International Lung Cancer Consortium: Coordinated association study of 10 potential lung cancer susceptibility variants
Background. Analysis of candidate genes in individual studies has had only limited success in identifying particular gene variants that are conclusively associated with lung cancer risk. In the International Lung Cancer Consortium (ILCCO), we conducted a coordinated genotyping study of 10 common var...
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| Veröffentlicht in: | Carcinogenesis (New York) 2010-04, Vol.31 (4), p.625-633 |
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| creator | Truong, Therese Sauter, Wiebke McKay, James D. Hosgood, H.Dean Gallagher, Carla Amos, Christopher I. Spitz, Margaret Muscat, Joshua Lazarus, Philip Illig, Thomas Wichmann, H.Erich Bickeböller, Heike Risch, Angela Dienemann, Hendrik Zhang, Zuo-Feng Naeim, Behnaz Pezeshki Yang, Ping Zienolddiny, Shanbeh Haugen, Aage Le Marchand, Loïc Hong, Yun-Chul Kim, Jin Hee Duell, Eric J. Andrew, Angeline S. Kiyohara, Chikako Shen, Hongbing Matsuo, Keitaro Suzuki, Takeshi Seow, Adeline Ng, Daniel P.K. Lan, Qing Zaridze, David Szeszenia-Dabrowska, Neonilia Lissowska, Jolanta Rudnai, Peter Fabianova, Eleonora Constantinescu, Vali Bencko, Vladimir Foretova, Lenka Janout, Vladimir Caporaso, Neil E. Albanes, Demetrius Thun, Michael Landi, Maria Teresa Trubicka, Joanna Lener, Marcin Lubiński, Jan Wang, Ying Chabrier, Amélie Boffetta, Paolo Brennan, Paul Hung, Rayjean J. |
| description | Background. Analysis of candidate genes in individual studies has had only limited success in identifying particular gene variants that are conclusively associated with lung cancer risk. In the International Lung Cancer Consortium (ILCCO), we conducted a coordinated genotyping study of 10 common variants selected because of their prior evidence of an association with lung cancer. These variants belonged to candidate genes from different cancer-related pathways including inflammation (IL1B), folate metabolism (MTHFR), regulatory function (AKAP9 and CAMKK1), cell adhesion (SEZL6) and apoptosis (FAS, FASL, TP53, TP53BP1 and BAT3). Methods. Genotype data from 15 ILCCO case–control studies were available for a total of 8431 lung cancer cases and 11 072 controls of European descent and Asian ethnic groups. Unconditional logistic regression was used to model the association between each variant and lung cancer risk. Results. Only the association between a non-synonymous variant of TP53BP1 (rs560191) and lung cancer risk was significant (OR = 0.91, P = 0.002). This association was more striking for squamous cell carcinoma (OR = 0.86, P = 6 × 10−4). No heterogeneity by center, ethnicity, smoking status, age group or sex was observed. In order to confirm this association, we included results for this variant from a set of independent studies (9966 cases/11 722 controls) and we reported similar results. When combining all these studies together, we reported an overall OR = 0.93 (0.89–0.97) (P = 0.001). This association was significant only for squamous cell carcinoma [OR = 0.89 (0.85–0.95), P = 1 × 10−4]. Conclusion. This study suggests that rs560191 is associated to lung cancer risk and further highlights the value of consortia in replicating or refuting published genetic associations. |
| doi_str_mv | 10.1093/carcin/bgq001 |
| format | Article |
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Analysis of candidate genes in individual studies has had only limited success in identifying particular gene variants that are conclusively associated with lung cancer risk. In the International Lung Cancer Consortium (ILCCO), we conducted a coordinated genotyping study of 10 common variants selected because of their prior evidence of an association with lung cancer. These variants belonged to candidate genes from different cancer-related pathways including inflammation (IL1B), folate metabolism (MTHFR), regulatory function (AKAP9 and CAMKK1), cell adhesion (SEZL6) and apoptosis (FAS, FASL, TP53, TP53BP1 and BAT3). Methods. Genotype data from 15 ILCCO case–control studies were available for a total of 8431 lung cancer cases and 11 072 controls of European descent and Asian ethnic groups. Unconditional logistic regression was used to