Cross Cancer Genomic Investigation of Inflammation Pathway for Five Common Cancers: Lung, Ovary, Prostate, Breast, and Colorectal Cancer
Inflammation has been hypothesized to increase the risk of cancer development as an initiator or promoter, yet no large-scale study of inherited variation across cancer sites has been conducted. We conducted a cross-cancer genomic analysis for the inflammation pathway based on 48 genome-wide associa...
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| creator | Hung, Rayjean J Ulrich, Cornelia M Goode, Ellen L Brhane, Yonathan Muir, Kenneth Chan, Andrew T Marchand, Loic Le Schildkraut, Joellen Witte, John S Eeles, Rosalind Boffetta, Paolo Spitz, Margaret R Poirier, Julia G Rider, David N Fridley, Brooke L Chen, Zhihua Haiman, Christopher Schumacher, Fredrick Easton, Douglas F Landi, Maria Teresa Brennan, Paul Houlston, Richard Christiani, David C Field, John K Bickeböller, Heike Risch, Angela Kote-Jarai, Zsofia Wiklund, Fredrik Grönberg, Henrik Chanock, Stephen Berndt, Sonja I Kraft, Peter Lindström, Sara Al Olama, Ali Amin Song, Honglin Phelan, Catherine Wentzensen, Nicholas Peters, Ulrike Slattery, Martha L Sellers, Thomas A Casey, Graham Gruber, Stephen B Hunter, David J Amos, Christopher I Henderson, Brian |
| description | Inflammation has been hypothesized to increase the risk of cancer development as an initiator or promoter, yet no large-scale study of inherited variation across cancer sites has been conducted.
We conducted a cross-cancer genomic analysis for the inflammation pathway based on 48 genome-wide association studies within the National Cancer Institute GAME-ON Network across five common cancer sites, with a total of 64 591 cancer patients and 74 467 control patients. Subset-based meta-analysis was used to account for possible disease heterogeneity, and hierarchical modeling was employed to estimate the effect of the subcomponents within the inflammation pathway. The network was visualized by enrichment map. All statistical tests were two-sided.
We identified three pleiotropic loci within the inflammation pathway, including one novel locus in Ch12q24 encoding SH2B3 (rs3184504), which reached GWAS significance with a P value of 1.78 x 10(-8), and it showed an association with lung cancer (P = 2.01 x 10(-6)), colorectal cancer (GECCO P = 6.72x10(-6); CORECT P = 3.32x10(-5)), and breast cancer (P = .009). We also identified five key subpathway components with genetic variants that are relevant for the risk of these five cancer sites: inflammatory response for colorectal cancer (P = .006), inflammation related cell cycle gene for lung cancer (P = 1.35x10(-6)), and activation of immune response for ovarian cancer (P = .009). In addition, sequence variations in immune system development played a role in breast cancer etiology (P = .001) and innate immune response was involved in the risk of both colorectal (P = .022) and ovarian cancer (P = .003).
Genetic variations in inflammation and its related subpathway components are keys to the development of lung, colorectal, ovary, and breast cancer, including SH2B3, which is associated with lung, colorectal, and breast cancer. |
| doi_str_mv | 10.1093/jnci/djv246 |
| format | Article |
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We conducted a cross-cancer genomic analysis for the inflammation pathway based on 48 genome-wide association studies within the National Cancer Institute GAME-ON Network across five common cancer sites, with a total of 64 591 cancer patients and 74 467 control patients. Subset-based meta-analysis was used to account for possible disease heterogeneity, and hierarchical modeling was employed to estimate the effect of the subcomponents within the inflammation pathway. The network was visualized by enrichment map. All statistical tests were two-sided.
We identified three pleiotropic loci within the inflammation pathway, including one novel locus in Ch12q24 encoding SH2B3 (rs3184504), which reached GWAS significance with a P value of 1.78 x 10(-8), and it showed an association with lung cancer (P = 2.01 x 10(-6)), colorectal cancer (GECCO P = 6.72x10(-6); CORECT P = 3.32x10(-5)), and breast cancer (P = .009). We also identified five key subpathway components with genetic variants that are relevant for the risk of these five cancer sites: inflammatory response for colorectal cancer (P = .006), inflammation related cell cycle gene for lung cancer (P = 1.35x10(-6)), and activation of immune response for ovarian cancer (P = .009). In addition, sequence variations in immune system development played a role in breast cancer etiology (P = .001) and innate immune response was involved in the risk of both colorectal (P = .022) and ovarian cancer (P = .003).
