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  • 1. Ferreiro-Iglesias, Aida
    et al.
    Lesseur, Corina
    McKay, James
    Hung, Rayjean J.
    Han, Younghun
    Zong, Xuchen
    Christiani, David
    Johansson, Mattias
    Xiao, Xiangjun
    Li, Yafang
    Qian, David C.
    Ji, Xuemei
    Liu, Geoffrey
    Caporaso, Neil
    Scelo, Ghislaine
    Zaridze, David
    Mukeriya, Anush
    Kontic, Milica
    Ognjanovic, Simona
    Lissowska, Jolanta
    Szolkowska, Malgorzata
    Swiatkowska, Beata
    Janout, Vladimir
    Holcatova, Ivana
    Bolca, Ciprian
    Savic, Milan
    Ognjanovic, Miodrag
    Bojesen, Stig Egil
    Wu, Xifeng
    Albanes, Demetrios
    Aldrich, Melinda C.
    Tardon, Adonina
    Fernandez-Somoano, Ana
    Fernandez-Tardon, Guillermo
    Le Marchand, Loic
    Rennert, Gadi
    Chen, Chu
    Doherty, Jennifer
    Goodman, Gary
    Bickeboeller, Heike
    Wichmann, H-Erich
    Risch, Angela
    Rosenberger, Albert
    Shen, Hongbing
    Dai, Juncheng
    Field, John K.
    Davies, Michael
    Woll, Penella
    Teare, M. Dawn
    Kiemeney, Lambertus A.
    van der Heijden, Erik H. F. M.
    Yuan, Jian-Min
    Hong, Yun-Chul
    Haugen, Aage
    Zienolddiny, Shanbeh
    Lam, Stephen
    Tsao, Ming-Sound
    Johansson, Mikael
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Grankvist, Kjell
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Clinical chemistry.
    Schabath, Matthew B.
    Andrew, Angeline
    Duell, Eric
    Melander, Olle
    Brunnstrom, Hans
    Lazarus, Philip
    Arnold, Susanne
    Slone, Stacey
    Byun, Jinyoung
    Kamal, Ahsan
    Zhu, Dakai
    Landi, Maria Teresa
    Amos, Christopher, I
    Brennan, Paul
    Fine mapping of MHC region in lung cancer highlights independent susceptibility loci by ethnicity2018In: Nature Communications, E-ISSN 2041-1723, Vol. 9, article id 3927Article in journal (Refereed)
    Abstract [en]

    Lung cancer has several genetic associations identified within the major histocompatibility complex (MHC); although the basis for these associations remains elusive. Here, we analyze MHC genetic variation among 26,044 lung cancer patients and 20,836 controls densely genotyped across the MHC, using the Illumina Illumina OncoArray or Illumina 660W SNP microarray. We impute sequence variation in classical HLA genes, fine-map MHC associations for lung cancer risk with major histologies and compare results between ethnicities. Independent and novel associations within HLA genes are identified in Europeans including amino acids in the HLA-B*0801 peptide binding groove and an independent HLA-DQB1*06 loci group. In Asians, associations are driven by two independent HLA allele sets that both increase risk in HLA-DQB1*0401 and HLA-DRB1*0701; the latter better represented by the amino acid Ala-104. These results implicate several HLA-tumor peptide interactions as the major MHC factor modulating lung cancer susceptibility.

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  • 2. Hung, Rayjean J.
    et al.
    Spitz, Margaret R.
    Houlston, Richard S.
    Schwartz, Ann G.
    Field, John K.
    Ying, Jun
    Li, Yafang
    Han, Younghun
    Ji, Xuemei
    Chen, Wei
    Wu, Xifeng
    Gorlov, Ivan P.
    Na, Jie
    de Andrade, Mariza
    Liu, Geoffrey
    Brhane, Yonathan
    Diao, Nancy
    Wenzlaff, Angela
    Davies, Michael P. A.
    Liloglou, Triantafillos
    Timofeeva, Maria
    Muley, Thomas
    Rennert, Hedy
    Saliba, Walid
    Ryan, Brid M.
    Bowman, Elise
    Barros-Dios, Juan-Miguel
    Perez-Rios, Monica
    Morgenstern, Hal
    Zienolddiny, Shanbeh
    Skaug, Vidar
    Ugolini, Donatella
    Bonassi, Stefano
    van der Heijden, Erik H. F. M.
    Tardon, Adonina
    Bojesen, Stig E.
    Landi, Maria Teresa
    Johansson, Mattias
    Bickeboeller, Heike
    Arnold, Susanne
    Le Marchand, Loic
    Melander, Olle
    Andrew, Angeline
    Grankvist, Kjell
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Clinical chemistry.
    Caporaso, Neil
    Teare, M. Dawn
    Schabath, Matthew B.
    Aldrich, Melinda C.
    Kiemeney, Lambertus A.
    Wichmann, H-Erich
    Lazarus, Philip
    Mayordomo, Jose
    Neri, Monica
    Haugen, Aage
    Zhang, Zuo-Feng
    Ruano-Ravina, Alberto
    Brenner, Hermann
    Harris, Curtis C.
    Orlow, Irene
    Rennert, Gadi
    Risch, Angela
    Brennan, Paul
    Christiani, David C.
    Amos, Christopher I.
    Yang, Ping
    Gorlova, Olga Y.
    Lung Cancer Risk in Never-Smokers of European Descent is Associated With Genetic Variation in the 5(p)15.33 TERT-CLPTM1Ll Region2019In: Journal of Thoracic Oncology, ISSN 1556-0864, E-ISSN 1556-1380, Vol. 14, no 8, p. 1360-1369Article in journal (Refereed)
    Abstract [en]