model the association between each variant and lung cancer risk. Results. Only the association between a non-synonymous variant of TP53BP1 (rs560191) and lung cancer risk was significant (OR = 0.91, P = 0.002). This association was more striking for squamous cell carcinoma (OR = 0.86, P = 6 × 10−4). No heterogeneity by center, ethnicity, smoking status, age group or sex was observed. In order to confirm this association, we included results for this variant from a set of independent studies (9966 cases/11 722 controls) and we reported similar results. When combining all these studies together, we reported an overall OR = 0.93 (0.89–0.97) (P = 0.001). This association was significant only for squamous cell carcinoma [OR = 0.89 (0.85–0.95), P = 1 × 10−4]. Conclusion. This study suggests that rs560191 is associated to lung cancer risk and further highlights the value of consortia in replicating or refuting published genetic associations.</description><identifier>ISSN: 0143-3334</identifier><identifier>EISSN: 1460-2180</identifier><identifier>DOI: 10.1093/carcin/bgq001</identifier><identifier>PMID: 20106900</identifier><language>eng</language><publisher>England: Oxford University Press</publisher><subject>Adult ; Aged ; Female ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Genotype ; Humans ; Intracellular Signaling Peptides and Proteins - genetics ; Lung Neoplasms - etiology ; Lung Neoplasms - genetics ; Male ; Methylenetetrahydrofolate Reductase (NADPH2) - genetics ; Middle Aged ; Molecular Chaperones - genetics ; Molecular Epidemiology ; Odds Ratio ; Tumor Suppressor p53-Binding Protein 1</subject><ispartof>Carcinogenesis (New York), 2010-04, Vol.31 (4), p.625-633</ispartof><rights>The Author 2010. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c490t-d51e97aa881472a2d67d0f6bf007b62b32b1fba8714a11c3dc412f0a8af344b73</citedby><cites>FETCH-LOGICAL-c490t-d51e97aa881472a2d67d0f6bf007b62b32b1fba8714a11c3dc412f0a8af344b73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20106900$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Truong, Therese</creatorcontrib><creatorcontrib>Sauter, Wiebke</creatorcontrib><creatorcontrib>McKay, James D.</creatorcontrib><creatorcontrib>Hosgood, H.Dean</creatorcontrib><creatorcontrib>Gallagher, Carla</creatorcontrib><creatorcontrib>Amos, Christopher I.</creatorcontrib><creatorcontrib>Spitz, Margaret</creatorcontrib><creatorcontrib>Muscat, Joshua</creatorcontrib><creatorcontrib>Lazarus, Philip</creatorcontrib><creatorcontrib>Illig, Thomas</creatorcontrib><creatorcontrib>Wichmann, H.Erich</creatorcontrib><creatorcontrib>Bickeböller, Heike</creatorcontrib><creatorcontrib>Risch, Angela</creatorcontrib><creatorcontrib>Dienemann, Hendrik</creatorcontrib><creatorcontrib>Zhang, Zuo-Feng</creatorcontrib><creatorcontrib>Naeim, Behnaz Pezeshki</creatorcontrib><creatorcontrib>Yang, Ping</creatorcontrib><creatorcontrib>Zienolddiny, Shanbeh</creatorcontrib><creatorcontrib>Haugen, Aage</creatorcontrib><creatorcontrib>Le Marchand, Loïc</creatorcontrib><creatorcontrib>Hong, Yun-Chul</creatorcontrib><creatorcontrib>Kim, Jin Hee</creatorcontrib><creatorcontrib>Duell, Eric J.</creatorcontrib><creatorcontrib>Andrew, Angeline S.</creatorcontrib><creatorcontrib>Kiyohara, Chikako</creatorcontrib><creatorcontrib>Shen, Hongbing</creatorcontrib><creatorcontrib>Matsuo, Keitaro</creatorcontrib><creatorcontrib>Suzuki, Takeshi</creatorcontrib><creatorcontrib>Seow, Adeline</creatorcontrib><creatorcontrib>Ng, Daniel P.K.</creatorcontrib><creatorcontrib>Lan, Qing</creatorcontrib><creatorcontrib>Zaridze, David</creatorcontrib><creatorcontrib>Szeszenia-Dabrowska, Neonilia</creatorcontrib><creatorcontrib>Lissowska, Jolanta</creatorcontrib><creatorcontrib>Rudnai, Peter</creatorcontrib><creatorcontrib>Fabianova, Eleonora</creatorcontrib><creatorcontrib>Constantinescu, Vali</creatorcontrib><creatorcontrib>Bencko, Vladimir</creatorcontrib><creatorcontrib>Foretova, Lenka</creatorcontrib><creatorcontrib>Janout, Vladimir</creatorcontrib><creatorcontrib>Caporaso, Neil E.