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Current research re-examines early tumorigenesis mechanisms, enabling a molecular era of cancer prevention.",{"@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/tumor-promoters-and-opportunities-for-molecular-cancer-prevention/329938/",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/tumor-promoters-and-opportunities-for-molecular-cancer-prevention/329938.png","ImageObject",300,407,{"name":42,"@type":43},"Ophelia","Person",{"url":19,"name":45,"@type":46},"DocShare","Organization","application/pdf","2026-11-08","2026-09-21",true,{"@type":52,"interactionType":53,"userInteractionCount":55},"InteractionCounter",{"@type":54},"ViewAction",12,{"@type":57,"mainEntity":58},"FAQPage",[59,65,69],{"name":60,"@type":61,"acceptedAnswer":62},"How do environmental carcinogens contribute to cancer incidence according to the document?","Question",{"text":63,"@type":64},"Environmental carcinogens increase cancer incidence through both mutagenic and non-mutagenic mechanisms. The text notes that not all carcinogen effects can be explained solely by inducing mutations.","Answer",{"name":66,"@type":61,"acceptedAnswer":67},"Why do oncogenic driver mutations not always lead to tumorigenesis?",{"text":68,"@type":64},"The document states that oncogenic driver mutations can be found in histologically normal tissue without evidence of disease. This suggests driver mutations are necessary but not always sufficient for tumor formation.",{"name":70,"@type":61,"acceptedAnswer":71},"What is the tumor promotion concept described in the document?",{"text":72,"@type":64},"A two-step model proposes an initiation step followed by a promotion step involving irritant inflammatory agents. Without promotion, mutant cells may remain dormant, while promoter exposure can still drive rapid tumorigenesis.","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},329938,1790686704,{"code":4,"msg":82,"data":83},"success",[84,88,92,96,101,106,111,115,120,123,127],{"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":112,"doc_module":4,"doc_module_name":25,"category_name":29,"show_sort_weight":113,"slug":114},8,30,"research-report",{"id":116,"doc_module":4,"doc_module_name":25,"category_name":117,"show_sort_weight":118,"slug":119},9,"Religion & Spirituality",20,"religion-spirituality",{"id":118,"doc_module":4,"doc_module_name":25,"category_name":121,"show_sort_weight":118,"slug":122},"World Cup","world-cup",{"id":124,"doc_module":4,"doc_module_name":25,"category_name":125,"show_sort_weight":124,"slug":126},10,"Lifestyle","lifestyle",{"id":128,"doc_module":4,"doc_module_name":25,"category_name":129,"show_sort_weight":97,"slug":130},19,"General","general",{"code":4,"msg":82,"data":132},{"doc_id":79,"user_id":133,"nickname":42,"user_avatar":134,"doc_module":4,"category_id":112,"category_name":29,"doc_title":10,"doc_description":12,"doc_content":135,"file_id":136,"file_url":137,"file_type":138,"file_size":139,"view_count":55,"is_deleted":4,"is_public":22,"is_downloadable":22,"audit_status":22,"page_count":140,"language":141,"language_code":8,"site_id":7,"html_lang":8,"table_of_contents":142,"faqs":143,"seo_title":144,"seo_description":12,"update_tm":145,"read_time":146,"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","Europe PMC unders uthManuscripts Europe M eC und Author Manuscripts  \n| Europe PMC Funders Group\u003Cbr>Author Manuscript\u003Cbr>Cancer Discov. Author manuscript; available in PMC 2024 September 11. |\n| --- |\n| Published in final edited form as:\u003Cbr>Cancer Discov. 2024 July 01; 14(7): 1154–1160. doi:10.1158/2159-8290.CD-24-0128 .\u003Cbr>Tumor Promoters and Opportunities for Molecular Cancer Prevention\u003Cbr>William Hill 1 , Clare E. Weeden 1 , Charles Swanton 1,2,3,\\#\u003Cbr>1Cancer Evolution and Genome Instability Laboratory, The Francis Crick Institute, London, UK.\u003Cbr>2Cancer Research UK Lung Cancer Centre of Excellence, University College London Cancer Institute, London, UK.\u003Cbr>3 Department of Oncology, University College London Hospitals, London, UK.