unconfounded effect of BMI on risk of EAC and BE. This was performed using a genetic risk score, derived from 29 genetic variants shown to be associated with BMI, as an instrument for lifetime BMI. A higher score indicates propensity to obesity. All tests were two-sided.

    RESULTS: The genetic risk score was not associated with potential confounders, including gastroesophageal reflux symptoms and smoking. In the instrumental variable analyses (IV), EAC risk increased by 16% (IV-odds ratio [OR] = 1.16, 95% confidence interval [CI] = 1.01 to 1.33) and BE risk increased by 12% (IV-OR = 1.12, 95% CI = 1.00 to 1.25) per 1kg/m(2) increase in BMI. BMI was statistically significantly associated with EAC and BE in conventional epidemiologic analyses.

    CONCLUSIONS: People with a high genetic propensity to obesity have higher risks of esophageal metaplasia and neoplasia than people with low genetic propensity. These analyses provide the strongest evidence to date that obesity is independently associated with BE and EAC, and is not due to confounding or bias inherent in conventional epidemiologic analyses.

  • 34. Travis, L. B.
    et al.
    Curtis, R. E.
    Glimelius, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology.
    Holowaty, E. J.
    van Leeuwen, F. E.
    Lynch, C. F.
    Hagenbeek, A.
    Stovall, M.
    Banks, P. M.
    Adami, Johanna
    Gospodarowicz, M.
    Wacholder, S.
    Inskip, P.
    Tucker, M.
    Boice, J.
    Bladder and kidney cancer following cyclophosphamide therapy for non-Hodgkin´s lymphoma1995In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 87, no 7, p. 524-530Article, book review (Other academic)
    Abstract [en]

    BACKGROUND: Cyclophosphamide is an established bladder carcinogen, but few studies have examined the relationship between dose and effect. The largest analysis to date included only seven cases of bladder cancer. No investigation has estimated the risk of kidney cancer. PURPOSE: The purpose of this study was to quantify the risk of bladder and kidney cancer following cyclophosphamide therapy. METHODS: Within a cohort of 6171 two-year survivors of non-Hodgkin's lymphoma (NHL), 48 patients with secondary cancer of the urinary tract were identified and matched to 136 control subjects with NHL who did not develop a second malignancy. Detailed information on chemotherapeutic drugs and cumulative dose received was collected for all subjects. Radiation dose to the target organ was estimated from individual radiotherapy records. Evaluations of the risk of second cancer as a result of treatment with cyclophosphamide alone, radiation alone, or both therapies were made relative to those patients who were exposed to neither treatment modality. RESULTS: A significant 4.5-fold risk of bladder cancer (95% confidence interval [CI] = 1.5-13.6) followed therapy with cyclophosphamide, and risk was dependent upon cumulative dose. Among patients who received a total amount of cyclophosphamide of less than 20 g, a nonsignificant 2.4-fold risk of bladder cancer was apparent. Significantly elevated sixfold (95% CI = 1.3-29) and 14.5-fold (95% CI = 2.3-94) risks of bladder malignancy followed cumulative doses of 20-49 g and 50 g or more, respectively (P value for trend = .004). Radiotherapy given without cyclophosphamide was associated with a nonsignificant increased risk of bladder malignancy. Excess bladder cancer risk following treatment with both radiotherapy and cyclophosphamide was as expected if individual risks were summed. Neither radiotherapy nor cyclophosphamide was associated with excesses of kidney cancer. CONCLUSIONS: Cyclophosphamide-related bladder cancer is dose dependent. For patients given cumulative doses between 20 and 49 g, the absolute risk of bladder cancer is on the order of three excess cancers per 100 NHL patients after 15 years of follow-up. At cumulative doses of 50 g or more, the excess risk increases to approximately seven excess bladder cancers per 100 NHL patients. IMPLICATIONS: The strong dose-response relationship and high absolute risk of bladder cancer underscore the importance of limiting the cumulative dose of cyclophosphamide to what is required to achieve therapeutic end points. The risk of secondary bladder malignancy and other late sequelae of therapy must be carefully weighted against the curative gains provided by cyclophosphamide. Moreover, long-term side effects of therapy that might be acceptable in cancer treatment may need to be re-evaluated for patients with non-neoplastic disorders.

