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Author (up) Fanidi, A.; Carreras-Torres, R.; Larose, T.L.; Yuan, J.-M.; Stevens, V.L.; Weinstein, S.J.; Albanes, D.; Prentice, R.; Pettinger, M.; Cai, Q.; Blot, W.J.; Arslan, A.A.; Zeleniuch-Jacquotte, A.; McCullough, M.L.; Le Marchand, L.; Wilkens, L.R.; Haiman, C.A.; Zhang, X.; Stampfer, M.J.; Smith-Warner, S.A.; Giovannucci, E.; Giles, G.G.; Hodge, A.M.; Severi, G.; Johansson, M.; Grankvist, K.; Langhammer, A.; Brumpton, B.M.; Wang, R.; Gao, Y.-T.; Ericson, U.; Bojesen, S.E.; Arnold, S.M.; Koh, W.-P.; Shu, X.-O.; Xiang, Y.-B.; Li, H.; Zheng, W.; Lan, Q.; Visvanathan, K.; Hoffman-Bolton, J.; Ueland, P.M.; Midttun, O.; Caporaso, N.E.; Purdue, M.; Freedman, N.D.; Buring, J.E.; Lee, I.-M.; Sesso, H.D.; Michael Gaziano, J.; Manjer, J.; Relton, C.L.; Hung, R.J.; Amos, C.I.; Johansson, M.; Brennan, P. url  doi
  Title Is high vitamin B12 status a cause of lung cancer? Type Journal Article
  Year 2018 Publication International Journal of Cancer Abbreviated Journal Int J Cancer  
  Volume Issue Pages  
  Keywords  
  Abstract Vitamin B supplementation can have side effects for human health, including cancer risk. We aimed to elucidate the role of vitamin B12 in lung cancer etiology via direct measurements of pre-diagnostic circulating vitamin B12 concentrations in a nested case-control study, complemented with a Mendelian randomization (MR) approach in an independent case-control sample. We used pre-diagnostic biomarker data from 5183 case-control pairs nested within 20 prospective cohorts, and genetic data from 29,266 cases and 56,450 controls. Exposures included directly measured circulating vitamin B12 in pre-diagnostic blood samples from the nested case-control study, and 8 single nucleotide polymorphisms associated with vitamin B12 concentrations in the MR study. Our main outcome of interest was increased risk for lung cancer, overall and by histological subtype, per increase in circulating vitamin B12 concentrations. We found circulating vitamin B12 to be positively associated with overall lung cancer risk in a dose response fashion (odds ratio for a doubling in B12 [ORlog2B12 ] = 1.15, 95% confidence interval (95%CI) = 1.06-1.25). The MR analysis based on 8 genetic variants also indicated that genetically determined higher vitamin B12 concentrations were positively associated with overall lung cancer risk (OR per 150 pmol/L standard deviation increase in B12 [ORSD ] = 1.08, 95%CI = 1.00-1.16). Considering the consistency of these two independent and complementary analyses, these findings support the hypothesis that high vitamin B12 status increases the risk of lung cancer.  
  Address Genetic Epidemiology Group, International Agency for Research on Cancer, Lyon, France  
  Corporate Author LC3 consortium and the TRICL consortium Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0020-7136 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:30499135 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 2080  
Permanent link to this record
 

 
Author (up) Fanidi, A.; Muller, D.C.; Yuan, J.-M.; Stevens, V.L.; Weinstein, S.J.; Albanes, D.; Prentice, R.; Thomsen, C.A.; Pettinger, M.; Cai, Q.; Blot, W.J.; Wu, J.; Arslan, A.A.; Zeleniuch-Jacquotte, A.; McCullough, M.L.; Le Marchand, L.; Wilkens, L.R.; Haiman, C.A.; Zhang, X.; Han, J.; Stampfer, M.J.; Smith-Warner, S.A.; Giovannucci, E.; Giles, G.G.; Hodge, A.M.; Severi, G.; Johansson, M.; Grankvist, K.; Langhammer, A.; Krokstad, S.; Naess, M.; Wang, R.; Gao, Y.-T.; Butler, L.M.; Koh, W.-P.; Shu, X.-O.; Xiang, Y.-B.; Li, H.; Zheng, W.; Lan, Q.; Visvanathan, K.; Bolton, J.H.; Ueland, P.M.; Midttun, O.; Ulvik, A.; Caporaso, N.E.; Purdue, M.; Ziegler, R.G.; Freedman, N.D.; Buring, J.E.; Lee, I.-M.; Sesso, H.D.; Gaziano, J.M.; Manjer, J.; Ericson, U.; Relton, C.; Brennan, P.; Johansson, M. url  doi
  Title Circulating Folate, Vitamin B6, and Methionine in Relation to Lung Cancer Risk in the Lung Cancer Cohort Consortium (LC3) Type Journal Article
  Year 2018 Publication Journal of the National Cancer Institute Abbreviated Journal J Natl Cancer Inst  
  Volume 110 Issue 1 Pages  
  Keywords Adult; Aged; Aged, 80 and over; Asia/epidemiology; Australia/epidemiology; Case-Control Studies; Cotinine/blood; Europe/epidemiology; Female; Folic Acid/*blood; Humans; Incidence; Lung Neoplasms/blood/*epidemiology; Male; Methionine/*blood; Middle Aged; Prospective Studies; Protective Factors; Risk Factors; Sex Factors; Smoking/blood/epidemiology; United States/epidemiology; Vitamin B 6/*blood  