</creatorcontrib><creatorcontrib>Albanes, Demetrius</creatorcontrib><creatorcontrib>Thun, Michael</creatorcontrib><creatorcontrib>Landi, Maria Teresa</creatorcontrib><creatorcontrib>Trubicka, Joanna</creatorcontrib><creatorcontrib>Lener, Marcin</creatorcontrib><creatorcontrib>Lubiński, Jan</creatorcontrib><creatorcontrib>Wang, Ying</creatorcontrib><creatorcontrib>Chabrier, Amélie</creatorcontrib><creatorcontrib>Boffetta, Paolo</creatorcontrib><creatorcontrib>Brennan, Paul</creatorcontrib><creatorcontrib>Hung, Rayjean J.</creatorcontrib><creatorcontrib>EPIC-lung</creatorcontrib><creatorcontrib>EPIC-lung</creatorcontrib><title>International Lung Cancer Consortium: Coordinated association study of 10 potential lung cancer susceptibility variants</title><title>Carcinogenesis (New York)</title><addtitle>Carcinogenesis</addtitle><description>Background. Analysis of candidate genes in individual studies has had only limited success in identifying particular gene variants that are conclusively associated with lung cancer risk. In the International Lung Cancer Consortium (ILCCO), we conducted a coordinated genotyping study of 10 common variants selected because of their prior evidence of an association with lung cancer. These variants belonged to candidate genes from different cancer-related pathways including inflammation (IL1B), folate metabolism (MTHFR), regulatory function (AKAP9 and CAMKK1), cell adhesion (SEZL6) and apoptosis (FAS, FASL, TP53, TP53BP1 and BAT3). Methods. Genotype data from 15 ILCCO case–control studies were available for a total of 8431 lung cancer cases and 11 072 controls of European descent and Asian ethnic groups. Unconditional logistic regression was used to model the association between each variant and lung cancer risk. Results. Only the association between a non-synonymous variant of TP53BP1 (rs560191) and lung cancer risk was significant (OR = 0.91, P = 0.002). This association was more striking for squamous cell carcinoma (OR = 0.86, P = 6 × 10−4). No heterogeneity by center, ethnicity, smoking status, age group or sex was observed. In order to confirm this association, we included results for this variant from a set of independent studies (9966 cases/11 722 controls) and we reported similar results. When combining all these studies together, we reported an overall OR = 0.93 (0.89–0.97) (P = 0.001). This association was significant only for squamous cell carcinoma [OR = 0.89 (0.85–0.95), P = 1 × 10−4]. Conclusion. This study suggests that rs560191 is associated to lung cancer risk and further highlights the value of consortia in replicating or refuting published genetic associations.</description><subject>Adult</subject><subject>Aged</subject><subject>Female</subject><subject>Genetic Predisposition to Disease</subject><subject>Genome-Wide Association Study</subject><subject>Genotype</subject><subject>Humans</subject><subject>Intracellular Signaling Peptides and Proteins - genetics</subject><subject>Lung Neoplasms - etiology</subject><subject>Lung Neoplasms - genetics</subject><subject>Male</subject><subject>Methylenetetrahydrofolate Reductase (NADPH2) - genetics</subject><subject>Middle Aged</subject><subject>Molecular Chaperones - genetics</subject><subject>Molecular Epidemiology</subject><subject>Odds Ratio</subject><subject>Tumor Suppressor p53-Binding Protein 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E.</creatorcontrib><creatorcontrib>Albanes, Demetrius</creatorcontrib><creatorcontrib>Thun, Michael</creatorcontrib><creatorcontrib>Landi, Maria Teresa</creatorcontrib><creatorcontrib>Trubicka, Joanna</creatorcontrib><creatorcontrib>Lener, Marcin</creatorcontrib><creatorcontrib>Lubiński, Jan</creatorcontrib><creatorcontrib>Wang, Ying</creatorcontrib><creatorcontrib>Chabrier, Amélie</creatorcontrib><creatorcontrib>Boffetta, Paolo</creatorcontrib><creatorcontrib>Brennan, Paul</creatorcontrib><creatorcontrib>Hung, Rayjean J.</creatorcontrib><creatorcontrib>EPIC-lung</creatorcontrib><creatorcontrib>EPIC-lung</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Carcinogenesis (New York)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Truong, Therese</au><au>Sauter, Wiebke</au><au>McKay, James D.</au><au>Hosgood, H.Dean</au><au>Gallagher, Carla</au><au>Amos, Christopher I.</au><au>Spitz, Margaret</au><au>Muscat, Joshua</au><au>Lazarus, Philip</au><au>Illig, Thomas</au><au>Wichmann, H.Erich</au><au>Bickeböller, Heike</au><au>Risch, Angela</au><au>Dienemann, Hendrik</au><au>Zhang, Zuo-Feng</au><au>Naeim, Behnaz Pezeshki</au><au>Yang, Ping</au><au>Zienolddiny, Shanbeh</au><au>Haugen, Aage</au><au>Le Marchand, Loïc</au><au>Hong, Yun-Chul</au><au>Kim, Jin Hee</au><au>Duell, Eric J.