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2. Gene–gene interaction of AhRwith and within the Wntcascade affects susceptibility to lung cancer

Author

Rosenberger, Albert, Muttray, Nils, Hung, Rayjean J., Christiani, David C., Caporaso, Neil E., Liu, Geoffrey, Bojesen, Stig E., Le Marchand, Loic, Albanes, Demetrios, Aldrich, Melinda C., Tardon, Adonina, Fernández-Tardón, Guillermo, Rennert, Gad, Field, John K., Davies, Michael P. A., Liloglou, Triantafillos, Kiemeney, Lambertus A., Lazarus, Philip, Wendel, Bernadette, Haugen, Aage, Zienolddiny, Shanbeh, Lam, Stephen, Schabath, Matthew B., Andrew, Angeline S., Duell, Eric J., Arnold, Susanne M., Goodman, Gary E., Chen, Chu, Doherty, Jennifer A., Taylor, Fiona, Cox, Angela, Woll, Penella J., Risch, Angela, Muley, Thomas R., Johansson, Mikael, Brennan, Paul, Landi, Maria Teresa, Shete, Sanjay S., Amos, Christopher I., and Bickeböller, Heike

Published
2022
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4. Cannabis smoking and lung cancer risk: Pooled analysis in the International Lung Cancer Consortium

Author

Zhang, Li Rita, Morgenstern, Hal, Greenland, Sander, Chang, Shen‐Chih, Lazarus, Philip, Teare, M Dawn, Woll, Penella J, Orlow, Irene, Cox, Brian, Zealand, on behalf of the Cannabis and Respiratory Disease Research Group of New, Brhane, Yonathan, Liu, Geoffrey, and Hung, Rayjean J

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Cannabinoid Research, Substance Misuse, Tobacco, Lung Cancer, Tobacco Smoke and Health, Cancer, Lung, Prevention, Women's Health, 2.2 Factors relating to the physical environment, 2.1 Biological and endogenous factors, Respiratory, Good Health and Well Being, Adenocarcinoma, Carcinoma, Squamous Cell, Case-Control Studies, Humans, Lung Neoplasms, Marijuana Smoking, Risk, lung cancer, Cannabis smoking, never smokers, marijuana smoking, Cannabis and Respiratory Disease Research Group of New Zealand, Lung cancer, Marijuana smoking, Never smokers, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract

To investigate the association between cannabis smoking and lung cancer risk, data on 2,159 lung cancer cases and 2,985 controls were pooled from 6 case-control studies in the US, Canada, UK, and New Zealand within the International Lung Cancer Consortium. Study-specific associations between cannabis smoking and lung cancer were estimated using unconditional logistic regression adjusting for sociodemographic factors, tobacco smoking status and pack-years; odds-ratio estimates were pooled using random effects models. Subgroup analyses were done for sex, histology and tobacco smoking status. The shapes of dose-response associations were examined using restricted cubic spline regression. The overall pooled OR for habitual versus nonhabitual or never users was 0.96 (95% CI: 0.66-1.38). Compared to nonhabitual or never users, the summary OR was 0.88 (95%CI: 0.63-1.24) for individuals who smoked 1 or more joint-equivalents of cannabis per day and 0.94 (95%CI: 0.67-1.32) for those consumed at least 10 joint-years. For adenocarcinoma cases the ORs were 1.73 (95%CI: 0.75-4.00) and 1.74 (95%CI: 0.85-3.55), respectively. However, no association was found for the squamous cell carcinoma based on small numbers. Weak associations between cannabis smoking and lung cancer were observed in never tobacco smokers. Spline modeling indicated a weak positive monotonic association between cumulative cannabis use and lung cancer, but precision was low at high exposure levels. Results from our pooled analyses provide little evidence for an increased risk of lung cancer among habitual or long-term cannabis smokers, although the possibility of potential adverse effect for heavy consumption cannot be excluded.

Published
2015

7. Identification of genetically predicted DNA methylation markers associated with non–small cell lung cancer risk among 34,964 cases and 448,579 controls

Author

Zhao, Xiaoyu, primary, Yang, Meiqi, additional, Fan, Jingyi, additional, Wang, Mei, additional, Wang, Yifan, additional, Qin, Na, additional, Zhu, Meng, additional, Jiang, Yue, additional, Gorlova, Olga Y., additional, Gorlov, Ivan P., additional, Albanes, Demetrius, additional, Lam, Stephen, additional, Tardón, Adonina, additional, Chen, Chu, additional, Goodman, Gary E., additional, Bojesen, Stig E., additional, Landi, Maria Teresa, additional, Johansson, Mattias, additional, Risch, Angela, additional, Wichmann, H.‐Erich, additional, Bickeböller, Heike, additional, Christiani, David C., additional, Rennert, Gad, additional, Arnold, Susanne M., additional, Brennan, Paul, additional, Field, John K., additional, Shete, Sanjay, additional, Le Marchand, Loïc, additional, Liu, Geoffrey, additional, Hung, Rayjean J., additional, Andrew, Angeline S., additional, Kiemeney, Lambertus A., additional, Zienolddiny, Shanbeh, additional, Grankvist, Kjell, additional, Johansson, Mikael, additional, Caporaso, Neil E., additional, Woll, Penella J., additional, Lazarus, Philip, additional, Schabath, Matthew B., additional, Aldrich, Melinda C., additional, Patel, Alpa V., additional, Davies, Michael P. A., additional, Ma, Hongxia, additional, Jin, Guangfu, additional, Hu, Zhibin, additional, Amos, Christopher I., additional, Shen, Hongbing, additional, and Dai, Juncheng, additional