Genetic variations in inflammation and its related subpathway components are keys to the development of lung, colorectal, ovary, and breast cancer, including SH2B3, which is associated with lung, colorectal, and breast cancer.</description><identifier>ISSN: 0027-8874</identifier><identifier>ISSN: 1460-2105</identifier><identifier>EISSN: 1460-2105</identifier><identifier>DOI: 10.1093/jnci/djv246</identifier><identifier>PMID: 26319099</identifier><language>eng</language><publisher>United States: Oxford University Press</publisher><subject>Adaptor Proteins, Signal Transducing ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Colorectal Neoplasms - genetics ; Colorectal Neoplasms - metabolism ; Female ; Genome-Wide Association Study ; Humans ; Inflammation - genetics ; Inflammation - metabolism ; Intracellular Signaling Peptides and Proteins ; Lung Neoplasms - genetics ; Lung Neoplasms - metabolism ; Male ; Ovarian Neoplasms - genetics ; Ovarian Neoplasms - metabolism ; Prostatic Neoplasms - genetics ; Prostatic Neoplasms - metabolism ; Proteins - genetics ; Signal Transduction</subject><ispartof>JNCI : Journal of the National Cancer Institute, 2015-11, Vol.107 (11), p.djv246</ispartof><rights>The Author 2015. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.</rights><rights>The Author 2015. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c419t-5581a027ebbf3bf9f7968a3f3297b3f3b99174e7f0462a8914dddddafd2917243</citedby><cites>FETCH-LOGICAL-c419t-5581a027ebbf3bf9f7968a3f3297b3f3b99174e7f0462a8914dddddafd2917243</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,550,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26319099$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:132650324$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Hung, Rayjean J</creatorcontrib><creatorcontrib>Ulrich, Cornelia M</creatorcontrib><creatorcontrib>Goode, Ellen L</creatorcontrib><creatorcontrib>Brhane, Yonathan</creatorcontrib><creatorcontrib>Muir, Kenneth</creatorcontrib><creatorcontrib>Chan, Andrew T</creatorcontrib><creatorcontrib>Marchand, Loic Le</creatorcontrib><creatorcontrib>Schildkraut, Joellen</creatorcontrib><creatorcontrib>Witte, John S</creatorcontrib><creatorcontrib>Eeles, Rosalind</creatorcontrib><creatorcontrib>Boffetta, Paolo</creatorcontrib><creatorcontrib>Spitz, Margaret R</creatorcontrib><creatorcontrib>Poirier, Julia G</creatorcontrib><creatorcontrib>Rider, David N</creatorcontrib><creatorcontrib>Fridley, Brooke L</creatorcontrib><creatorcontrib>Chen, Zhihua</creatorcontrib><creatorcontrib>Haiman, Christopher</creatorcontrib><creatorcontrib>Schumacher, Fredrick</creatorcontrib><creatorcontrib>Easton, Douglas F</creatorcontrib><creatorcontrib>Landi, Maria Teresa</creatorcontrib><creatorcontrib>Brennan, Paul</creatorcontrib><creatorcontrib>Houlston, Richard</creatorcontrib><creatorcontrib>Christiani, David C</creatorcontrib><creatorcontrib>Field, John K</creatorcontrib><creatorcontrib>Bickeböller, Heike</creatorcontrib><creatorcontrib>Risch, Angela</creatorcontrib><creatorcontrib>Kote-Jarai, Zsofia</creatorcontrib><creatorcontrib>Wiklund, Fredrik</creatorcontrib><creatorcontrib>Grönberg, Henrik</creatorcontrib><creatorcontrib>Chanock, Stephen</creatorcontrib><creatorcontrib>Berndt, Sonja I</creatorcontrib><creatorcontrib>Kraft, Peter</creatorcontrib><creatorcontrib>Lindström, Sara</creatorcontrib><creatorcontrib>Al Olama, Ali Amin</creatorcontrib><creatorcontrib>Song, Honglin</creatorcontrib><creatorcontrib>Phelan, Catherine</creatorcontrib><creatorcontrib>Wentzensen, Nicholas</creatorcontrib><creatorcontrib>Peters, Ulrike</creatorcontrib><creatorcontrib>Slattery, Martha L</creatorcontrib><creatorcontrib>Sellers, Thomas A</creatorcontrib><creatorcontrib>Casey, Graham</creatorcontrib><creatorcontrib>Gruber, Stephen B</creatorcontrib><creatorcontrib>Hunter, David J</creatorcontrib><creatorcontrib>Amos, Christopher I</creatorcontrib><creatorcontrib>Henderson, Brian</creatorcontrib><creatorcontrib>DRIVE</creatorcontrib><creatorcontrib>CORECT</creatorcontrib><creatorcontrib>FOCI</creatorcontrib><creatorcontrib>GAME-ON Network</creatorcontrib><creatorcontrib>GECCO</creatorcontrib><creatorcontrib>for FOCI</creatorcontrib><creatorcontrib>for GECCO</creatorcontrib><creatorcontrib>for CORECT</creatorcontrib><creatorcontrib>for DRIVE</creatorcontrib><creatorcontrib>on behalf of the GAME-ON Network</creatorcontrib><title>Cross Cancer Genomic Investigation of Inflammation Pathway for Five Common Cancers: Lung, Ovary, Prostate, Breast, and Colorectal Cancer</title><title>JNCI : Journal of the National Cancer Institute</title><addtitle>J Natl Cancer Inst</addtitle><description>Inflammation has been hypothesized to increase the risk of cancer development as an initiator or promoter, yet no large-scale study of inherited variation across cancer sites has been conducted.