    Introduction: Inherited susceptibility to lung cancer risk in never-smokers is poorly understood. The major reason for this gap in knowledge is that this disease is relatively uncommon (except in Asians), making it difficult to assemble an adequate study sample. In this study we conducted a genome-wide association study on the largest, to date, set of European-descent never-smokers with lung cancer. Methods: We conducted a two-phase (discovery and replication) genome-wide association study in never-smokers of European descent. We further augmented the sample by performing a meta-analysis with never-smokers from the recent OncoArray study, which resulted in a total of 3636 cases and 6295 controls. We also compare our findings with those in smokers with lung cancer. Results: We detected three genome-wide statistically significant single nucleotide polymorphisms rs31490 (odds ratio [OR]: 0.769, 95% confidence interval [CI]: 0.722-0.820; p value 5.31 x 10(-16)), rs380286 (OR: 0.770, 95% CI: 0.723-0.820; p value 4.32 x 10(-16)), and rs4975616 OR: 0.778, 95% CI: 0.730-0.829; p value 1.04 x 10(-14)). All three mapped to Chromosome 5 CLPTM1L-TERT region, previously shown to be associated with lung cancer risk in smokers and in never-smoker Asian women, and risk of other cancers including breast, ovarian, colorectal, and prostate. Conclusions: We found that genetic susceptibility to lung cancer in never-smokers is associated to genetic variants with pan-cancer risk effects. The comparison with smokers shows that top variants previously shown to be associated with lung cancer risk only confer risk in the presence of tobacco exposure, underscoring the importance of gene-environment interactions in the etiology of this disease. (C) 2019 International Association for the Study of Lung Cancer. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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  • 3. Rosenberger, Albert
    et al.
    Hung, Rayjean J.
    Christiani, David C.
    Caporaso, Neil E.
    Liu, Geoffrey
    Bojesen, Stig E.
    Le Marchand, Loic
    Haiman, Ch. A.
    Albanes, Demetrios
    Aldrich, Melinda C.
    Tardon, Adonina
    Fernandez-Tardon, G.
    Rennert, Gad
    Field, John K.
    Kiemeney, B.
    Lazarus, Philip
    Haugen, Aage
    Zienolddiny, Shanbeh
    Lam, Stephen
    Schabath, Matthew B.
    Andrew, Angeline S.
    Brunnsstom, Hans
    Goodman, Gary E.
    Doherty, Jennifer A.
    Chen, Chu
    Teare, M. Dawn
    Wichmann, H. -Erich
    Manz, Judith
    Risch, Angela
    Muley, Thomas R.
    Johansson, Mikael
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Brennan, Paul
    Landi, Maria Teresa
    Amos, Christopher I.
    Pesch, Beate
    Johnen, Georg
    Bruening, Thomas
    Bickeboeller, Heike
    Gomolka, Maria
    Genetic modifiers of radon-induced lung cancer risk: a genome-wide interaction study in former uranium miners2018In: International Archives of Occupational and Environmental Health, ISSN 0340-0131, E-ISSN 1432-1246, Vol. 91, no 8, p. 937-950Article in journal (Refereed)
    Abstract [en]

    Purpose: Radon is a risk factor for lung cancer and uranium miners are more exposed than the general population. A genome-wide interaction analysis was carried out to identify genomic loci, genes or gene sets that modify the susceptibility to lung cancer given occupational exposure to the radioactive gas radon.

    Methods: Samples from 28 studies provided by the International Lung Cancer Consortium were pooled with samples of former uranium miners collected by the German Federal Office of Radiation Protection. In total, 15,077 cases and 13,522 controls, all of European ancestries, comprising 463 uranium miners were compared. The DNA of all participants was genotyped with the OncoArray. We fitted single-marker and in multi-marker models and performed an exploratory gene-set analysis to detect cumulative enrichment of significance in sets of genes.