Published
2023
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8. Gemcitabine and docetaxel versus doxorubicin as first-line treatment in previously untreated advanced unresectable or metastatic soft-tissue sarcomas (GeDDiS): a randomised controlled phase 3 trial

Author

Seddon, Beatrice, Strauss, Sandra J, Whelan, Jeremy, Leahy, Michael, Woll, Penella J, Cowie, Fiona, Rothermundt, Christian, Wood, Zoe, Benson, Charlotte, Ali, Nasim, Marples, Maria, Veal, Gareth J, Jamieson, David, Küver, Katja, Tirabosco, Roberto, Forsyth, Sharon, Nash, Stephen, Dehbi, Hakim-Moulay, and Beare, Sandy

Published
2017
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9. Carboplatin versus two doses of cisplatin in combination with gemcitabine in the treatment of advanced non-small-cell lung cancer: Results from a British Thoracic Oncology Group randomised phase III trial

Author

Ferry, David, Billingham, Lucinda, Jarrett, Hugh, Dunlop, David, Woll, Penella J., Nicolson, Marianne, Shah, Riyaz, Thompson, Joyce, Spicer, James, Muthukumar, D., Skailes, Geraldine, Leonard, Pauline, Chetiyawardana, A.D., Wells, Paula, Lewanski, Conrad, Crosse, Barbara, Hill, Michelle, Gaunt, Piers, and O'Byrne, Kenneth

Published
2017
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10. Concurrent once-daily versus twice-daily chemoradiotherapy in patients with limited-stage small-cell lung cancer (CONVERT): an open-label, phase 3, randomised, superiority trial

Author

Faivre-Finn, Corinne, Snee, Michael, Ashcroft, Linda, Appel, Wiebke, Barlesi, Fabrice, Bhatnagar, Adityanarayan, Bezjak, Andrea, Cardenal, Felipe, Fournel, Pierre, Harden, Susan, Le Pechoux, Cecile, McMenemin, Rhona, Mohammed, Nazia, O'Brien, Mary, Pantarotto, Jason, Surmont, Veerle, Van Meerbeeck, Jan P, Woll, Penella J, Lorigan, Paul, and Blackhall, Fiona

Published
2017
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12. Candidate pathway analysis of surfactant proteins identifies CTSH and SFTA2 that influences lung cancer risk

Author

Luyapan, Jennifer, primary, Bossé, Yohan, additional, Li, Zhonglin, additional, Xiao, Xiangjun, additional, Rosenberger, Albert, additional, Hung, Rayjean J, additional, Lam, Stephen, additional, Zienolddiny, Shanbeh, additional, Liu, Geoffrey, additional, Kiemeney, Lambertus A, additional, Chen, Chu, additional, McKay, James, additional, Johansson, Mattias, additional, Johansson, Mikael, additional, Tardon, Adonina, additional, Fernandez-Tardon, Guillermo, additional, Brennan, Paul, additional, Field, John K, additional, Davies, Michael P, additional, Woll, Penella J, additional, Cox, Angela, additional, Taylor, Fiona, additional, Arnold, Susanne M, additional, Lazarus, Philip, additional, Grankvist, Kjell, additional, Landi, Maria Teresa, additional, Christiani, David C, additional, MacKenzie, Todd A, additional, and Amos, Christopher I, additional

Published
2023
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13. Candidate pathway analysis of surfactant proteins identifies CTSH and SFTA2 that influences lung cancer risk