We conducted a cross-cancer genomic analysis for the inflammation pathway based on 48 genome-wide association studies within the National Cancer Institute GAME-ON Network across five common cancer sites, with a total of 64 591 cancer patients and 74 467 control patients. Subset-based meta-analysis was used to account for possible disease heterogeneity, and hierarchical modeling was employed to estimate the effect of the subcomponents within the inflammation pathway. The network was visualized by enrichment map. All statistical tests were two-sided.
We identified three pleiotropic loci within the inflammation pathway, including one novel locus in Ch12q24 encoding SH2B3 (rs3184504), which reached GWAS significance with a P value of 1.78 x 10(-8), and it showed an association with lung cancer (P = 2.01 x 10(-6)), colorectal cancer (GECCO P = 6.72x10(-6); CORECT P = 3.32x10(-5)), and breast cancer (P = .009). We also identified five key subpathway components with genetic variants that are relevant for the risk of these five cancer sites: inflammatory response for colorectal cancer (P = .006), inflammation related cell cycle gene for lung cancer (P = 1.35x10(-6)), and activation of immune response for ovarian cancer (P = .009). In addition, sequence variations in immune system development played a role in breast cancer etiology (P = .001) and innate immune response was involved in the risk of both colorectal (P = .022) and ovarian cancer (P = .003).
Genetic variations in inflammation and its related subpathway components are keys to the development of lung, colorectal, ovary, and breast cancer, including SH2B3, which is associated with lung, colorectal, and breast cancer.</description><subject>Adaptor Proteins, Signal Transducing</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Colorectal Neoplasms - genetics</subject><subject>Colorectal Neoplasms - metabolism</subject><subject>Female</subject><subject>Genome-Wide Association Study</subject><subject>Humans</subject><subject>Inflammation - genetics</subject><subject>Inflammation - metabolism</subject><subject>Intracellular Signaling Peptides and Proteins</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - metabolism</subject><subject>Male</subject><subject>Ovarian Neoplasms - genetics</subject><subject>Ovarian Neoplasms - metabolism</subject><subject>Prostatic Neoplasms - genetics</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>Proteins - genetics</subject><subject>Signal Transduction</subject><issn>0027-8874</issn><issn>1460-2105</issn><issn>1460-2105</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>D8T</sourceid><recordid>eNpVUU1v1DAQtRAVXVpO3JGPSN1Q23E-zAGJRm2ptFJ7gLM1Seytl8QutjdV_wE_u46yVHQu45l582Y8D6GPlHyhROTnO9uZ8343MV6-QSvKS5IxSoq3aEUIq7K6rvgxeh_CjiQTjL9Dx6zMqSBCrNDfxrsQcAO2Ux5fK-tG0-EbO6kQzRaicRY7nRJ6gHFc4juI94_whLXz-MpMCjduHFN-IQlf8WZvt2t8O4F_WuO7NCBCVGt84RWEuMZg-9QyOK-6CMOh7RQdaRiC-nDwJ-jX1eXP5ke2ub2-ab5vso5TEbOiqCmkb6m21Xmrha5EWUOucyaqNrlWCFpxVWnCSwa1oLyfDXTPUoHx_ARlC294VA_7Vj54M6Y9pQMjD6nf6aVkQdMRi4T_tuBTZVR9p2z0MLxqe12x5l5u3SR5WRWUkETw-UDg3Z99OqscTejUMIBVbh8krUhdi7rgM_RsgXazKF7plzGUyFlrOWstF60T-tP_m71g_4mbPwNO86kf</recordid><startdate>20151101</startdate><enddate>20151101</enddate><creator>Hung, Rayjean J</creator><creator>Ulrich, Cornelia M</creator><creator>Goode, Ellen L</creator><creator>Brhane, Yonathan</creator><creator>Muir, Kenneth</creator><creator>Chan, Andrew T</creator><creator>Marchand, Loic Le</creator><creator>Schildkraut, Joellen</creator><creator>Witte, John S</creator><creator>Eeles, Rosalind</creator><creator>Boffetta, Paolo</creator><creator>Spitz, Margaret R</creator><creator>Poirier, Julia G</creator><creator>Rider, David