[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"doc-seo-330263-105":3,"detail-sidebar-cat-0-en-105":81,"doc-detail-330263-en":130},{"code":4,"msg":5,"data":6},0,"ok",{"site_id":7,"language":8,"slug":9,"title":10,"keywords":11,"description":12,"schema_data":13,"social_meta":74,"head_meta":76,"extra_data":78,"updated_unix":80},105,"en","inflammation-promotes-aging-associated-oncogenesis-in-the-lung","Inflammation promotes aging-associated oncogenesis in the lung","","Lung cancer remains the leading cause of cancer death, and although smoking is a major preventable risk factor, advanced age also strongly increases susceptibility. Aging-related chronic low-grade inflammation, termed inflammaging, is well described, yet its mechanistic role in higher lung cancer incidence is not fully understood. This study links lung aging-associated changes to cancer risk by integrating human gene-expression datasets and mouse models, then testing inflammation-dependent effects on oncogenesis.",{"@graph":14,"@context":73},[15,34,56],{"@type":16,"itemListElement":17},"BreadcrumbList",[18,23,27,31],{"item":19,"name":20,"@type":21,"position":22},"https://docshare.wps.com","Home","ListItem",1,{"item":24,"name":25,"@type":21,"position":26},"https://docshare.wps.com/document/","Document",2,{"item":28,"name":29,"@type":21,"position":30},"https://docshare.wps.com/document/research-report/","Research & Report",3,{"item":32,"name":10,"@type":21,"position":33},"https://docshare.wps.com/document/inflammation-promotes-aging-associated-oncogenesis-in-the-lung/330263/",4,{"url":32,"name":10,"@type":35,"image":36,"author":41,"headline":10,"publisher":44,"fileFormat":47,"inLanguage":8,"description":12,"dateModified":48,"datePublished":49,"encodingFormat":47,"isAccessibleForFree":50,"interactionStatistic":51},"DigitalDocument",{"url":37,"@type":38,"width":39,"height":40},"https://docshare.wps.com/thumbnails/inflammation-promotes-aging-associated-oncogenesis-in-the-lung/330263.png","ImageObject",300,407,{"name":42,"@type":43},"Finn","Person",{"url":19,"name":45,"@type":46},"DocShare","Organization","application/pdf","2026-11-03","2026-09-21",true,{"@type":52,"interactionType":53,"userInteractionCount":55},"InteractionCounter",{"@type":54},"ViewAction",8,{"@type":57,"mainEntity":58},"FAQPage",[59,65,69],{"name":60,"@type":61,"acceptedAnswer":62},"How does the study connect inflammaging to lung cancer risk?","Question",{"text":63,"@type":64},"It analyzes human gene-expression profiles across age groups and uses mouse models to determine which aging-related changes depend on inflammation and influence oncogenesis.","Answer",{"name":66,"@type":61,"acceptedAnswer":67},"What gene-expression pathways increase with age in human lung cancer datasets?",{"text":68,"@type":64},"Comparisons across age groups show upregulated inflammatory response pathways, including TNFA signaling via NF-κB and interferon-gamma response.",{"name":70,"@type":61,"acceptedAnswer":71},"What do mouse experiments show about inflammation and tumor development in aging?",{"text":72,"@type":64},"Transgenic expression of alpha-1 antitrypsin partially reverses aging-associated inflammation markers and immune dysregulation, while NLRP3 knockout in old mice reduces lung tumor volumes, supporting an inflammation-driven contribution to aging-associated oncogenesis.","https://schema.org",{"og:url":32,"og:type":75,"og:title":10,"og:site_name":45,"og:description":12},"article",{"robots":77,"canonical":32},"index,follow",{"doc_id":79,"site_id":7},330263,1790179816,{"code":4,"msg":82,"data":83},"success",[84,88,92,96,101,106,111,114,119,122,126],{"id":22,"doc_module":4,"doc_module_name":25,"category_name":85,"show_sort_weight":86,"slug":87},"Story & Novel",90,"story-novel",{"id":26,"doc_module":4,"doc_module_name":25,"category_name":89,"show_sort_weight":90,"slug":91},"Literature",80,"literature",{"id":33,"doc_module":4,"doc_module_name":25,"category_name":93,"show_sort_weight":94,"slug":95},"Exam",70,"exam",{"id":97,"doc_module":4,"doc_module_name":25,"category_name":98,"show_sort_weight":99,"slug":100},5,"Comic",60,"comic",{"id":102,"doc_module":4,"doc_module_name":25,"category_name":103,"show_sort_weight":104,"slug":105},6,"Technology",50,"technology",{"id":107,"doc_module":4,"doc_module_name":25,"category_name":108,"show_sort_weight":109,"slug":110},7,"Healthcare",40,"healthcare",{"id":55,"doc_module":4,"doc_module_name":25,"category_name":29,"show_sort_weight":112,"slug":113},30,"research-report",{"id":115,"doc_module":4,"doc_module_name":25,"category_name":116,"show_sort_weight":117,"slug":118},9,"Religion & Spirituality",20,"religion-spirituality",{"id":117,"doc_module":4,"doc_module_name":25,"category_name":120,"show_sort_weight":117,"slug":121},"World Cup","world-cup",{"id":123,"doc_module":4,"doc_module_name":25,"category_name":124,"show_sort_weight":123,"slug":125},10,"Lifestyle","lifestyle",{"id":127,"doc_module":4,"doc_module_name":25,"category_name":128,"show_sort_weight":97,"slug":129},19,"General","general",{"code":4,"msg":82,"data":131},{"doc_id":79,"user_id":132,"nickname":42,"user_avatar":133,"doc_module":4,"category_id":55,"category_name":29,"doc_title":10,"doc_description":12,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":55,"is_deleted":4,"is_public":22,"is_downloadable":22,"audit_status":22,"page_count":139,"language":140,"language_code":8,"site_id":7,"html_lang":8,"table_of_contents":141,"faqs":142,"seo_title":143,"seo_description":12,"update_tm":144,"read_time":145,"preview_page_count":4},34359740700684,"https://ap-avatar.wpscdn.com/avatar/1f400023980c374ae676?