  • 35.
    Travis, Lois B
    et al.
    National Cancer Institute, USA.
    Gospodarowicz, Mary
    Canada.
    Curtis, Rochelle E
    National Cancer Institute, USA.
    Clarke, E Aileen
    Toronto.
    Andersson, Michael
    Denmark.
    Glimelius, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Radiology, Oncology and Radiation Science, Oncology.
    Joensuu, Timo
    Finland.
    Lynch, Charles F
    Iowa.
    van Leeuwen, Flora E
    The Netherlands.
    Holowaty, Eric
    Toronto.
    Storm, Hans
    Denmark.
    Glimelius, Ingrid
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Radiology, Oncology and Radiation Science. Karolinska Institutet.
    Pukkala, Eero
    Finland.
    Stovall, Marilyn
    Houston.
    Fraumeni, Joseph F
    National Cancer Institute, USA.
    Boice, John D
    USA.
    Gilbert, Ethel
    National Cancer Institute, USA.
    Lung cancer following chemotherapy and radiotherapy for Hodgkin's disease2002In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 94, no 3, p. 182-192Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Lung cancer is a frequent cause of death in patients cured of Hodgkin's disease, but the contributions of chemotherapy, radiotherapy, and smoking are not well described. We quantified the risk of treatment-associated lung cancer, taking into account tobacco use.

    METHODS: Within a population-based cohort of 19 046 Hodgkin's disease patients (diagnosed from 1965 through 1994), a case-control study of lung cancer was conducted. The cumulative amount of cytotoxic drugs, the radiation dose to the specific location in the lung where cancer developed, and tobacco use were compared for 222 patients who developed lung cancer and for 444 matched control patients. All statistical tests were two-sided.

    RESULTS: Treatment with alkylating agents without radiotherapy was associated with increased lung cancer risk (relative risk [RR] = 4.2; 95% confidence interval [CI] = 2.1 to 8.8), as was radiation dose of 5 Gy or more without alkylating agents (RR = 5.9; 95% CI = 2.7 to 13.5). Risk increased with both increasing number of cycles of alkylating agents and increasing radiation dose (P for trend <.001). Among patients treated with mechlorethamine, vincristine, procarbazine, and prednisone (MOPP), risk increased with cumulative amounts of mechlorethamine and procarbazine (P<.001) when evaluated separately. Statistically significantly elevated risks of lung cancer were apparent within 1-4 years after treatment with alkylating agents, whereas excess risk after radiotherapy began 5 years after treatment and persisted for more than 20 years. Risk after treatment with alkylating agents and radiotherapy together was as expected if individual excess risks were summed. Tobacco use increased lung cancer risk more than 20-fold; risks from smoking appeared to multiply risks from treatment.

    CONCLUSIONS: Past treatments with alkylating agents and radiation therapy for Hodgkin's disease were associated with an increased risk of lung cancer in a dose-dependent and additive fashion. The precise risk estimates, however, should be interpreted cautiously, given the possible residual and enhancing effects of tobacco.

  • 36. Travis, Lois B.
    et al.
    Hill, Deirdre
    Dores, Graça M.
    Gospodarowicz, Mary
    van Leeuwen, Flora E.
    Holowaty, Eric
    Glimelius, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology.
    Andersson, Michael
    Pukkala, Eero
    Lynch, Charles F.
    Pee, David
    Smith, Susan A.
    Van't Veer, Mars B.
    Joensuu, Timo
    Storm, Hans
    Stovall, Marilyn
    Boice, John D.
    Gilbert, Ethel
    Gail, Mitchell H.
    Cumulative absolute breast cancer risk for young women treated for Hodgkin lymphoma2005In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 97, no 19, p. 1428-37Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Many women develop breast cancer after treatment for Hodgkin lymphoma (HL) at a young age. We estimated this future risk, taking into account age and calendar year of HL diagnosis, HL treatment information, population breast cancer incidence rates, and competing causes of death. METHODS: Relative risks of breast cancer for categories defined by radiation dose to the chest (0, 20- < 40 Gy, or > or = 40 Gy) and use of alkylating agents (yes or no) were estimated from a case-control study conducted within an international population-based cohort of 3817 female 1-year survivors of HL diagnosed at age 30 years or younger from January 1, 1965, through December 31, 1994. To compute cumulative absolute risks of breast cancer, we used modified standardized incidence ratios to relate cohort breast cancer risks to those in the general population, enabling application of population-based breast cancer rates, and we allowed for competing risks by using population-based mortality rates in female HL survivors. RESULTS: Cumulative absolute risks of breast cancer increased with age at end of follow-up, time since HL diagnosis, and radiation dose. For an HL survivor who was treated at age 25 years with a chest radiation dose of at least 40 Gy without alkylating agents, estimated cumulative absolute risks of breast cancer by age 35, 45, and 55 years were 1.4% (95% confidence interval [CI] = 0.9% to 2.1%), 11.1% (95% CI = 7.4% to 16.3%), and 29.0% (95% CI = 20.2% to 40.1%), respectively. Cumulative absolute risks were lower in women treated with alkylating agents. CONCLUSIONS: Breast cancer projections varied considerably by type of HL therapy, time since HL diagnosis, and age at end of follow-up. These estimates are applicable to HL survivors treated with regimens of the past and can be used to counsel such patients and plan management and preventive strategies. Projections should be used with caution, however, in patients treated with more recent approaches, including limited-field radiotherapy and/or ovary-sparing chemotherapy.