  Abstract Background: Circulating concentrations of B vitamins and factors related to one-carbon metabolism have been found to be strongly inversely associated with lung cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) study. The extent to which these associations are present in other study populations is unknown. Methods: Within 20 prospective cohorts from the National Cancer Institute Cohort Consortium, a nested case-control study was designed including 5364 incident lung cancer case patients and 5364 control subjects who were individually matched to case patients by age, sex, cohort, and smoking status. Centralized biochemical analyses were performed to measure circulating concentrations of vitamin B6, folate, and methionine, as well as cotinine as an indicator of recent tobacco exposure. The association between these biomarkers and lung cancer risk was evaluated using conditional logistic regression models. Results: Participants with higher circulating concentrations of vitamin B6 and folate had a modestly decreased risk of lung cancer risk overall, the odds ratios when comparing the top and bottom fourths (OR 4vs1 ) being 0.88 (95% confidence interval [CI] = 0.78 to 1.00) and 0.86 (95% CI = 0.74 to 0.99), respectively. We found stronger associations among men (vitamin B6: OR 4vs1 = 0.74, 95% CI = 0.62 to 0.89; folate: OR 4vs1 = 0.75, 95% CI = 0.61 to 0.93) and ever smokers (vitamin B6: OR 4vs1 = 0.78, 95% CI = 0.67 to 0.91; folate: OR 4vs1 = 0.87, 95% CI = 0.73 to 1.03). We further noted that the association of folate was restricted to Europe/Australia and Asia, whereas no clear association was observed for the United States. Circulating concentrations of methionine were not associated with lung cancer risk overall or in important subgroups. Conclusions: Although confounding by tobacco exposure or reverse causation cannot be ruled out, these study results are compatible with a small decrease in lung cancer risk in ever smokers who avoid low concentrations of circulating folate and vitamin B6.  
  Address Genetic Epidemiology Group, International Agency for Research on Cancer, Lyon, France; Department of Epidemiology and Biostatistics, Imperial College London, London, UK; Division of Cancer Control and Population Sciences, University of Pittsburgh Cancer Institute, Pittsburgh, PA; Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA; Epidemiology Research Program, American Cancer Society, Inc., Atlanta, GA; Division of Cancer Epidemiology and Genetics and Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD; Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA; Health Promotion Sciences, Mel and Enid Zuckerman College of Public Health, University of Arizona, Tucson, AZ; Division of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN; International Epidemiology Institute, Rockville, MD; Departments of Obstetrics and Gynecology, Population Health and Environmental Medicine and Population Health, New York University School of Medicine, New York, NY; Epidemiology Program, Cancer Research Center of Hawaii, University of Hawaii, Honolulu, HI; Channing Division of Network Medicine, Division of Preventive Medicine, and Division of Aging, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA; Department of Epidemiology and Department of Nutrition, Harvard T. H. Chan School of Public Health, Boston, MA; Cancer Epidemiology Centre, Cancer Council Victoria, Melbourne, Australia; Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Victoria, Australia; Molecular end Epidemiology Unit, HuGeF, Human Genetics Foundation, Torino, Italy; Inserm (Institut National de la Sante et de la Recherche Medicale), Centre for Research in Epidemiology and Population Health, Villejuif, France; Umea, University, Umea, Sweden; HUNT Research Centre, Department of Public Health and General Practice, NTNU, Norwegian University of Science and Technology, Levanger, Norway; Department of Epidemiology, Shanghai Cancer Institute, Shanghai Jiaotong University, Shanghai, China; Duke-NUS Graduate Medical School Singapore, Singapore; Department of Epidemiology, George W Comstock Center for Public Health Research and Prevention Health Monitoring Unit, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD; Laboratory of Clinical Biochemistry, Department of Clinical Science, University of Bergen, Bergen, Norway; Haukeland University Hospital, Bergen, Norway; Bevital AS, Bergen, Norway; Boston VA Medical Center, Boston, MA; Department of Surgery, Skane University Hospital Malmo, Lund University, Malmo, Sweden; Department of Clinical Sciences, Malmo, Lund University, Lund, Sweden; Institute of Genetic Medicine, Newcastle University, Newcastle, UK; MRC Integrative Epidemiology Unit, School of Social and Community Medicine, University of Bristol, Bristol, UK  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0027-8874 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:28922778; PMCID:PMC5989622 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 2081  
Permanent link to this record
 

 
Author (up) Hung, R.J.; McKay, J.D.; Gaborieau, V.; Boffetta, P.; Hashibe, M.; Zaridze, D.; Mukeria, A.; Szeszenia-Dabrowska, N.; Lissowska, J.; Rudnai, P.; Fabianova, E.; Mates, D.; Bencko, V.; Foretova, L.; Janout, V.; Chen, C.; Goodman, G.; Field, J.K.; Liloglou, T.; Xinarianos, G.; Cassidy, A.; McLaughlin, J.; Liu, G.; Narod, S.; Krokan, H.E.; Skorpen, F.; Elvestad, M.B.; Hveem, K.; Vatten, L.; Linseisen, J.; Clavel-Chapelon, F.; Vineis, P.; Bueno-de-Mesquita, H.B.; Lund, E.; Martinez, C.; Bingham, S.; Rasmuson, T.; Hainaut, P.; Riboli, E.; Ahrens, W.; Benhamou, S.; Lagiou, P.; Trichopoulos, D.; Holcatova, I.; Merletti, F.; Kjaerheim, K.; Agudo, A.; Macfarlane, G.; Talamini, R.; Simonato, L.; Lowry, R.; Conway, D.I.; Znaor, A.; Healy, C.; Zelenika, D.; Boland, A.; Delepine, M.; Foglio, M.; Lechner, D.; Matsuda, F.; Blanche, H.; Gut, I.; Heath, S.; Lathrop, M.; Brennan, P. url  doi
  Title A susceptibility locus for lung cancer maps to nicotinic acetylcholine receptor subunit genes on 15q25 Type Journal Article