</au><au>Andrew, Angeline S.</au><au>Kiyohara, Chikako</au><au>Shen, Hongbing</au><au>Matsuo, Keitaro</au><au>Suzuki, Takeshi</au><au>Seow, Adeline</au><au>Ng, Daniel P.K.</au><au>Lan, Qing</au><au>Zaridze, David</au><au>Szeszenia-Dabrowska, Neonilia</au><au>Lissowska, Jolanta</au><au>Rudnai, Peter</au><au>Fabianova, Eleonora</au><au>Constantinescu, Vali</au><au>Bencko, Vladimir</au><au>Foretova, Lenka</au><au>Janout, Vladimir</au><au>Caporaso, Neil E.</au><au>Albanes, Demetrius</au><au>Thun, Michael</au><au>Landi, Maria Teresa</au><au>Trubicka, Joanna</au><au>Lener, Marcin</au><au>Lubiński, Jan</au><au>Wang, Ying</au><au>Chabrier, Amélie</au><au>Boffetta, Paolo</au><au>Brennan, Paul</au><au>Hung, Rayjean J.</au><aucorp>EPIC-lung</aucorp><aucorp>EPIC-lung</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>International Lung Cancer Consortium: Coordinated association study of 10 potential lung cancer susceptibility variants</atitle><jtitle>Carcinogenesis (New York)</jtitle><addtitle>Carcinogenesis</addtitle><date>2010-04-01</date><risdate>2010</risdate><volume>31</volume><issue>4</issue><spage>625</spage><epage>633</epage><pages>625-633</pages><issn>0143-3334</issn><eissn>1460-2180</eissn><abstract>Background. Analysis of candidate genes in individual studies has had only limited success in identifying particular gene variants that are conclusively associated with lung cancer risk. In the International Lung Cancer Consortium (ILCCO), we conducted a coordinated genotyping study of 10 common variants selected because of their prior evidence of an association with lung cancer. These variants belonged to candidate genes from different cancer-related pathways including inflammation (IL1B), folate metabolism (MTHFR), regulatory function (AKAP9 and CAMKK1), cell adhesion (SEZL6) and apoptosis (FAS, FASL, TP53, TP53BP1 and BAT3). Methods. Genotype data from 15 ILCCO case–control studies were available for a total of 8431 lung cancer cases and 11 072 controls of European descent and Asian ethnic groups. Unconditional logistic regression was used to model the association between each variant and lung cancer risk. Results. Only the association between a non-synonymous variant of TP53BP1 (rs560191) and lung cancer risk was significant (OR = 0.91, P = 0.002). This association was more striking for squamous cell carcinoma (OR = 0.86, P = 6 × 10−4). No heterogeneity by center, ethnicity, smoking status, age group or sex was observed. In order to confirm this association, we included results for this variant from a set of independent studies (9966 cases/11 722 controls) and we reported similar results. When combining all these studies together, we reported an overall OR = 0.93 (0.89–0.97) (P = 0.001). This association was significant only for squamous cell carcinoma [OR = 0.89 (0.85–0.95), P = 1 × 10−4]. Conclusion. This study suggests that rs560191 is associated to lung cancer risk and further highlights the value of consortia in replicating or refuting published genetic associations.</abstract><cop>England</cop><pub>Oxford University Press</pub><pmid>20106900</pmid><doi>10.1093/carcin/bgq001</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0143-3334 |
| ispartof | Carcinogenesis (New York), 2010-04, Vol.31 (4), p.625-633 |
| issn | 0143-3334 1460-2180 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2847090 |
| source | MEDLINE; Oxford University Press Journals All Titles (1996-Current); EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Adult Aged Female Genetic Predisposition to Disease Genome-Wide Association Study Genotype Humans Intracellular Signaling Peptides and Proteins - genetics Lung Neoplasms - etiology Lung Neoplasms - genetics Male Methylenetetrahydrofolate Reductase (NADPH2) - genetics Middle Aged Molecular Chaperones - genetics Molecular Epidemiology Odds Ratio Tumor Suppressor p53-Binding Protein 1 |
| title | International Lung Cancer Consortium: Coordinated association study of 10 potential lung cancer susceptibility variants |
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