  • 37. Urayama, Kevin Y.
    et al.
    Jarrett, Ruth F.
    Hjalgrim, Henrik
    Diepstra, Arjan
    Kamatani, Yoichiro
    Chabrier, Amelie
    Gaborieau, Valerie
    Boland, Anne
    Nieters, Alexandra
    Becker, Nikolaus
    Foretova, Lenka
    Benavente, Yolanda
    Maynadie, Marc
    Staines, Anthony
    Shield, Lesley
    Lake, Annette
    Montgomery, Dorothy
    Taylor, Malcolm
    Smedby, Karin Ekstrom
    Amini, Rose-Marie
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Molecular and Morphological Pathology.
    Adami, Hans-Olov
    Glimelius, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Radiology, Oncology and Radiation Science, Oncology.
    Feenstra, Bjarke
    Nolte, Ilja M.
    Visser, Lydia
    van Imhoff, Gustaaf W.
    Lightfoot, Tracy
    Cocco, Pierluigi
    Kiemeney, Lambertus
    Vermeulen, Sita H.
    Holcatova, Ivana
    Vatten, Lars
    Macfarlane, Gary J.
    Thomson, Peter
    Conway, David I.
    Benhamou, Simone
    Agudo, Antonio
    Healy, Claire M.
    Overvad, Kim
    Tjonneland, Anne
    Melin, Beatrice
    Canzian, Federico
    Khaw, Kay-Tee
    Travis, Ruth C.
    Peeters, Petra H. M.
    Gonzalez, Carlos A.
    Quiros, Jose Ramon
    Sanchez, Maria-Jose
    Maria Huerta, Jose
    Ardanaz, Eva
    Dorronsoro, Miren
    Clavel-Chapelon, Francoise
    Bueno-de-Mesquita, H. Bas
    Riboli, Elio
    Roman, Eve
    Boffetta, Paolo
    de Sanjose, Silvia
    Zelenika, Diana
    Melbye, Mads
    van den Berg, Anke
    Lathrop, Mark
    Brennan, Paul
    McKay, James D.
    Genome-Wide Association Study of Classical Hodgkin Lymphoma and Epstein-Barr Virus Status-Defined Subgroups2012In: Journal of the National Cancer Institute, ISSN 0027-8874, E-ISSN 1460-2105, Vol. 104, no 3, p. 240-253Article in journal (Refereed)
    Abstract [en]

    Accumulating evidence suggests that risk factors for classical Hodgkin lymphoma (cHL) differ by tumor Epstein-Barr virus (EBV) status. This potential etiological heterogeneity is not recognized in current disease classification. We conducted a genome-wide association study of 1200 cHL patients and 6417 control subjects, with validation in an independent replication series, to identify common genetic variants associated with total cHL and subtypes defined by tumor EBV status. Multiple logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs) assuming a log-additive genetic model for the variants. All statistical tests were two-sided. Two novel loci associated with total cHL irrespective of EBV status were identified in the major histocompatibility complex region; one resides adjacent to MICB (rs2248462: OR = 0.61, 95% CI = 0.53 to 0.69, P = 1.3 x 10(-13)) and the other at HLA-DRA (rs2395185: OR = 0.56, 95% CI = 0.50 to 0.62, P = 8.3 x 10(-25)) with both results confirmed in an independent replication series. Consistent with previous reports, associations were found between EBV-positive cHL and genetic variants within the class I region (rs2734986, HLA-A: OR = 2.45, 95% CI = 2.00 to 3.00, P = 1.2 x 10(-15); rs6904029, HCG9: OR = 0.46, 95% CI = 0.36 to 0.59, P = 5.5 x 10(-10)) and between EBV-negative cHL and rs6903608 within the class II region (rs6903608, HLA-DRA: OR = 2.08, 95% CI = 1.84 to 2.35, P = 6.1 x 10(-31)). The association between rs6903608 and EBV-negative cHL was confined to the nodular sclerosis histological subtype. Evidence for an association between EBV-negative cHL and rs20541 (5q31, IL13: OR = 1.53, 95% CI = 1.32 to 1.76, P = 5.4 x 10(-9)), a variant previously linked to psoriasis and asthma, was observed; however, the evidence for replication was less clear. Notably, one additional psoriasis-associated variant, rs27524 (5q15, ERAP1), showed evidence of an association with cHL in the genome-wide association study (OR = 1.21, 95% CI = 1.10 to 1.33, P = 1.5 x 10(-4)) and replication series (P = .03). Overall, these results provide strong evidence that EBV status is an etiologically important classification of cHL and also suggest that some components of the pathological process are common to both EBV-positive and EBV-negative patients.

1 - 37 of 37
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