N</creator><creator>Fridley, Brooke L</creator><creator>Chen, Zhihua</creator><creator>Haiman, Christopher</creator><creator>Schumacher, Fredrick</creator><creator>Easton, Douglas F</creator><creator>Landi, Maria Teresa</creator><creator>Brennan, Paul</creator><creator>Houlston, Richard</creator><creator>Christiani, David C</creator><creator>Field, John K</creator><creator>Bickeböller, Heike</creator><creator>Risch, Angela</creator><creator>Kote-Jarai, Zsofia</creator><creator>Wiklund, Fredrik</creator><creator>Grönberg, Henrik</creator><creator>Chanock, Stephen</creator><creator>Berndt, Sonja I</creator><creator>Kraft, Peter</creator><creator>Lindström, Sara</creator><creator>Al Olama, Ali Amin</creator><creator>Song, Honglin</creator><creator>Phelan, Catherine</creator><creator>Wentzensen, Nicholas</creator><creator>Peters, Ulrike</creator><creator>Slattery, Martha L</creator><creator>Sellers, Thomas A</creator><creator>Casey, Graham</creator><creator>Gruber, Stephen B</creator><creator>Hunter, David J</creator><creator>Amos, Christopher I</creator><creator>Henderson, Brian</creator><general>Oxford University Press</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>D8T</scope><scope>ZZAVC</scope></search><sort><creationdate>20151101</creationdate><title>Cross Cancer Genomic Investigation of Inflammation Pathway for Five Common Cancers: Lung, Ovary, Prostate, Breast, and Colorectal Cancer</title><author>Hung, Rayjean J ; Ulrich, Cornelia M ; Goode, Ellen L ; Brhane, Yonathan ; Muir, Kenneth ; Chan, Andrew T ; Marchand, Loic Le ; Schildkraut, Joellen ; Witte, John S ; Eeles, Rosalind ; Boffetta, Paolo ; Spitz, Margaret R ; Poirier, Julia G ; Rider, David N ; Fridley, Brooke L ; Chen, Zhihua ; Haiman, Christopher ; Schumacher, Fredrick ; Easton, Douglas F ; Landi, Maria Teresa ; Brennan, Paul ; Houlston, Richard ; Christiani, David C ; Field, John K ; Bickeböller, Heike ; Risch, Angela ; Kote-Jarai, Zsofia ; Wiklund, Fredrik ; Grönberg, Henrik ; Chanock, Stephen ; Berndt, Sonja I ; Kraft, Peter ; Lindström, Sara ; Al Olama, Ali Amin ; Song, Honglin ; Phelan, Catherine ; Wentzensen, Nicholas ; Peters, Ulrike ; Slattery, Martha L ; Sellers, Thomas A ; Casey, Graham ; Gruber, Stephen B ; Hunter, David J ; Amos, Christopher I ; Henderson, Brian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c419t-5581a027ebbf3bf9f7968a3f3297b3f3b99174e7f0462a8914dddddafd2917243</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Adaptor Proteins, Signal Transducing</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Colorectal Neoplasms - genetics</topic><topic>Colorectal Neoplasms - metabolism</topic><topic>Female</topic><topic>Genome-Wide Association Study</topic><topic>Humans</topic><topic>Inflammation - genetics</topic><topic>Inflammation - metabolism</topic><topic>Intracellular Signaling Peptides and Proteins</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - metabolism</topic><topic>Male</topic><topic>Ovarian Neoplasms - genetics</topic><topic>Ovarian Neoplasms - metabolism</topic><topic>Prostatic Neoplasms - genetics</topic><topic>Prostatic Neoplasms - metabolism</topic><topic>Proteins - genetics</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hung, Rayjean J</creatorcontrib><creatorcontrib>Ulrich, Cornelia M</creatorcontrib><creatorcontrib>Goode, Ellen L</creatorcontrib><creatorcontrib>Brhane, Yonathan</creatorcontrib><creatorcontrib>Muir, Kenneth</creatorcontrib><creatorcontrib>Chan, Andrew T</creatorcontrib><creatorcontrib>Marchand, Loic Le</creatorcontrib><creatorcontrib>Schildkraut, Joellen</creatorcontrib><creatorcontrib>Witte, John