  Year 2008 Publication Nature Abbreviated Journal Nature  
  Volume 452 Issue 7187 Pages 633-637  
  Keywords HUNT2; Chromosomes, Human, Pair 15/*genetics; Europe; Genetic Predisposition to Disease/*genetics; Genotype; Humans; Lung Neoplasms/*genetics; Odds Ratio; Polymorphism, Single Nucleotide/genetics; Protein Subunits/*genetics; Receptors, Nicotinic/*genetics  
  Abstract Lung cancer is the most common cause of cancer death worldwide, with over one million cases annually. To identify genetic factors that modify disease risk, we conducted a genome-wide association study by analysing 317,139 single-nucleotide polymorphisms in 1,989 lung cancer cases and 2,625 controls from six central European countries. We identified a locus in chromosome region 15q25 that was strongly associated with lung cancer (P = 9 x 10(-10)). This locus was replicated in five separate lung cancer studies comprising an additional 2,513 lung cancer cases and 4,752 controls (P = 5 x 10(-20) overall), and it was found to account for 14% (attributable risk) of lung cancer cases. Statistically similar risks were observed irrespective of smoking status or propensity to smoke tobacco. The association region contains several genes, including three that encode nicotinic acetylcholine receptor subunits (CHRNA5, CHRNA3 and CHRNB4). Such subunits are expressed in neurons and other tissues, in particular alveolar epithelial cells, pulmonary neuroendocrine cells and lung cancer cell lines, and they bind to N'-nitrosonornicotine and potential lung carcinogens. A non-synonymous variant of CHRNA5 that induces an amino acid substitution (D398N) at a highly conserved site in the second intracellular loop of the protein is among the markers with the strongest disease associations. Our results provide compelling evidence of a locus at 15q25 predisposing to lung cancer, and reinforce interest in nicotinic acetylcholine receptors as potential disease candidates and chemopreventative targets.  
  Address International Agency for Research on Cancer (IARC), Lyon 69008, France  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0028-0836 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:18385738 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1678  
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Author (up) Larose, T.L.; Guida, F.; Fanidi, A.; Langhammer, A.; Kveem, K.; Stevens, V.L.; Jacobs, E.J.; Smith-Warner, S.A.; Giovannucci, E.; Albanes, D.; Weinstein, S.J.; Freedman, N.D.; Prentice, R.; Pettinger, M.; Thomson, C.A.; Cai, Q.; Wu, J.; Blot, W.J.; Arslan, A.A.; Zeleniuch-Jacquotte, A.; Le Marchand, L.; Wilkens, L.R.; Haiman, C.A.; Zhang, X.; Stampfer, M.J.; Hodge, A.M.; Giles, G.G.; Severi, G.; Johansson, M.; Grankvist, K.; Wang, R.; Yuan, J.-M.; Gao, Y.-T.; Koh, W.-P.; Shu, X.-O.; Zheng, W.; Xiang, Y.-B.; Li, H.; Lan, Q.; Visvanathan, K.; Hoffman Bolton, J.; Ueland, P.M.; Midttun, O.; Caporaso, N.; Purdue, M.; Sesso, H.D.; Buring, J.E.; Lee, I.-M.; Gaziano, J.M.; Manjer, J.; Brunnstrom, H.; Brennan, P.; Johansson, M. url  doi
  Title Circulating cotinine concentrations and lung cancer risk in the Lung Cancer Cohort Consortium (LC3) Type Journal Article
  Year 2018 Publication International Journal of Epidemiology Abbreviated Journal Int J Epidemiol  
  Volume 47 Issue 6 Pages 1760-1771  
  Keywords  
  Abstract Background: Self-reported smoking is the principal measure used to assess lung cancer risk in epidemiological studies. We evaluated if circulating cotinine-a nicotine metabolite and biomarker of recent tobacco exposure-provides additional information on lung cancer risk. Methods: The study was conducted in the Lung Cancer Cohort Consortium (LC3) involving 20 prospective cohort studies. Pre-diagnostic serum cotinine concentrations were measured in one laboratory on 5364 lung cancer cases and 5364 individually matched controls. We used conditional logistic regression to evaluate the association between circulating cotinine and lung cancer, and assessed if cotinine provided additional risk-discriminative information compared with self-reported smoking (smoking status, smoking intensity, smoking duration), using receiver-operating characteristic (ROC) curve analysis. Results: We observed a strong positive association between cotinine and lung cancer risk for current smokers [odds ratio (OR ) per 500 nmol/L increase in cotinine (OR500): 1.39, 95% confidence interval (CI): 1.32-1.47]. Cotinine concentrations consistent with active smoking (>/=115 nmol/L) were common in former smokers (cases: 14.6%; controls: 9.2%) and rare in never smokers (cases: 2.7%; controls: 0.8%). Former and never smokers with cotinine concentrations indicative of active smoking (>/=115 nmol/L) also showed increased lung cancer risk. For current smokers, the risk-discriminative performance of cotinine combined with self-reported smoking (AUCintegrated: 0.69, 95% CI: 0.68-0.71) yielded a small improvement over self-reported smoking alone (AUCsmoke: 0.66, 95% CI: 0.64-0.68) (P = 1.5x10-9). Conclusions: Circulating cotinine concentrations are consistently associated with lung cancer risk for current smokers and provide additional risk-discriminative information compared with self-report smoking alone.  