Author

Luyapan, Jennifer, Bossé, Yohan, Li, Zhonglin, Xiao, Xiangjun, Rosenberger, Albert, Hung, Rayjean J., Lam, Stephen, Zienolddiny, Shanbeh, Liu, Geoffrey, Kiemeney, Lambertus A., Chen, Chu, McKay, James, Johansson, Mattias, Johansson, Mikael, Tardon, Adonina, Fernandez-Tardon, Guillermo, Brennan, Paul, Field, John K., Davies, Michael P., Woll, Penella J., Cox, Angela, Taylor, Fiona, Arnold, Susanne M., Lazarus, Philip, Grankvist, Kjell, Landi, Maria T., Christiani, David C., MacKenzie, Todd A., Amos, Christopher I., Luyapan, Jennifer, Bossé, Yohan, Li, Zhonglin, Xiao, Xiangjun, Rosenberger, Albert, Hung, Rayjean J., Lam, Stephen, Zienolddiny, Shanbeh, Liu, Geoffrey, Kiemeney, Lambertus A., Chen, Chu, McKay, James, Johansson, Mattias, Johansson, Mikael, Tardon, Adonina, Fernandez-Tardon, Guillermo, Brennan, Paul, Field, John K., Davies, Michael P., Woll, Penella J., Cox, Angela, Taylor, Fiona, Arnold, Susanne M., Lazarus, Philip, Grankvist, Kjell, Landi, Maria T., Christiani, David C., MacKenzie, Todd A., and Amos, Christopher I.

Abstract

Pulmonary surfactant is a lipoprotein synthesized and secreted by alveolar type II cells in lung. We evaluated the associations between 200,139 single nucleotide polymorphisms (SNPs) of 40 surfactant-related genes and lung cancer risk using genotyped data from two independent lung cancer genome-wide association studies. Discovery data included 18,082 cases and 13,780 controls of European ancestry. Replication data included 1,914 cases and 3,065 controls of European descent. Using multivariate logistic regression, we found novel SNPs in surfactant-related genes CTSH [rs34577742 C > T, odds ratio (OR) = 0.90, 95% confidence interval (CI) = 0.89-0.93, P = 7.64 × 10-9] and SFTA2 (rs3095153 G > A, OR = 1.16, 95% CI = 1.10-1.21, P = 1.27 × 10-9) associated with overall lung cancer in the discovery data and validated in an independent replication data-CTSH (rs34577742 C > T, OR = 0.88, 95% CI = 0.80-0.96, P = 5.76 × 10-3) and SFTA2 (rs3095153 G > A, OR = 1.14, 95% CI = 1.01-1.28, P = 3.25 × 10-2). Among ever smokers, we found SNPs in CTSH (rs34577742 C > T, OR = 0.89, 95% CI = 0.85-0.92, P = 1.94 × 10-7) and SFTA2 (rs3095152 G > A, OR = 1.20, 95% CI = 1.14-1.27, P = 4.25 × 10-11) associated with overall lung cancer in the discovery data and validated in the replication data-CTSH (rs34577742 C > T, OR = 0.88, 95% CI = 0.79-0.97, P = 1.64 × 10-2) and SFTA2 (rs3095152 G > A, OR = 1.15, 95% CI = 1.01-1.30, P = 3.81 × 10-2). Subsequent transcriptome-wide association study using expression weights from a lung expression quantitative trait loci study revealed genes most strongly associated with lung cancer are CTSH (PTWAS = 2.44 × 10-4) and SFTA2 (PTWAS = 2.32 × 10-6).

Published
2023
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14. MESO-02 Trial Protocol from Ganetespib in Combination with Pemetrexed–Platinum Chemotherapy in Patients with Pleural Mesothelioma (MESO-02): A Phase Ib Trial

Author

Fennell, Dean A., primary, Danson, Sarah, primary, Woll, Penella J., primary, Forster, Martin, primary, Talbot, Denis, primary, Child, Jennifer, primary, Farrelly, Laura, primary, Sharkey, Annabel, primary, Busacca, Sara, primary, Ngai, Yenting, primary, Hackshaw, Allan, primary, and Wheeler, Graham M., primary

Published
2023
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15. Supplementary Data from Ganetespib in Combination with Pemetrexed–Platinum Chemotherapy in Patients with Pleural Mesothelioma (MESO-02): A Phase Ib Trial

Author

Fennell, Dean A., primary, Danson, Sarah, primary, Woll, Penella J., primary, Forster, Martin, primary, Talbot, Denis, primary, Child, Jennifer, primary, Farrelly, Laura, primary, Sharkey, Annabel, primary, Busacca, Sara, primary, Ngai, Yenting, primary, Hackshaw, Allan, primary, and Wheeler, Graham M., primary

Published
2023
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16. Maintenance pazopanib versus placebo in Non-Small Cell Lung Cancer patients non-progressive after first line chemotherapy: A double blind randomised phase III study of the lung cancer group, EORTC 08092 (EudraCT: 2010-018566-23, NCT01208064)

Author

O’Brien, Mary E.R., Gaafar, Rabab, Hasan, Baktiar, Menis, Jessica, Cufer, Tanja, Popat, Sanjay, Woll, Penella J., Surmont, Veerle, Georgoulias, Vassilis, Montes, Ana, Blackhall, Fiona, Hennig, Ivo, Schmid-Bindert, Gerald, and Baas, Paul

Published
2015
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18. Neuropeptide growth factors and small cell lung cancer

Author

Woll, Penella J.