    Results: We discovered a genome-wide significant interaction of the marker rs12440014 within the gene CHRNB4 (OR = 0.26, 95% CI 0.11–0.60, p = 0.0386 corrected for multiple testing). At least suggestive significant interaction of linkage disequilibrium blocks was observed at the chromosomal regions 18q21.23 (p = 1.2 × 10−6), 5q23.2 (p = 2.5 × 10−6), 1q21.3 (p = 3.2 × 10−6), 10p13 (p = 1.3 × 10−5) and 12p12.1 (p = 7.1 × 10−5). Genes belonging to the Gene Ontology term “DNA dealkylation involved in DNA repair” (GO:0006307; p = 0.0139) or the gene family HGNC:476 “microRNAs” (p = 0.0159) were enriched with LD-blockwise significance.

    Conclusion: The well-established association of the genomic region 15q25 to lung cancer might be influenced by exposure to radon among uranium miners. Furthermore, lung cancer susceptibility is related to the functional capability of DNA damage signaling via ubiquitination processes and repair of radiation-induced double-strand breaks by the single-strand annealing mechanism.

  • 4. Zhu, Ying
    et al.
    Wei, Yongyue
    Zhang, Ruyang
    Dong, Xuesi
    Shen, Sipeng
    Zhao, Yang
    Bai, Jianling
    Albanes, Demetrius
    Caporaso, Neil E.
    Landi, Maria Teresa
    Zhu, Bin
    Chanock, Stephen J.
    Gu, Fangyi
    Lam, Stephen
    Tsao, Ming-Sound
    Shepherd, Frances A.
    Tardon, Adonina
    Fernandez-Somoano, Ana
    Fernandez-Tardon, Guillermo
    Chen, Chu
    Barnett, Matthew J.
    Doherty, Jennifer
    Bojesen, Stig E.
    Johansson, Mattias
    Brennan, Paul
    Mckay, James D.
    Carreras-Torres, Robert
    Muley, Thomas
    Risch, Angela
    Wichmann, Heunz-Erich
    Bickeboeller, Heike
    Rosenberger, Albert
    Rennert, Gad
    Saliba, Walid
    Arnold, Susanne M.
    Field, John K.
    Davies, Michael P. A.
    Marcus, Michael W.
    Wu, Xifeng
    Ye, Yuanqing
    Le Marchand, Loic
    Wilkens, Lynne R.
    Melander, Olle
    Manjer, Jonas
    Brunnstrom, Hans
    Hung, Rayjean J.
    Liu, Geoffrey
    Brhane, Yonathan
    Kachuri, Linda
    Andrew, Angeline S.
    Duell, Eric J.
    Kiemeney, Lambertus A.
    van der Heijden, Erik H. F. M.
    Haugen, Aage
    Zienolddiny, Shanbeh
    Skaug, Vidar
    Grankvist, Kjell
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Clinical chemistry.
    Johansson, Mikael
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology.
    Woll, Penella J.
    Cox, Angela
    Taylor, Fiona
    Teare, Dawn M.
    Lazarus, Philip
    Schabath, Matthew B.
    Aldrich, Melinda C.
    Houlston, Richard S.
    McLaughlin, John
    Stevens, Victoria L.
    Shen, Hongbing
    Hu, Zhibin
    Dai, Juncheng
    Amos, Christopher I.
    Han, Younghun
    Zhu, Dakai
    Goodman, Gary E.
    Chen, Feng
    Christiani, David C.
    Elevated Platelet Count Appears to Be Causally Associated with Increased Risk of Lung Cancer: A Mendelian Randomization Analysis2019In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 28, no 5, p. 935-942Article in journal (Refereed)
    Abstract [en]

    Background: Platelets are a critical element in coagulation and inflammation, and activated platelets are linked to cancer risk through diverse mechanisms. However, a causal relationship between platelets and risk of lung cancer remains unclear. Methods: We performed single and combined multiple instrumental variable Mendelian randomization analysis by an inverse-weighted method, in addition to a series of sensitivity analyses. Summary data for associations between SNPs and platelet count are from a recent publication that included 48,666 Caucasian Europeans, and the International Lung Cancer Consortium and Transdisciplinary Research in Cancer of the Lung data consisting of 29,266 cases and 56,450 controls to analyze associations between candidate SNPs and lung cancer risk. Results: Multiple instrumental variable analysis incorporating six SNPs showed a 62% increased risk of overall nonsmall cell lung cancer [NSCLC; OR, 1.62; 95% confidence interval (CI), 1.15-2.27; P = 0.005] and a 200% increased risk for small-cell lung cancer (OR, 3.00; 95% CI, 1.27-7.06; P = 0.01). Results showed only a trending association with NSCLC histologic subtypes, which may be due to insufficient sample size and/or weak effect size. A series of sensitivity analysis retained these findings. Conclusions: Our findings suggest a causal relationship between elevated platelet count and increased risk of lung cancer and provide evidence of possible antiplatelet interventions for lung cancer prevention. Impact: These findings provide a better understanding of lung cancer etiology and potential evidence for antiplatelet interventions for lung cancer prevention.

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