  Address Genetic Epidemiology Group, International Agency for Research on Cancer, Lyon, France  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0300-5771 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:29901778; PMCID:PMC6280953 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 2126  
Permanent link to this record
 

 
Author (up) Machiela, M.J.; Hofmann, J.N.; Carreras-Torres, R.; Brown, K.M.; Johansson, M.; Wang, Z.; Foll, M.; Li, P.; Rothman, N.; Savage, S.A.; Gaborieau, V.; McKay, J.D.; Ye, Y.; Henrion, M.; Bruinsma, F.; Jordan, S.; Severi, G.; Hveem, K.; Vatten, L.J.; Fletcher, T.; Koppova, K.; Larsson, S.C.; Wolk, A.; Banks, R.E.; Selby, P.J.; Easton, D.F.; Pharoah, P.; Andreotti, G.; Freeman, L.E.B.; Koutros, S.; Albanes, D.; Mannisto, S.; Weinstein, S.; Clark, P.E.; Edwards, T.E.; Lipworth, L.; Gapstur, S.M.; Stevens, V.L.; Carol, H.; Freedman, M.L.; Pomerantz, M.M.; Cho, E.; Kraft, P.; Preston, M.A.; Wilson, K.M.; Gaziano, J.M.; Sesso, H.S.; Black, A.; Freedman, N.D.; Huang, W.-Y.; Anema, J.G.; Kahnoski, R.J.; Lane, B.R.; Noyes, S.L.; Petillo, D.; Colli, L.M.; Sampson, J.N.; Besse, C.; Blanche, H.; Boland, A.; Burdette, L.; Prokhortchouk, E.; Skryabin, K.G.; Yeager, M.; Mijuskovic, M.; Ognjanovic, M.; Foretova, L.; Holcatova, I.; Janout, V.; Mates, D.; Mukeriya, A.; Rascu, S.; Zaridze, D.; Bencko, V.; Cybulski, C.; Fabianova, E.; Jinga, V.; Lissowska, J.; Lubinski, J.; Navratilova, M.; Rudnai, P.; Szeszenia-Dabrowska, N.; Benhamou, S.; Cancel-Tassin, G.; Cussenot, O.; Bueno-de-Mesquita, H.B.A.; Canzian, F.; Duell, E.J.; Ljungberg, B.; Sitaram, R.T.; Peters, U.; White, E.; Anderson, G.L.; Johnson, L.; Luo, J.; Buring, J.; Lee, I.-M.; Chow, W.-H.; Moore, L.E.; Wood, C.; Eisen, T.; Larkin, J.; Choueiri, T.K.; Lathrop, G.M.; Teh, B.T.; Deleuze, J.-F.; Wu, X.; Houlston, R.S.; Brennan, P.; Chanock, S.J.; Scelo, G.; Purdue, M.P. url  doi
  Title Corrigendum re “Genetic Variants Related to Longer Telomere Length are Associated with Increased Risk of Renal Cell Carcinoma” [Eur Urol 2017;72:747-54] Type Published Erratum
  Year 2018 Publication European Urology Abbreviated Journal Eur Urol  
  Volume 74 Issue 3 Pages e85-e86  
  Keywords  
  Abstract  
  Address Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department Health and Human Services, Bethesda, MS, USA. Electronic address: purduem@mail.nih.gov  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0302-2838 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:29853305 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 2130  
Permanent link to this record
 

 
Author (up) Machiela, M.J.; Hofmann, J.N.; Carreras-Torres, R.; Brown, K.M.; Johansson, M.; Wang, Z.; Foll, M.; Li, P.; Rothman, N.; Savage, S.A.; Gaborieau, V.; McKay, J.D.; Ye, Y.; Henrion, M.; Bruinsma, F.; Jordan, S.; Severi, G.; Hveem, K.; Vatten, L.J.; Fletcher, T.; Koppova, K.; Larsson, S.C.; Wolk, A.; Banks, R.E.; Selby, P.J.; Easton, D.F.; Pharoah, P.; Andreotti, G.; Freeman, L.E.B.; Koutros, S.; Albanes, D.; Mannisto, S.; Weinstein, S.; Clark, P.E.; Edwards, T.E.; Lipworth, L.; Gapstur, S.M.; Stevens, V.L.; Carol, H.; Freedman, M.L.; Pomerantz, M.M.; Cho, E.; Kraft, P.; Preston, M.A.; Wilson, K.M.; Gaziano, J.M.; Sesso, H.S.; Black, A.; Freedman, N.D.; Huang, W.-Y.; Anema, J.G.; Kahnoski, R.J.; Lane, B.R.; Noyes, S.L.; Petillo, D.; Colli, L.M.; Sampson, J.N.; Besse, C.; Blanche, H.; Boland, A.; Burdette, L.; Prokhortchouk, E.; Skryabin, K.G.; Yeager, M.; Mijuskovic, M.; Ognjanovic, M.; Foretova, L.; Holcatova, I.; Janout, V.; Mates, D.; Mukeriya, A.; Rascu, S.; Zaridze, D.; Bencko, V.; Cybulski, C.; Fabianova, E.; Jinga, V.; Lissowska, J.; Lubinski, J.; Navratilova, M.; Rudnai, P.; Szeszenia-Dabrowska, N.; Benhamou, S.; Cancel-Tassin, G.; Cussenot, O.; Bueno-de-Mesquita, H.B.; Canzian, F.; Duell, E.J.; Ljungberg, B.; Sitaram, R.T.; Peters, U.; White, E.; Anderson, G.L.; Johnson, L.; Luo, J.; Buring, J.; Lee, I.-M.; Chow, W.-H.; Moore, L.E.; Wood, C.; Eisen, T.; Larkin, J.; Choueiri, T.K.; Lathrop, G.M.; Teh, B.T.; Deleuze, J.-F.; Wu, X.; Houlston, R.S.; Brennan, P.; Chanock, S.J.; Scelo, G.; Purdue, M.P. url  doi
  Title Genetic Variants Related to Longer Telomere Length are Associated with Increased Risk of Renal Cell Carcinoma Type Journal Article
  Year 2017 Publication European Urology Abbreviated Journal Eur Urol  
  Volume 72 Issue 5 Pages 747-754  
  Keywords Genetic variants; Mendelian randomization; Renal cell carcinoma; Risk; Telomere length  