Subjects
616.99
Abstract

Quiescent cultures of Swiss 3T3 cells are a useful model system for elucidating the mechanisms of mitogenesis. Here, Swiss 3T3 cells were used to test novel mitogens and characterise bombesin antagonists. Bradykinin was identified as a potent mitogen, acting in synergy with insulin. Two groups of antagonists were characterised: the substance P analogues [DArg1, DPro2, DTrp7,9, Leu11]- substance P (antagonist A), [DArg1, DPhe5, DTrp7,9, Leu11]- substance P (antagonist D) and [Arg6, DTrp7,9, Leu11] substance P(6-11) (antagonist G); and the bombesin-specific antagonists (Leu13-psi(CH2NH)Leu14]bombesin and N- acetyl-GRP(20-26). The substance P antagonists appear to interact with a common domain on the receptors for three mitogenic neuropeptides in Swiss 3T3 cells: bombesin, vasopressin and bradykinin. The bombesin-specific antagonists did not interact with other receptors. Small cell lung cancer (SCLC) is an aggressive form of lung cancer. The bombesin-like peptides, including gastrin- releasing peptide (GRP), have been postulated to act as autocrine growth factors for these tumours. In SCLC cell lines, all the antagonists were shown to block the early effect of bombesin, mobilisation of cytosolic Ca2+. The substance P antagonists also inhibited SCLC growth in liquid and semisolid media, in a reversible, dose-dependent fashion. The bombesin-specific antagonists did not inhibit SCLC growth, suggesting that other growth factors blocked by the substance P antagonists may be more important for regulating SCLC growth. A variety of peptides and hormones were tested for their ability to mobilise cytosolic Ca2+ in SCLG cell lines. Ca2+ signals were induced by GRP, vasopressin, bradykinin, cholecystokinin, galanin and neurotensin, and all were blocked by antagonists D and G. These neuropeptides are suggested as possible growth factors for SCLC.

Published
1990

23. Overall Survival Improvement in Patients with Lung Cancer and Bone Metastases Treated with Denosumab Versus Zoledronic Acid: Subgroup Analysis from a Randomized Phase 3 Study

Author

Scagliotti, Giorgio Vittorio, Hirsh, Vera, Siena, Salvatore, Henry, David H., Woll, Penella J., Manegold, Christian, Solal-Celigny, Philippe, Rodriguez, Gladys, Krzakowski, Maciej, Mehta, Nilesh D., Lipton, Lara, García-Sáenz, José Angel, Pereira, José Rodrigues, Prabhash, Kumar, Ciuleanu, Tudor-Eliade, Kanarev, Vladimir, Wang, Huei, Balakumaran, Arun, and Jacobs, Ira

Published
2012
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24. First-line erlotinib in patients with advanced non-small-cell lung cancer unsuitable for chemotherapy (TOPICAL): a double-blind, placebo-controlled, phase 3 trial

Author

Lee, Siow Ming, Khan, Iftekhar, Upadhyay, Sunil, Lewanski, Conrad, Falk, Stephen, Skailes, Geraldine, Marshall, Ernie, Woll, Penella J, Hatton, Matthew, Lal, Rohit, Jones, Richard, Toy, Elizabeth, Chao, David, Middleton, Gary, Bulley, Sue, Ngai, Yenting, Rudd, Robin, Hackshaw, Allan, and Boshoff, Chris

Published
2012
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26. Increased risk of lung cancer in individuals with a family history of the disease: A pooled analysis from the International Lung Cancer Consortium

Author

Coté, Michele L., Liu, Mei, Bonassi, Stefano, Neri, Monica, Schwartz, Ann G., Christiani, David C., Spitz, Margaret R., Muscat, Joshua E., Rennert, Gad, Aben, Katja K., Andrew, Angeline S., Bencko, Vladimir, Bickeböller, Heike, Boffetta, Paolo, Brennan, Paul, Brenner, Hermann, Duell, Eric J., Fabianova, Eleonora, Field, John K., Foretova, Lenka, Friis, Søren, Harris, Curtis C., Holcatova, Ivana, Hong, Yun-Chul, Isla, Dolores, Janout, Vladimir, Kiemeney, Lambertus A., Kiyohara, Chikako, Lan, Qing, Lazarus, Philip, Lissowska, Jolanta, Le Marchand, Loic, Mates, Dana, Matsuo, Keitaro, Mayordomo, Jose I., McLaughlin, John R., Morgenstern, Hal, Müeller, Heiko, Orlow, Irene, Park, Bernard J., Pinchev, Mila, Raji, Olaide Y., Rennert, Hedy S., Rudnai, Peter, Seow, Adeline, Stucker, Isabelle, Szeszenia-Dabrowska, Neonila, Dawn Teare, M., Tjønnelan, Anne, Ugolini, Donatella, van der Heijden, Henricus F.M., Wichmann, Erich, Wiencke, John K., Woll, Penella J., Yang, Ping, Zaridze, David, Zhang, Zuo-Feng, Etzel, Carol J., and Hung, Rayjean J.