S</creatorcontrib><creatorcontrib>Eeles, Rosalind</creatorcontrib><creatorcontrib>Boffetta, Paolo</creatorcontrib><creatorcontrib>Spitz, Margaret R</creatorcontrib><creatorcontrib>Poirier, Julia G</creatorcontrib><creatorcontrib>Rider, David N</creatorcontrib><creatorcontrib>Fridley, Brooke L</creatorcontrib><creatorcontrib>Chen, Zhihua</creatorcontrib><creatorcontrib>Haiman, Christopher</creatorcontrib><creatorcontrib>Schumacher, Fredrick</creatorcontrib><creatorcontrib>Easton, Douglas F</creatorcontrib><creatorcontrib>Landi, Maria Teresa</creatorcontrib><creatorcontrib>Brennan, Paul</creatorcontrib><creatorcontrib>Houlston, Richard</creatorcontrib><creatorcontrib>Christiani, David C</creatorcontrib><creatorcontrib>Field, John K</creatorcontrib><creatorcontrib>Bickeböller, Heike</creatorcontrib><creatorcontrib>Risch, Angela</creatorcontrib><creatorcontrib>Kote-Jarai, Zsofia</creatorcontrib><creatorcontrib>Wiklund, Fredrik</creatorcontrib><creatorcontrib>Grönberg, Henrik</creatorcontrib><creatorcontrib>Chanock, Stephen</creatorcontrib><creatorcontrib>Berndt, Sonja I</creatorcontrib><creatorcontrib>Kraft, Peter</creatorcontrib><creatorcontrib>Lindström, Sara</creatorcontrib><creatorcontrib>Al Olama, Ali Amin</creatorcontrib><creatorcontrib>Song, Honglin</creatorcontrib><creatorcontrib>Phelan, Catherine</creatorcontrib><creatorcontrib>Wentzensen, Nicholas</creatorcontrib><creatorcontrib>Peters, Ulrike</creatorcontrib><creatorcontrib>Slattery, Martha L</creatorcontrib><creatorcontrib>Sellers, Thomas A</creatorcontrib><creatorcontrib>Casey, Graham</creatorcontrib><creatorcontrib>Gruber, Stephen B</creatorcontrib><creatorcontrib>Hunter, David J</creatorcontrib><creatorcontrib>Amos, Christopher I</creatorcontrib><creatorcontrib>Henderson, Brian</creatorcontrib><creatorcontrib>DRIVE</creatorcontrib><creatorcontrib>CORECT</creatorcontrib><creatorcontrib>FOCI</creatorcontrib><creatorcontrib>GAME-ON Network</creatorcontrib><creatorcontrib>GECCO</creatorcontrib><creatorcontrib>for FOCI</creatorcontrib><creatorcontrib>for GECCO</creatorcontrib><creatorcontrib>for CORECT</creatorcontrib><creatorcontrib>for DRIVE</creatorcontrib><creatorcontrib>on behalf of the GAME-ON Network</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Freely available online</collection><collection>SwePub Articles full text</collection><jtitle>JNCI : Journal of the National Cancer Institute</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hung, Rayjean J</au><au>Ulrich, Cornelia M</au><au>Goode, Ellen L</au><au>Brhane, Yonathan</au><au>Muir, Kenneth</au><au>Chan, Andrew T</au><au>Marchand, Loic Le</au><au>Schildkraut, Joellen</au><au>Witte, John S</au><au>Eeles, Rosalind</au><au>Boffetta, Paolo</au><au>Spitz, Margaret R</au><au>Poirier, Julia G</au><au>Rider, David N</au><au>Fridley, Brooke L</au><au>Chen, Zhihua</au><au>Haiman, Christopher</au><au>Schumacher, Fredrick</au><au>Easton, Douglas F</au><au>Landi, Maria Teresa</au><au>Brennan, Paul</au><au>Houlston, Richard</au><au>Christiani, David C</au><au>Field, John K</au><au>Bickeböller, Heike</au><au>Risch, Angela</au><au>Kote-Jarai, Zsofia</au><au>Wiklund, Fredrik</au><au>Grönberg, Henrik</au><au>Chanock, Stephen</au><au>Berndt, Sonja I</au><au>Kraft, Peter</au><au>Lindström, Sara</au><au>Al Olama, Ali Amin</au><au>Song, Honglin</au><au>Phelan, Catherine</au><au>Wentzensen, Nicholas</au><au>Peters, Ulrike</au><au>Slattery, Martha L</au><au>Sellers, Thomas A</au><au>Casey, Graham</au><au>Gruber, Stephen B</au><au>Hunter, David J</au><au>Amos, Christopher I</au><au>Henderson, Brian</au><aucorp>DRIVE</aucorp><aucorp>CORECT</aucorp><aucorp>FOCI</aucorp><aucorp>GAME-ON Network</aucorp><aucorp>GECCO</aucorp><aucorp>for FOCI</aucorp><aucorp>for