\u003Cbr>Abstract\u003Cbr>Environmental carcinogens increase cancer incidence via both mutagenic and non-mutagenic mechanisms. There are over 500 known or suspected carcinogens classified by the International Agency for Research on Cancer. Sequencing of both cancerous and histologically non-cancerous tissue has been instrumental in improving our understanding of how environmental carcinogens cause cancer. Understanding how and defining which environmental or lifestyle exposures drive cancer will support cancer prevention. Recent research is revisiting the mechanisms of early tumorigenesis, paving the way for an era of molecular cancer prevention.\u003Cbr>Cancer Initiation: Beyond the Genome\u003Cbr>A longstanding model of carcinogenesis is that acquisition of mutations is the rate-limiting step toward tumor formation and that many environmental carcinogens act via mutagenesis. However, several lines of evidence, including seminal breakthroughs from the Mutographs Cancer Grand Challenges team, paint a more nuanced view of cancer initiation. (i) Somatic cells become replete with oncogenic mutations over time. Recent studies of sequencing histologically normal tissue from a range of tissue sites have identified oncogenic driver mutations without any evidence of disease, suggesting driver mutations are necessary but not always sufficient for tumorigenesis (1) . (ii) Common oncogenic driver mutations may not be directly induced by cancer risk factors. Mutational signature analysis can be used to study the etiology and origins of mutations in the genome, but many oncogenic driver mutations do not arise within well-established environmental mutational signatures. For example, in silico analysis suggests common oncogenic drivers (KRASG12D, TP53R175H, and NRASQ61K) correspond within an aging-associated mutational signature (2) . These observations challenge the notion that the mechanism of action for environmental carcinogens, such as UV light and tobacco smoking, are solely mutagenic (2) . (iii) Many carcinogens drive cancer without altering mutational burden or leaving a clear mutational signature. A recent study by Balmain and colleagues of 20 International Agency for\u003Cbr>This work is licensed under a BY 4.0 International license.\u003Cbr>\\#Corresponding Author: Prof Charles Swanton, 1 Midland Road, Francis Crick Institute, London, NW1 1AT, +44 203 796 2047. |\n\nEurope PMC unders uthManuscripts Europe M eC und Author Manuscripts  \nHill et al. Page 2  \nResearch on Cancer group-one carcinogens found only three increased mutational burden and led to mutational signatures, whereas the majority accelerated cancer independently of mutagenesis (3) . (iv) Mutational profiling alone may not fully explain geographical differences in esophageal cancer incidence. Profiling of over 500 whole genomes from esophageal tumors from eight different countries with varying esophageal cancer incidence rates revealed that the mutational profiles were strikingly similar (4) . This lack of any clear mutational difference between tumors from high-risk and low-risk areas suggests that carcinogens that leave no measurable genomic imprint may promote cancer initiation. (v) In lung cancer arising in people who smoke (a clear mutagen), 8% of lung cancers lacke","cbCaidGyG0XJERuP","https://ap.wps.com/l/cbCaidGyG0XJERuP","pdf",652396,15,"English","# Abstract\n# Cancer Initiation: Beyond the Genome\n# Cancer Promotion\n# Examples of Tumor promotion","[{\"question\":\"How do environmental carcinogens contribute to cancer incidence according to the document?\",\"answer\":\"Environmental carcinogens increase cancer incidence through both mutagenic and non-mutagenic mechanisms. The text notes that not all carcinogen effects can be explained solely by inducing mutations.\"},{\"question\":\"Why do oncogenic driver mutations not always lead to tumorigenesis?\",\"answer\":\"The document states that oncogenic driver mutations can be found in histologically normal tissue without evidence of disease. This suggests driver mutations are necessary but not always sufficient for tumor formation.\"},{\"question\":\"What is the tumor promotion concept described in the document?\",\"answer\":\"A two-step model proposes an initiation step followed by a promotion step involving irritant inflammatory agents. Without promotion, mutant cells may remain dormant, while promoter exposure can still drive rapid tumorigenesis.\"}]","Tumor Promoters and Opportunities for Molecular Cancer Prevention | PDF",1789986215,38]