Published
2012
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27. Gene–gene interaction of AhR with and within the Wnt cascade affects susceptibility to lung cancer

Author

Rosenberger, Albert, Muttray, Nils, Hung, Rayjean J., Christiani, David C., Caporaso, Neil E., Liu, Geoffrey, Bojesen, Stig E., Le Marchand, Loic, Albanes, Demetrios, Aldrich, Melinda C., Tardon, Adonina, Fernández-Tardón, Guillermo, Rennert, Gad, Field, John K., Davies, Michael P. A., Liloglou, Triantafillos, Kiemeney, Lambertus A., Lazarus, Philip, Wendel, Bernadette, Haugen, Aage, Zienolddiny, Shanbeh, Lam, Stephen, Schabath, Matthew B., Andrew, Angeline S., Duell, Eric J., Arnold, Susanne M., Goodman, Gary E., Chen, Chu, Doherty, Jennifer A., Taylor, Fiona, Cox, Angela, Woll, Penella J., Risch, Angela, Muley, Thomas R., Johansson, Mikael, Brennan, Paul, Landi, Maria Teresa, Shete, Sanjay S., Amos, Christopher I., Bickeböller, Heike, Rosenberger, Albert, Muttray, Nils, Hung, Rayjean J., Christiani, David C., Caporaso, Neil E., Liu, Geoffrey, Bojesen, Stig E., Le Marchand, Loic, Albanes, Demetrios, Aldrich, Melinda C., Tardon, Adonina, Fernández-Tardón, Guillermo, Rennert, Gad, Field, John K., Davies, Michael P. A., Liloglou, Triantafillos, Kiemeney, Lambertus A., Lazarus, Philip, Wendel, Bernadette, Haugen, Aage, Zienolddiny, Shanbeh, Lam, Stephen, Schabath, Matthew B., Andrew, Angeline S., Duell, Eric J., Arnold, Susanne M., Goodman, Gary E., Chen, Chu, Doherty, Jennifer A., Taylor, Fiona, Cox, Angela, Woll, Penella J., Risch, Angela, Muley, Thomas R., Johansson, Mikael, Brennan, Paul, Landi, Maria Teresa, Shete, Sanjay S., Amos, Christopher I., and Bickeböller, Heike

Abstract

Background: Aberrant Wnt signalling, regulating cell development and stemness, influences the development of many cancer types. The Aryl hydrocarbon receptor (AhR) mediates tumorigenesis of environmental pollutants. Complex interaction patterns of genes assigned to AhR/Wnt-signalling were recently associated with lung cancer susceptibility. Aim: To assess the association and predictive ability of AhR/Wnt-genes with lung cancer in cases and controls of European descent. Methods: Odds ratios (OR) were estimated for genomic variants assigned to the Wnt agonist and the antagonistic genes DKK2, DKK3, DKK4, FRZB, SFRP4 and Axin2. Logistic regression models with variable selection were trained, validated and tested to predict lung cancer, at which other previously identified SNPs that have been robustly associated with lung cancer risk could also enter the model. Furthermore, decision trees were created to investigate variant × variant interaction. All analyses were performed for overall lung cancer and for subgroups. Results: No genome-wide significant association of AhR/Wnt-genes with overall lung cancer was observed, but within the subgroups of ever smokers (e.g., maker rs2722278 SFRP4; OR = 1.20; 95% CI 1.13–1.27; p = 5.6 × 10–10) and never smokers (e.g., maker rs1133683 Axin2; OR = 1.27; 95% CI 1.19–1.35; p = 1.0 × 10–12). Although predictability is poor, AhR/Wnt-variants are unexpectedly overrepresented in optimized prediction scores for overall lung cancer and for small cell lung cancer. Remarkably, the score for never-smokers contained solely two AhR/Wnt-variants. The optimal decision tree for never smokers consists of 7 AhR/Wnt-variants and only two lung cancer variants. Conclusions: The role of variants belonging to Wnt/AhR-pathways in lung cancer susceptibility may be underrated in main-effects association analysis. Complex interaction patterns in individuals of European descent have moderate predictive capacity for lung cancer or subgroups thereof, especially i

Published
2022
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29. BMC Bioinformatics / I am hiQ—a novel pair of accuracy indices for imputed genotypes

Author

Rosenberger, Albert, Tozzi, Viola, Bickeböller, Heike, Hung, Rayjean J., Christiani, David C., Caporaso, Neil E., Albanes, Demetrios, Landi, Maria Teresa, Liu, Geoffrey, Bojesen, Stig Egil, Marchand, Loic Le, Aldrich, Melinda C., Tardon, Adonina, Fernández-Tardón, Guillermo, Rennert, Gad, Field, John, Davies, Mike, Liloglou, Triantafillos, Kiemeney, Lambertus A., Lazarus, Philip, Haugen, Aage, Zienolddiny, Shanbeh, Lam, Stephen, Schabath, Matthew B., Andrew, Angeline S., Duell, Eric J., Arnold, Susanne Margaretha, Brunnström, Hans, Melander, Olle, Chen, Chu, Doherty, Jennifer A., Teare, Marion Dawn, Cox, Angela, Woll, Penella J., Risch, Angela, Muley, Thomas R., Vejdemo-Johansson, Mikael, Brennan, Paul, Shete, Sanjay S., and Amos, Christopher I.