  Abstract BACKGROUND: Relative telomere length in peripheral blood leukocytes has been evaluated as a potential biomarker for renal cell carcinoma (RCC) risk in several studies, with conflicting findings. OBJECTIVE: We performed an analysis of genetic variants associated with leukocyte telomere length to assess the relationship between telomere length and RCC risk using Mendelian randomization, an approach unaffected by biases from temporal variability and reverse causation that might have affected earlier investigations. DESIGN, SETTING, AND PARTICIPANTS: Genotypes from nine telomere length-associated variants for 10 784 cases and 20 406 cancer-free controls from six genome-wide association studies (GWAS) of RCC were aggregated into a weighted genetic risk score (GRS) predictive of leukocyte telomere length. OUTCOME MEASUREMENTS AND STATISTICAL ANALYSIS: Odds ratios (ORs) relating the GRS and RCC risk were computed in individual GWAS datasets and combined by meta-analysis. RESULTS AND LIMITATIONS: Longer genetically inferred telomere length was associated with an increased risk of RCC (OR=2.07 per predicted kilobase increase, 95% confidence interval [CI]:=1.70-2.53, p<0.0001). As a sensitivity analysis, we excluded two telomere length variants in linkage disequilibrium (R(2)>0.5) with GWAS-identified RCC risk variants (rs10936599 and rs9420907) from the telomere length GRS; despite this exclusion, a statistically significant association between the GRS and RCC risk persisted (OR=1.73, 95% CI=1.36-2.21, p<0.0001). Exploratory analyses for individual histologic subtypes suggested comparable associations with the telomere length GRS for clear cell (N=5573, OR=1.93, 95% CI=1.50-2.49, p<0.0001), papillary (N=573, OR=1.96, 95% CI=1.01-3.81, p=0.046), and chromophobe RCC (N=203, OR=2.37, 95% CI=0.78-7.17, p=0.13). CONCLUSIONS: Our investigation adds to the growing body of evidence indicating some aspect of longer telomere length is important for RCC risk. PATIENT SUMMARY: Telomeres are segments of DNA at chromosome ends that maintain chromosomal stability. Our study investigated the relationship between genetic variants associated with telomere length and renal cell carcinoma risk. We found evidence suggesting individuals with inherited predisposition to longer telomere length are at increased risk of developing renal cell carcinoma.  
  Address Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department Health and Human Services, Bethesda, MS, USA. Electronic address: purduem@mail.nih.gov  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0302-2838 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:28797570; PMCID:PMC5641242 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1959  
Permanent link to this record
 

 
Author (up) Muller, D.C.; Hodge, A.M.; Fanidi, A.; Albanes, D.; Mai, X.M.; Shu, X.O.; Weinstein, S.J.; Larose, T.L.; Zhang, X.; Han, J.; Stampfer, M.J.; Smith-Warner, S.A.; Ma, J.; Gaziano, J.M.; Sesso, H.D.; Stevens, V.L.; McCullough, M.L.; Layne, T.M.; Prentice, R.; Pettinger, M.; Thomson, C.A.; Zheng, W.; Gao, Y.T.; Rothman, N.; Xiang, Y.B.; Cai, H.; Wang, R.; Yuan, J.M.; Koh, W.P.; Butler, L.M.; Cai, Q.; Blot, W.J.; Wu, J.; Ueland, P.M.; Midttun, O.; Langhammer, A.; Hveem, K.; Johansson, M.; Hultdin, J.; Grankvist, K.; Arslan, A.A.; Le Marchand, L.; Severi, G.; Johansson, M.; Brennan, P. url  doi
  Title No association between circulating concentrations of vitamin D and risk of lung cancer: an analysis in 20 prospective studies in the Lung Cancer Cohort Consortium (LC3) Type Journal Article
  Year 2018 Publication Annals of Oncology : Official Journal of the European Society for Medical Oncology Abbreviated Journal Ann Oncol  
  Volume 29 Issue 6 Pages 1468-1475  
  Keywords  
  Abstract Background: There is observational evidence suggesting that high vitamin D concentrations may protect against lung cancer. To investigate this hypothesis in detail, we measured circulating vitamin D concentrations in prediagnostic blood from 20 cohorts participating in the Lung Cancer Cohort Consortium (LC3). Patients and methods: The study included 5313 lung cancer cases and 5313 controls. Blood samples for the cases were collected, on average, 5 years before lung cancer diagnosis. Controls were individually matched to the cases by cohort, sex, age, race/ethnicity, date of blood collection, and smoking status in five categories. Liquid chromatography coupled with tandem mass spectrometry was used to separately analyze 25-hydroxyvitamin D2 [25(OH)D2] and 25-hydroxyvitamin D3 [25(OH)D3] and their concentrations were combined to give an overall measure of 25(OH)D. We used conditional logistic regression to calculate odds ratios (ORs) and 95% confidence intervals (CIs) for 25(OH)D as both continuous and categorical variables. Results: Overall, no apparent association between 25(OH)D and risk of lung cancer was observed (multivariable adjusted OR for a doubling in concentration: 0.98, 95% CI: 0.91, 1.06). Similarly, we found no clear evidence of interaction by cohort, sex, age, smoking status, or histology. Conclusion: This study did not support an association between vitamin D concentrations and lung cancer risk.  