_k=1777273430885731487","bioRxiv preprint doi: [https://doi.org/10.1101/2024.03.01.583044](https://doi.org/10.1101/2024.03.01.583044); this version posted March 5, 2024. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made  \navailable under aCC-BY-NC-ND 4.0 International license.  \nInflammation promotes aging-associated oncogenesis in the lung.  \nCatherine Pham-Danis1,* , Shi B Chia 1,* , Hannah A Scarborough1 , Etienne Danis2,6 , Travis Nemkov 1 , Emily K Kleczko5 , Andre Navarro5 , Andrew Goodspeed2,6 , Elizabeth A. Bonney3 , Charles A. Dinarello5 , Carlo Marchetti5 , Raphael A. Nemenoff5 , Kirk Hansen 1 , James DeGregori 1,4,5  \n1 Departments of Biochemistry and Molecular Genetics, 2 Biomedical Informatics ,  \n4 Immunology and Microbiology , 5 Medicine , 6 University of Colorado Cancer Center, University of Colorado Anschutz Medical Campus , Aurora, CO, United States ,  \n3 Department of Obstetrics, Gynecology and Reproductive Sciences, Larner College of Medicine, University of Vermont , Burlington, VT, United States.  \n*C. P-H. and S. B.C. contributed equally to these studies.  \n[Email Correspondence to James DeGregori:](Email Correspondence to James DeGregori: james.degregori@cuanschutz.edu)[ j](Email Correspondence to James DeGregori: james.degregori@cuanschutz.edu)[ames.degregori@cuanschutz.edu](Email Correspondence to James DeGregori: james.degregori@cuanschutz.edu)  \nbioRxiv preprint doi: [https://doi.org/10.1101/2024.03.01.583044](https://doi.org/10.1101/2024.03.01.583044); this version posted March 5, 2024. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made  \navailable under aCC-BY-NC-ND 4.0 International license.  \nABSTRACT  \nBackground: Lung cancer is the leading cause of cancer death in the world. While cigarette smoking is the major preventable factor for cancers in general and lung cancer in particular, old age is also a major risk factor. Aging-related chronic, low-level inflammation, termed inflammaging, has been widely documented; however, it remains unclear how inflammaging contributes to increased lung cancer incidence.  \nAim: To establish connections between aging-associated changes in the lungs and cancer risk.  \nMethods: We analyzed public databases of gene expression for normal and cancerous human lungs and used mouse models to understand which changes were dependent on inflammation, as well as to assess the impact on oncogenesis.  \nResults: Analyses of GTEx and TCGA databases comparing gene expression profiles from normal lungs, lung adenocarcinoma, lung squamous cell carcinoma of subjects across age groups revealed upregulated pathways such as inflammatory response, TNFA signaling via NF􀁎B, and interferon-gamma response. Similar pathways were identified comparing the gene expression profiles of young and old mouse lungs.  \nTransgenic expression of alpha 1 antitrypsin (AAT) partially reverses increases in  \nmarkers of aging-associated inflammation and immune deregulation. Using an orthotopic model of lung cancer using cells derived from EML4-ALK fusion-induced adenomas , we demonstrated an increased tumor outgrowth in lungs of old mice while NLRP3 knockout in old mice decreased tumor volumes , suggesting that inflammation contributes to increased lung cancer development in aging organisms.  \nbioRxiv preprint doi: [https://doi.org/10.1101/2024.03.01.583044](https://doi.org/10.1101/2024.03.01.583044); this version posted March 5, 2024. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made  \navailable under aCC-BY-NC-ND 4.0 International license.  \nConclusions: These studies reveal how expression of an anti-inflammatory mediator (AAT) ca","cbCaiuHsWqLo6HK8","https://ap.wps.com/l/cbCaiuHsWqLo6HK8","pdf",6484665,39,"English","# Abstract\n## Background\n## Aim\n## Methods\n## Results\n## Conclusions\n# Introduction","[{\"question\":\"How does the study connect inflammaging to lung cancer risk?\",\"answer\":\"It analyzes human gene-expression profiles across age groups and uses mouse models to determine which aging-related changes depend on inflammation and influence oncogenesis.\"},{\"question\":\"What gene-expression pathways increase with age in human lung cancer datasets?\",\"answer\":\"Comparisons across age groups show upregulated inflammatory response pathways, including TNFA signaling via NF-κB and interferon-gamma response.\"},{\"question\":\"What do mouse experiments show about inflammation and tumor development in aging?\",\"answer\":\"Transgenic expression of alpha-1 antitrypsin partially reverses aging-associated inflammation markers and immune dysregulation, while NLRP3 knockout in old mice reduces lung tumor volumes, supporting an inflammation-driven contribution to aging-associated oncogenesis.\"}]","Inflammation promotes aging-associated oncogenesis in the lung | PDF",1789987939,98]