Subjects
Genotype imputation, High-throughput genotyping, Accuracy measures, GWAS
Abstract

Background: Imputation of untyped markers is a standard tool in genome-wide association studies to close the gap between directly genotyped and other known DNA variants. However, high accuracy with which genotypes are imputed is fundamental. Several accuracy measures have been proposed and some are implemented in imputation software, unfortunately diversely across platforms. In the present paper, we introduce Iam hiQ, an independent pair of accuracy measures that can be applied to dosage files, the output of all imputation software. Iam (imputation accuracy measure) quantifies the average amount of individual-specific versus population-specific genotype information in a linear manner. hiQ (heterogeneity in quantities of dosages) addresses the inter-individual heterogeneity between dosages of a marker across the sample at hand. Results: Applying both measures to a large case–control sample of the International Lung Cancer Consortium (ILCCO), comprising 27,065 individuals, we found meaningful thresholds for Iam and hiQ suitable to classify markers of poor accuracy. We demonstrate how Manhattan-like plots and moving averages of Iam and hiQ can be useful to identify regions enriched with less accurate imputed markers, whereas these regions would by missed when applying the accuracy measure info (implemented in IMPUTE2). Conclusion: We recommend using Iam hiQ additional to other accuracy scores for variant filtering before stepping into the analysis of imputed GWAS data.

Published
2022
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30. Additional file 1 of Gene���gene interaction of AhRwith and within the Wntcascade affects susceptibility to lung cancer

Author

Rosenberger, Albert, Muttray, Nils, Hung, Rayjean J., Christiani, David C., Caporaso, Neil E., Liu, Geoffrey, Bojesen, Stig E., Le Marchand, Loic, Albanes, Demetrios, Aldrich, Melinda C., Tardon, Adonina, Fern��ndez-Tard��n, Guillermo, Rennert, Gad, Field, John K., Davies, Michael P. A., Liloglou, Triantafillos, Kiemeney, Lambertus A., Lazarus, Philip, Wendel, Bernadette, Haugen, Aage, Zienolddiny, Shanbeh, Lam, Stephen, Schabath, Matthew B., Andrew, Angeline S., Duell, Eric J., Arnold, Susanne M., Goodman, Gary E., Chen, Chu, Doherty, Jennifer A., Taylor, Fiona, Cox, Angela, Woll, Penella J., Risch, Angela, Muley, Thomas R., Johansson, Mikael, Brennan, Paul, Landi, Maria Teresa, Shete, Sanjay S., Amos, Christopher I., and Bickeb��ller, Heike

Subjects
respiratory tract diseases
Abstract

Additional file 1: Table S1. List of investigated SNPs (AhR/Wnt-markers and LC-markers). Table S2. Association of AhR/Wnt-marker within subgroups. Table S3. Association of markers reported elsewhere. Table S4. Score composition and importance ratio. Table S5. Discriminability of prediction scores. Table S6. Prediction accuracy of the decision trees. Table S7. Prediction accuracy in never smokers by histological subtypes. Table S8. Expression in normal tissue of the lung according LungGENS. Table S9. Expression in normal tissue of the lung according the Human Protein Atlas. Figure S1. Association of AhR/Wnt-markers within never and ever smokers. Figure S2. Decision tree for overall LC. Figure S3. LC-risk score: model selection and ROCs for overall LC. Figure S4. LC-risk score: model selection and ROCs for SCLC and Never smoker. Figure S5. Decision tree for early onset LC (age ���55 years). Figure S6. Decision tree for SqCLC. Figure S7. Decision tree for SCLC. Figure S8. Decision tree for ever smoker. Figure S9. Expression profiles according to the Human Protein Atlas.