  Address Genetic Epidemiology Group, International Agency for Research on Cancer, Lyon, France  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0923-7534 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:29617726; PMCID:PMC6005063 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 2139  
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Author (up) Purdue, M.P.; Johansson, M.; Zelenika, D.; Toro, J.R.; Scelo, G.; Moore, L.E.; Prokhortchouk, E.; Wu, X.; Kiemeney, L.A.; Gaborieau, V.; Jacobs, K.B.; Chow, W.-H.; Zaridze, D.; Matveev, V.; Lubinski, J.; Trubicka, J.; Szeszenia-Dabrowska, N.; Lissowska, J.; Rudnai, P.; Fabianova, E.; Bucur, A.; Bencko, V.; Foretova, L.; Janout, V.; Boffetta, P.; Colt, J.S.; Davis, F.G.; Schwartz, K.L.; Banks, R.E.; Selby, P.J.; Harnden, P.; Berg, C.D.; Hsing, A.W.; Grubb, R.L. 3rd; Boeing, H.; Vineis, P.; Clavel-Chapelon, F.; Palli, D.; Tumino, R.; Krogh, V.; Panico, S.; Duell, E.J.; Quiros, J.R.; Sanchez, M.-J.; Navarro, C.; Ardanaz, E.; Dorronsoro, M.; Khaw, K.-T.; Allen, N.E.; Bueno-de-Mesquita, H.B.; Peeters, P.H.M.; Trichopoulos, D.; Linseisen, J.; Ljungberg, B.; Overvad, K.; Tjonneland, A.; Romieu, I.; Riboli, E.; Mukeria, A.; Shangina, O.; Stevens, V.L.; Thun, M.J.; Diver, W.R.; Gapstur, S.M.; Pharoah, P.D.; Easton, D.F.; Albanes, D.; Weinstein, S.J.; Virtamo, J.; Vatten, L.; Hveem, K.; Njolstad, I.; Tell, G.S.; Stoltenberg, C.; Kumar, R.; Koppova, K.; Cussenot, O.; Benhamou, S.; Oosterwijk, E.; Vermeulen, S.H.; Aben, K.K.H.; van der Marel, S.L.; Ye, Y.; Wood, C.G.; Pu, X.; Mazur, A.M.; Boulygina, E.S.; Chekanov, N.N.; Foglio, M.; Lechner, D.; Gut, I.; Heath, S.; Blanche, H.; Hutchinson, A.; Thomas, G.; Wang, Z.; Yeager, M.; Fraumeni, J.F.J.; Skryabin, K.G.; McKay, J.D.; Rothman, N.; Chanock, S.J.; Lathrop, M.; Brennan, P. url  doi
  Title Genome-wide association study of renal cell carcinoma identifies two susceptibility loci on 2p21 and 11q13.3 Type Journal Article
  Year 2011 Publication Nature Genetics Abbreviated Journal Nat Genet  
  Volume 43 Issue 1 Pages 60-65  
  Keywords HUNT2; Carcinoma, Renal Cell/*genetics; Case-Control Studies; Chromosomes, Human, Pair 11/*genetics; Chromosomes, Human, Pair 2/*genetics; *Genetic Predisposition to Disease/genetics; Genome, Human; *Genome-Wide Association Study; Humans; Kidney Neoplasms/*genetics; Polymorphism, Single Nucleotide; Risk Factors  
  Abstract We conducted a two-stage genome-wide association study of renal cell carcinoma (RCC) in 3,772 affected individuals (cases) and 8,505 controls of European background from 11 studies and followed up 6 SNPs in 3 replication studies of 2,198 cases and 4,918 controls. Two loci on the regions of 2p21 and 11q13.3 were associated with RCC susceptibility below genome-wide significance. Two correlated variants (r(2) = 0.99 in controls), rs11894252 (P = 1.8 x 10(-)(8)) and rs7579899 (P = 2.3 x 10(-)(9)), map to EPAS1 on 2p21, which encodes hypoxia-inducible-factor-2 alpha, a transcription factor previously implicated in RCC. The second locus, rs7105934, at 11q13.3, contains no characterized genes (P = 7.8 x 10(-)(1)(4)). In addition, we observed a promising association on 12q24.31 for rs4765623, which maps to SCARB1, the scavenger receptor class B, member 1 gene (P = 2.6 x 10(-)(8)). Our study reports previously unidentified genomic regions associated with RCC risk that may lead to new etiological insights.  
