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Chronic, low-level aging inflammation known as “inflammaging” has been documented, yet its role in higher lung cancer incidence remains unclear. This study links aging-related lung changes to cancer risk by combining public gene-expression analyses and mouse models to test inflammation dependency and impacts on oncogenesis. Results highlight inflammatory, TNFα/NFκB, and interferon-gamma pathways and show that alpha 1 antitrypsin and NLRP3 loss modulate tumor outgrowth in aged organisms.",{"@graph":69,"@context":126},[70,84,105],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":40,"@type":76,"position":81},"https://docshare.wps.com/document/research-report/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/inflammation-promotes-aging-associated-oncogenesisin-the-lung-original-article/331769/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/inflammation-promotes-aging-associated-oncogenesisin-the-lung-original-article/331769.png","ImageObject",300,407,{"name":92,"@type":93},"Ophelia","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-30","2026-09-21",true,{"@type":102,"interactionType":103,"userInteractionCount":39},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118,122],{"name":109,"@type":110,"acceptedAnswer":111},"What risk factors for lung cancer are emphasized in the study?","Question",{"text":112,"@type":113},"The study highlights cigarette smoking as a major preventable factor and identifies old age as a prominent prognostic risk factor. It also focuses on chronic, low-level inflammation termed “inflammaging.”","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"How did the researchers investigate links between aging and cancer risk?",{"text":117,"@type":113},"They analyzed public gene-expression databases (GTEx and TCGA) for normal and cancerous human lungs across age groups, and used mouse models to determine inflammation-dependent changes and their oncogenic impact.",{"name":119,"@type":110,"acceptedAnswer":120},"What did the study find about inflammation-related pathways across age groups?",{"text":121,"@type":113},"Comparisons across human age groups and young versus old mouse lungs showed upregulated inflammatory response pathways, including TNFα signaling via NFκB and interferon-gamma response.",{"name":123,"@type":110,"acceptedAnswer":124},"How do alpha 1 antitrypsin and NLRP3 affect tumor outcomes in aged mice?",{"text":125,"@type":113},"Transgenic alpha 1 antitrypsin partially reverses markers of aging-associated inflammation and immune deregulation. In an orthotopic lung cancer model, old mice showed increased tumor outgrowth, while NLRP3 knockout in old mice reduced tumor volumes, supporting a role for inflammation in age-related tumor development.","https://schema.org",{"og:url":83,"og:type":128,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":130,"canonical":83},"index,follow",{"doc_id":132,"site_id":62},331769,1790193904,{"code":4,"msg":5,"data":135},{"doc_id":132,"user_id":136,"nickname":92,"user_avatar":137,"doc_module":4,"category_id":39,"category_name":40,"doc_title":65,"doc_description":67,"doc_content":138,"file_id":139,"file_url":140,"file_type":141,"file_size":142,"view_count":39,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":143,"language":144,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":145,"faqs":146,"seo_title":147,"seo_description":67,"update_tm":148,"read_time":36,"preview_page_count":4},7971461741311,"https://ap-avatar.wpscdn.com/avatar/74000253aff267980c6?x-image-process=image/resize,m_fixed,w_180,h_180&k=1779345379180704826","Aging and Cancer  \nORIGINAL ARTICLE   \nInflammation Promotes Aging-Associated Oncogenesisin the Lung  \nCatherine Pham-Danis1  Shi B. Chia1   Hannah A. Scarborough1  Etienne Danis2, 3  Travis Nemkov1  Vadym Zaberezhnyy1  Jessica L. Christenson4  Emily K. Kleczko5  Andre Navarro5  Andrew Goodspeed2, 3  Elizabeth A. Bonney6  Charles A. Dinarello5  Carlo Marchetti5  Raphael A. Nemenoff5  Kirk C. Hansen1  James DeGregori1, 7, 5   \n1 Department of Biochemistry and Molecular Genetics, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA  2 Department of Biomedical Informatics, University of Colorado Anschutz Medical Campus, University of Colorado Cancer Center, Aurora, Colorado, USA  3University of Colorado Cancer Center, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA  4 Department of Pathology, University of Colorado Anschutz Medical Campus, University of Colorado Cancer Center, Aurora, Colorado, USA  5 Department of Medicine, University of Colorado Anschutz Medical Campus, University of Colorado Cancer Center, Aurora, Colorado, USA  6 Department of Obstetrics, Gynecology and Reproductive Sciences, Larner College of Medicine, University of Vermont, Burlington, Vermont, USA  7 Department of Immunology and Microbiology, University of Colorado Anschutz Medical Campus, University of Colorado Cancer Center, Aurora, Colorado, USA  \nCorrespondence: James DeGregori ([james.degregori@cuanschutz.edu](james.degregori@cuanschutz.edu))  \nReceived: 4 March 2024  Revised: 6 July 2024  Accepted: 13 August 2024  \nFunding: This study received funding from Veteran’s Administration (1 I01 BX004495), University of Vermont College of Medicine, and National Cancer Institute (T32CA174648 and P30CA046934) .  \nKeywords: aging | inflammation | lung cancer | microenvironment | alpha 1 antitrypsin  \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: The aim of this study was to establish connections between aging-associated changes in the lungs and cancer risk. Methods: 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, and lung squamous cell carcinoma of subjects across age groups revealed upregulated pathways such as inflammatory response, TNFA signaling via NFκB, and interferon-gamma response. Similar pathways were identified comparing the gene expression profiles of young and old mouse lungs. Transgenic expression of alpha 1 antitrypsin (AAT) partially reverses increases in markers 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.  \n\n| Catherine Pham-Danis and Shi B. Chia contributed equally to this study.\u003Cbr>|\n| --- |\n| This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.\u003Cbr>© 2024 The Author(s). Aging and Cancer published by Wiley Periodicals LLC. |\n\nAging and Cancer, 2025; 6:3–18 3 of 18  \n[https://doi.org/10.1002/","cbCainUbhw4YpOaT","https://ap.wps.com/l/cbCainUbhw4YpOaT","pdf",8253215,16,"English","# Background\n## Aim\n## Methods\n## Results\n## Conclusions\n# Introduction","[{\"question\":\"What risk factors for lung cancer are emphasized in the study?\",\"answer\":\"The study highlights cigarette smoking as a major preventable factor and identifies old age as a prominent prognostic risk factor. It also focuses on chronic, low-level inflammation termed “inflammaging.”\"},{\"question\":\"How did the researchers investigate links between aging and cancer risk?\",\"answer\":\"They analyzed public gene-expression databases (GTEx and TCGA) for normal and cancerous human lungs across age groups, and used mouse models to determine inflammation-dependent changes and their oncogenic impact.\"},{\"question\":\"What did the study find about inflammation-related pathways across age groups?\",\"answer\":\"Comparisons across human age groups and young versus old mouse lungs showed upregulated inflammatory response pathways, including TNFα signaling via NFκB and interferon-gamma response.\"},{\"question\":\"How do alpha 1 antitrypsin and NLRP3 affect tumor outcomes in aged mice?\",\"answer\":\"Transgenic alpha 1 antitrypsin partially reverses markers of aging-associated inflammation and immune deregulation. In an orthotopic lung cancer model, old mice showed increased tumor outgrowth, while NLRP3 knockout in old mice reduced tumor volumes, supporting a role for inflammation in age-related tumor development.\"}]","Inflammation Promotes Aging-Associated Oncogenesisin the Lung - Original Article | PDF",1789995029]