Published
2022
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33. Angiosarcoma

Author

Young, Robin J, Brown, Nicola J, Reed, Malcolm W, Hughes, David, and Woll, Penella J

Published
2010
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35. Olaparib as Maintenance Treatment in Patients with Chemosensitive Small Cell Lung Cancer (STOMP): A Randomised, Double-Blind, Placebo-Controlled Phase II Trial

Author

Woll, Penella J., primary, Gaunt, Piers, additional, Danson, Sarah, additional, Steele, Nicola, additional, Ahmed, Samreen, additional, Mulatero, Clive, additional, Shah, Riyaz, additional, Bhosle, Jaishree, additional, Hodgkinson, Elizabeth, additional, Watkins, Ben, additional, and Billingham, Lucinda J., additional

Published
2022
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39. Gene-gene Interaction of AhR with and within the Wnt Cascade Affects Susceptibility to Lung Cancer

Author

Rosenberger, Albert, primary, Muttray, Nils, additional, Hung, Rayjean J, additional, Christiani, David C, additional, Caporaso, Neil E, additional, Liu, Geoffrey, additional, Bojesen, Stig E, additional, Marchand, Loic Le, additional, Albanes, Demetrios, additional, Aldrich, Melinda C, additional, Tardon, Adonina, additional, Fernández-Tardón, Guillermo, additional, Rennert, Gad, additional, Field, John K, additional, Davies, Michael P.A., additional, Liloglou, Triantafillos, additional, Kiemeney, Lambertus A, additional, Lazarus, Philip, additional, Wendel, Bernadette, additional, Haugen, Aage, additional, Zienolddiny, Shanbeh, additional, Lam, Stephen, additional, Schabath, Matthew B, additional, Andrew, Angeline S, additional, Duell, Eric J, additional, Arnold, Susanne M, additional, Goodman, Gary E, additional, Chen, Chu, additional, Doherty, Jennifer A, additional, Taylor, Fiona, additional, Cox, Angela, additional, Woll, Penella J, additional, Risch, Angela, additional, Muley, Thomas R, additional, Johansson, Mikael, additional, Brennan, Paul, additional, Landi, Maria Teresa, additional, Shete, Sanjay S, additional, Amos, Christopher I, additional, Bickeböller, Heike, additional, and consortium, INTEGRAL-ILCCO, additional

Published
2021
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41. I’am hiQ – A Novel Accuracy Index for Imputed Genotypes

Author

Rosenberger, Albert, primary, Tozzi, Viola, additional, Hung, Rayjean J, additional, Christiani, David C, additional, Caporaso, Neil E, additional, Liu, Geoffrey, additional, Bojesen, Stig E, additional, Marchand, Loic Le, additional, Albanes, Demetrios, additional, Aldrich, Melinda C, additional, Tardon, Adonina, additional, Fernández-Tardón, Guillermo, additional, Rennert, Gad, additional, Field, John K, additional, Davies, Mike, additional, Liloglou, Triantafillos, additional, Kiemeney, Lambertus A, additional, Lazarus, Philip, additional, Haugen, Aage, additional, Zienolddiny, Shanbeh, additional, Lam, Stephen, additional, Schabath, Matthew B, additional, Andrew, Angeline S, additional, Duell, Eric J, additional, Arnold, Susanne M, additional, Brunnsstöm, Hans, additional, Melander, Olle, additional, Goodman, Gary E, additional, Chen, Chu, additional, Doherty, Jennifer A, additional, Teare, Marion Dawn, additional, Cox, Angela, additional, Woll, Penella J, additional, Risch, Angela, additional, Muley, Thomas R, additional, Johansson, Mikael, additional, Brennan, Paul, additional, Landi, Maria Teresa, additional, Shete, Sanjay S, additional, Amos, Christopher I, additional, and Bickeböller, Heike, additional

Published
2021
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43. Ganetespib in Combination with Pemetrexed–Platinum Chemotherapy in Patients with Pleural Mesothelioma (MESO-02): A Phase Ib Trial

Author

Fennell, Dean A., primary, Danson, Sarah, additional, Woll, Penella J., additional, Forster, Martin, additional, Talbot, Denis, additional, Child, Jennifer, additional, Farrelly, Laura, additional, Sharkey, Annabel, additional, Busacca, Sara, additional, Ngai, Yenting, additional, Hackshaw, Allan, additional, and Wheeler, Graham M., additional

Published
2020
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44. Association Analysis of Driver Gene–Related Genetic Variants Identified Novel Lung Cancer Susceptibility Loci with 20,871 Lung Cancer Cases and 15,971 Controls

Author

Wang, Yuzhuo, primary, Gorlova, Olga Y., additional, Gorlov, Ivan P., additional, Zhu, Meng, additional, Dai, Juncheng, additional, Albanes, Demetrius, additional, Lam, Stephen, additional, Tardon, Adonina, additional, Chen, Chu, additional, Goodman, Gary E., additional, Bojesen, Stig E., additional, Landi, Maria Teresa, additional, Johansson, Mattias, additional, Risch, Angela, additional, Wichmann, Heunz-Erich, additional, Bickeboller, Heike, additional, Christiani, David C., additional, Rennert, Gad, additional, Arnold, Susanne M., additional, Brennan, Paul, additional, Field, John K., additional, Shete, Sanjay, additional, Le Marchand, Loïc, additional, Melander, Olle, additional, Brunnstrom, Hans, additional, Liu, Geoffrey, additional, Hung, Rayjean J., additional, Andrew, Angeline S., additional, Kiemeney, Lambertus A., additional, Zienolddiny, Shanbeh, additional, Grankvist, Kjell, additional, Johansson, Mikael, additional, Caporaso, Neil E., additional, Woll, Penella J., additional, Lazarus, Philip, additional, Schabath, Matthew B., additional, Aldrich, Melinda C., additional, Stevens, Victoria L., additional, Ma, Hongxia, additional, Jin, Guangfu, additional, Hu, Zhibin, additional, Amos, Christopher I., additional, and Shen, Hongbing, additional