  Address Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department Health and Human Services, Bethesda, Maryland, USA  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 1061-4036 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:21131975; PMC3049257 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1697  
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Author (up) Scelo, G.; Purdue, M.P.; Brown, K.M.; Johansson, M.; Wang, Z.; Eckel-Passow, J.E.; Ye, Y.; Hofmann, J.N.; Choi, J.; Foll, M.; Gaborieau, V.; Machiela, M.J.; Colli, L.M.; Li, P.; Sampson, J.N.; Abedi-Ardekani, B.; Besse, C.; Blanche, H.; Boland, A.; Burdette, L.; Chabrier, A.; Durand, G.; Le Calvez-Kelm, F.; Prokhortchouk, E.; Robinot, N.; Skryabin, K.G.; Wozniak, M.B.; Yeager, M.; Basta-Jovanovic, G.; Dzamic, Z.; Foretova, L.; Holcatova, I.; Janout, V.; Mates, D.; Mukeriya, A.; Rascu, S.; Zaridze, D.; Bencko, V.; Cybulski, C.; Fabianova, E.; Jinga, V.; Lissowska, J.; Lubinski, J.; Navratilova, M.; Rudnai, P.; Szeszenia-Dabrowska, N.; Benhamou, S.; Cancel-Tassin, G.; Cussenot, O.; Baglietto, L.; Boeing, H.; Khaw, K.-T.; Weiderpass, E.; Ljungberg, B.; Sitaram, R.T.; Bruinsma, F.; Jordan, S.J.; Severi, G.; Winship, I.; Hveem, K.; Vatten, L.J.; Fletcher, T.; Koppova, K.; Larsson, S.C.; Wolk, A.; Banks, R.E.; Selby, P.J.; Easton, D.F.; Pharoah, P.; Andreotti, G.; Freeman, L.E.B.; Koutros, S.; Albanes, D.; Mannisto, S.; Weinstein, S.; Clark, P.E.; Edwards, T.L.; Lipworth, L.; Gapstur, S.M.; Stevens, V.L.; Carol, H.; Freedman, M.L.; Pomerantz, M.M.; Cho, E.; Kraft, P.; Preston, M.A.; Wilson, K.M.; Michael Gaziano, J.; Sesso, H.D.; Black, A.; Freedman, N.D.; Huang, W.-Y.; Anema, J.G.; Kahnoski, R.J.; Lane, B.R.; Noyes, S.L.; Petillo, D.; Teh, B.T.; Peters, U.; White, E.; Anderson, G.L.; Johnson, L.; Luo, J.; Buring, J.; Lee, I.-M.; Chow, W.-H.; Moore, L.E.; Wood, C.; Eisen, T.; Henrion, M.; Larkin, J.; Barman, P.; Leibovich, B.C.; Choueiri, T.K.; Mark Lathrop, G.; Rothman, N.; Deleuze, J.-F.; McKay, J.D.; Parker, A.S.; Wu, X.; Houlston, R.S.; Brennan, P.; Chanock, S.J. url  doi
  Title Genome-wide association study identifies multiple risk loci for renal cell carcinoma Type Journal Article
  Year 2017 Publication Nature Communications Abbreviated Journal Nat Commun  
  Volume 8 Issue Pages 15724  
  Keywords  
  Abstract Previous genome-wide association studies (GWAS) have identified six risk loci for renal cell carcinoma (RCC). We conducted a meta-analysis of two new scans of 5,198 cases and 7,331 controls together with four existing scans, totalling 10,784 cases and 20,406 controls of European ancestry. Twenty-four loci were tested in an additional 3,182 cases and 6,301 controls. We confirm the six known RCC risk loci and identify seven new loci at 1p32.3 (rs4381241, P=3.1 x 10(-10)), 3p22.1 (rs67311347, P=2.5 x 10(-8)), 3q26.2 (rs10936602, P=8.8 x 10(-9)), 8p21.3 (rs2241261, P=5.8 x 10(-9)), 10q24.33-q25.1 (rs11813268, P=3.9 x 10(-8)), 11q22.3 (rs74911261, P=2.1 x 10(-10)) and 14q24.2 (rs4903064, P=2.2 x 10(-24)). Expression quantitative trait analyses suggest plausible candidate genes at these regions that may contribute to RCC susceptibility.  