GECCO</aucorp><aucorp>for CORECT</aucorp><aucorp>for DRIVE</aucorp><aucorp>on behalf of the GAME-ON Network</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cross Cancer Genomic Investigation of Inflammation Pathway for Five Common Cancers: Lung, Ovary, Prostate, Breast, and Colorectal Cancer</atitle><jtitle>JNCI : Journal of the National Cancer Institute</jtitle><addtitle>J Natl Cancer Inst</addtitle><date>2015-11-01</date><risdate>2015</risdate><volume>107</volume><issue>11</issue><spage>djv246</spage><pages>djv246-</pages><issn>0027-8874</issn><issn>1460-2105</issn><eissn>1460-2105</eissn><abstract>Inflammation has been hypothesized to increase the risk of cancer development as an initiator or promoter, yet no large-scale study of inherited variation across cancer sites has been conducted.
We conducted a cross-cancer genomic analysis for the inflammation pathway based on 48 genome-wide association studies within the National Cancer Institute GAME-ON Network across five common cancer sites, with a total of 64 591 cancer patients and 74 467 control patients. Subset-based meta-analysis was used to account for possible disease heterogeneity, and hierarchical modeling was employed to estimate the effect of the subcomponents within the inflammation pathway. The network was visualized by enrichment map. All statistical tests were two-sided.
We identified three pleiotropic loci within the inflammation pathway, including one novel locus in Ch12q24 encoding SH2B3 (rs3184504), which reached GWAS significance with a P value of 1.78 x 10(-8), and it showed an association with lung cancer (P = 2.01 x 10(-6)), colorectal cancer (GECCO P = 6.72x10(-6); CORECT P = 3.32x10(-5)), and breast cancer (P = .009). We also identified five key subpathway components with genetic variants that are relevant for the risk of these five cancer sites: inflammatory response for colorectal cancer (P = .006), inflammation related cell cycle gene for lung cancer (P = 1.35x10(-6)), and activation of immune response for ovarian cancer (P = .009). In addition, sequence variations in immune system development played a role in breast cancer etiology (P = .001) and innate immune response was involved in the risk of both colorectal (P = .022) and ovarian cancer (P = .003).
Genetic variations in inflammation and its related subpathway components are keys to the development of lung, colorectal, ovary, and breast cancer, including SH2B3, which is associated with lung, colorectal, and breast cancer.</abstract><cop>United States</cop><pub>Oxford University Press</pub><pmid>26319099</pmid><doi>10.1093/jnci/djv246</doi><oa>free_for_read</oa></addata></record> |
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| language | eng |
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| source | MEDLINE; Free E-Journal (出版社公開部分のみ）; Oxford Journals Online; Alma/SFX Local Collection; SWEPUB Freely available online |
| subjects | Adaptor Proteins, Signal Transducing Breast Neoplasms - genetics Breast Neoplasms - metabolism Colorectal Neoplasms - genetics Colorectal Neoplasms - metabolism Female Genome-Wide Association Study Humans Inflammation - genetics Inflammation - metabolism Intracellular Signaling Peptides and Proteins Lung Neoplasms - genetics Lung Neoplasms - metabolism Male Ovarian Neoplasms - genetics Ovarian Neoplasms - metabolism Prostatic Neoplasms - genetics Prostatic Neoplasms - metabolism Proteins - genetics Signal Transduction |
| title | Cross Cancer Genomic Investigation of Inflammation Pathway for Five Common Cancers: Lung, Ovary, Prostate, Breast, and Colorectal Cancer |
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