Published
2020
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48. Association Analysis of Driver Gene-Related Genetic Variants Identified Novel Lung Cancer Susceptibility Loci with 20,871 Lung Cancer Cases and 15,971 Controls

Author

Wang, Yuzhuo, Gorlova, Olga Y., Gorlov, Ivan P., Zhu, Meng, Dai, Juncheng, Albanes, Demetrius, Lam, Stephen, Tardon, Adonina, Chen, Chu, Goodman, Gary E., Bojesen, Stig E., Landi, Maria Teresa, Johansson, Mattias, Risch, Angela, Wichmann, Heunz-Erich, Bickeboller, Heike, Christiani, David C., Rennert, Gad, Arnold, Susanne M., Brennan, Paul, Field, John K., Shete, Sanjay, Le Marchand, Loic, Melander, Olle, Brunnstrom, Hans, Liu, Geoffrey, Hung, Rayjean J., Andrew, Angeline S., Kiemeney, Lambertus A., Zienolddiny, Shanbeh, Grankvist, Kjell, Johansson, Mikael, Caporaso, Neil E., Woll, Penella J., Lazarus, Philip, Schabath, Matthew B., Aldrich, Melinda C., Stevens, Victoria L., Ma, Hongxia, Jin, Guangfu, Hu, Zhibin, Amos, Christopher I., Shen, Hongbing, Wang, Yuzhuo, Gorlova, Olga Y., Gorlov, Ivan P., Zhu, Meng, Dai, Juncheng, Albanes, Demetrius, Lam, Stephen, Tardon, Adonina, Chen, Chu, Goodman, Gary E., Bojesen, Stig E., Landi, Maria Teresa, Johansson, Mattias, Risch, Angela, Wichmann, Heunz-Erich, Bickeboller, Heike, Christiani, David C., Rennert, Gad, Arnold, Susanne M., Brennan, Paul, Field, John K., Shete, Sanjay, Le Marchand, Loic, Melander, Olle, Brunnstrom, Hans, Liu, Geoffrey, Hung, Rayjean J., Andrew, Angeline S., Kiemeney, Lambertus A., Zienolddiny, Shanbeh, Grankvist, Kjell, Johansson, Mikael, Caporaso, Neil E., Woll, Penella J., Lazarus, Philip, Schabath, Matthew B., Aldrich, Melinda C., Stevens, Victoria L., Ma, Hongxia, Jin, Guangfu, Hu, Zhibin, Amos, Christopher I., and Shen, Hongbing

Abstract

Background: A substantial proportion of cancer driver genes (CDG) are also cancer predisposition genes. However, the associations between genetic variants in lung CDGs and the susceptibility to lung cancer have rarely been investigated. Methods: We selected expression-related single-nucleotide polymorphisms (eSNP) and nonsynonymous variants of lung CDGs, and tested their associations with lung cancer risk in two large-scale genome-wide association studies (20,871 cases and 15,971 controls of European descent). Conditional and joint association analysis was performed to identify independent risk variants. The associations of independent risk variants with somatic alterations in lung CDGs or recurrently altered pathways were investigated using data from The Cancer Genome Atlas (TCGA) project. Results: We identified seven independent SNPs in five lung CDGs that were consistently associated with lung cancer risk in discovery (P < 0.001) and validation (P < 0.05) stages. Among these loci, rs78062588 in TPM3 (1q21.3) was a new lung cancer susceptibility locus (OR = 0.86, P = 1.65 x 10(-6)). Subgroup analysis by histologic types further identified nine lung CDGs. Analysis of somatic alterations found that in lung adenocarcinomas, rs78062588[C] allele (TPM3 in 1q21.3) was associated with elevated somatic copy number of TPM3 (OR = 1.16, P = 0.02). In lung adenocarcinomas, rs1611182 (HLA-A in 6p22.1) was associated with truncation mutations of the transcriptional misregulation in cancer pathway (OR = 0.66, P = 1.76 x 10(-3)). Conclusions: Genetic variants can regulate functions of lung CDGs and influence lung cancer susceptibility. Impact: Our findings might help unravel biological mechanisms underlying lung cancer susceptibility.

Published
2020
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