  Address Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department Health and Human Services, Bethesda, Maryland 20892, USA  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 2041-1723 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:28598434; PMCID:PMC5472706 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1976  
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Author (up) Theofylaktopoulou, D.; Midttun, O.; Ueland, P.M.; Meyer, K.; Fanidi, A.; Zheng, W.; Shu, X.-O.; Xiang, Y.-B.; Prentice, R.; Pettinger, M.; Thomson, C.A.; Giles, G.G.; Hodge, A.; Cai, Q.; Blot, W.J.; Wu, J.; Johansson, M.; Hultdin, J.; Grankvist, K.; Stevens, V.L.; McCullough, M.M.; Weinstein, S.J.; Albanes, D.; Ziegler, R.; Freedman, N.D.; Langhammer, A.; Hveem, K.; Naess, M.; Sesso, H.D.; Gaziano, J.M.; Buring, J.E.; Lee, I.-M.; Severi, G.; Zhang, X.; Stampfer, M.J.; Han, J.; Smith-Warner, S.A.; Zeleniuch-Jacquotte, A.; Le Marchand, L.; Yuan, J.-M.; Wang, R.; Butler, L.M.; Koh, W.-P.; Gao, Y.-T.; Rothman, N.; Ericson, U.; Sonestedt, E.; Visvanathan, K.; Jones, M.R.; Relton, C.; Brennan, P.; Johansson, M.; Ulvik, A. url  doi
  Title Impaired functional vitamin B6 status is associated with increased risk of lung cancer Type Journal Article
  Year 2018 Publication International Journal of Cancer Abbreviated Journal Int J Cancer  
  Volume 142 Issue 12 Pages 2425-2434  
  Keywords Aged; Biomarkers/blood; Carcinoma, Squamous Cell/*blood/*pathology; Case-Control Studies; Cohort Studies; Female; Humans; Lung Neoplasms/*blood/*pathology; Male; Middle Aged; Odds Ratio; Risk Factors; Vitamin B 6/*blood; *3-hydroxykynurenine:xanthurenic acid; *Lung Cancer Cohort Consortium; *functional vitamin B6 marker; *pyridoxal 5'-phosphate  
  Abstract Circulating vitamin B6 levels have been found to be inversely associated with lung cancer. Most studies have focused on the B6 form pyridoxal 5'-phosphate (PLP), a direct biomarker influenced by inflammation and other factors. Using a functional B6 marker allows further investigation of the potential role of vitamin B6 status in the pathogenesis of lung cancer. We prospectively evaluated the association of the functional marker of vitamin B6 status, the 3-hydroxykynurenine:xanthurenic acid (HK:XA) ratio, with risk of lung cancer in a nested case-control study consisting of 5,364 matched case-control pairs from the Lung Cancer Cohort Consortium (LC3). We used conditional logistic regression to evaluate the association between HK:XA and lung cancer, and random effect models to combine results from different cohorts and regions. High levels of HK:XA, indicating impaired functional B6 status, were associated with an increased risk of lung cancer, the odds ratio comparing the fourth and the first quartiles (OR4thvs.1st ) was 1.25 (95% confidence interval, 1.10-1.41). Stratified analyses indicated that this association was primarily driven by cases diagnosed with squamous cell carcinoma. Notably, the risk associated with HK:XA was approximately 50% higher in groups with a high relative frequency of squamous cell carcinoma, i.e., men, former and current smokers. This risk of squamous cell carcinoma was present in both men and women regardless of smoking status.  
  Address Bevital AS, Bergen, Norway  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0020-7136 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:29238985; PMCID:PMC5908731 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 2182  
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Author (up) Theofylaktopoulou, D.; Midttun, O.; Ueland, P.M.; Meyer, K.; Fanidi, A.; Zheng, W.; Shu, X.-O.; Xiang, Y.-B.; Prentice, R.; Pettinger, M.; Thomson, C.A.; Giles, G.G.; Hodge, A.; Cai, Q.; Blot, W.J.; Wu, J.; Johansson, M.; Hultdin, J.; Grankvist, K.; Stevens, V.L.; McCullough, M.M.; Weinstein, S.J.; Albanes, D.; Ziegler, R.; Freedman, N.D.; Langhammer, A.; Hveem, K.; Naess, M.; Sesso, H.D.; Gaziano, J.M.; Buring, J.E.; Lee, I.-M.; Severi, G.; Zhang, X.; Stampfer, M.J.; Han, J.; Smith-Warner, S.A.; Zeleniuch-Jacquotte, A.; Le Marchand, L.; Yuan, J.-M.; Wang, R.; Butler, L.M.; Koh, W.-P.; Gao, Y.-T.; Rothman, N.; Ericson, U.; Sonestedt, E.; Visvanathan, K.; Jones, M.R.; Relton, C.; Brennan, P.; Johansson, M.; Ulvik, A. url  doi
  Title Impaired functional vitamin B6 status is associated with increased risk of lung cancer Type Journal Article
  Year 2017 Publication International Journal of Cancer Abbreviated Journal Int J Cancer  
  Volume Issue Pages  
  Keywords 3-hydroxykynurenine:xanthurenic acid; Lung Cancer Cohort Consortium; functional vitamin B6 marker; pyridoxal 5'-phosphate  
  Abstract Circulating vitamin B6 levels have been found to be inversely associated with lung cancer. Most studies have focused on the B6 form pyridoxal 5'-phosphate (PLP), a direct biomarker influenced by inflammation and other factors. Using a functional B6 marker allows further investigation of the potential role of vitamin B6 status in the pathogenesis of lung cancer. We prospectively evaluated the association of the functional marker of vitamin B6 status, the 3-hydroxykynurenine:xanthurenic acid (HK:XA) ratio, with risk of lung cancer in a nested case-control study consisting of 5,364 matched case-control pairs from the Lung Cancer Cohort Consortium (LC3). We used conditional logistic regression to evaluate the association between HK:XA and lung cancer, and random effect models to combine results from different cohorts and regions. High levels of HK:XA, indicating impaired functional B6 status, were associated with an increased risk of lung cancer, the odds ratio comparing the fourth and the first quartiles (OR4thvs.1st ) was 1.25 (95% confidence interval, 1.10-1.41). Stratified analyses indicated that this association was primarily driven by cases diagnosed with squamous cell carcinoma. Notably, the risk associated with HK:XA was approximately 50% higher in groups with a high relative frequency of squamous cell carcinoma, i.e., men, former and current smokers. This risk of squamous cell carcinoma was present in both men and women regardless of smoking status.  
  Address Bevital AS, Bergen, Norway  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0020-7136 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:29238985 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 2011  
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