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This study profiled MAM in Barrett’s esophagus (BE) and across an esophageal adenocarcinoma (EAC) progression sequence, then assessed links to host genotoxic changes. 16S rRNA sequencing compared nonneoplastic BE (N), adjacent EAC-associated BE (ADJ), and EAC tumors (T), with correlations to TP53 mutation, telomere length, and DNA methylation of candidate genes and genome-wide RRBS methylation. Adjacent/tumor groups showed reduced microbial alpha diversity and increased DNA methylation Z scores, with hyper-methylated sites near transcription start sites involving metabolic pathways. Results support pathogenic interaction between host genotoxic change and MAM dysbiosis.",{"@graph":69,"@context":122},[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/distinct-microbiome-dysbiosis-and-epigenetic-anomaly-in-esophageal-adenocarcinoma-and-its-underlying-barretts-esophagus/331647/",{"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/distinct-microbiome-dysbiosis-and-epigenetic-anomaly-in-esophageal-adenocarcinoma-and-its-underlying-barretts-esophagus/331647.png","ImageObject",300,407,{"name":92,"@type":93},"Genevieve","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-11-03","2026-09-21",true,{"@type":102,"interactionType":103,"userInteractionCount":34},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"What tissue groups were compared in the study of MAM and EAC progression?","Question",{"text":112,"@type":113},"The study analyzed three biopsy groups: nonneoplastic Barrett’s esophagus without cancer (N), biopsies from adjacent areas associated with EAC (ADJ), and biopsies from EAC tumor tissues (T).","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"How were MAM and host genotoxic changes measured?",{"text":117,"@type":113},"MAM was profiled using 16S rRNA gene sequencing, while host genotoxic changes were assessed via TP53 mutation status, telomere length, and DNA methylation of candidate genes and genome-wide DNA methylation using RRBS.",{"name":119,"@type":110,"acceptedAnswer":120},"What key association did the integrated analysis reveal?",{"text":121,"@type":113},"Hyper-methylated genome sites were associated with lower microbial alpha diversity and were enriched near transcription start sites, with genes involved in metabolic processes.","https://schema.org",{"og:url":83,"og:type":124,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":126,"canonical":83},"index,follow",{"doc_id":128,"site_id":62},331647,1790160040,{"code":4,"msg":5,"data":131},{"doc_id":128,"user_id":132,"nickname":92,"user_avatar":133,"doc_module":4,"category_id":39,"category_name":40,"doc_title":65,"doc_description":67,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":34,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":139,"language":140,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":141,"faqs":142,"seo_title":143,"seo_description":67,"update_tm":144,"read_time":145,"preview_page_count":4},1374391974585,"https://ap-avatar.wpscdn.com/davatar_276721f389ce27ea32af1340a28f341c","Shijimaya et al. Clinical Epigenetics (2024) 16:184 [https://doi.org/10.1186/s13148-024-01801-z](https://doi.org/10.1186/s13148-024-01801-z)  \nClinical Epigenetics  \n RESEARCH Open Access  \nDistinct microbiome dysbiosis and epigenetic anomaly in esophageal adenocarcinoma and its underlying Barrett’s esophagus  \nTakuya Shijimaya1, Tomomitsu Tahara1,4*, Jumpei Yamazaki2,3, Sanshiro Kobayashi 1, Yasushi Matsumoto 1, Naohiro Nakamura 1, Yu Takahashi1, Takashi Tomiyama1, Toshiro Fukui 1, Tomoyuki Shibata4 and Makoto Naganuma 1  \nAbstract  \nInteraction between host genotoxic changes and mucosa-associated microbiome (MAM) dysbiosis may have a role in various digestive cancers. We investigated MAM in Barrett’s esophagus (BE) and esophageal adenocarcinoma (EAC) progression sequence and its association with host genotoxic changes. 16S rRNA gene sequencing was performed in three different groups of biopsies from nonneoplastic BE from patients without cancer (N, normal group; n = 47) and with EAC (ADJ, adjacent group; n = 27) . Endoscopic biopsies were also obtained from EAC tissues (T, tumor group; n = 22) . Results were correlated with TP53 mutation, telomere length and DNA methylation of candidate genes (N33, DPYS, SLC16A12, miR124A3 and miR34bc) . Genome-wide DNA methylation examined by reduced representation bisulfite sequencing (RRBS) was available for 32 samples (n = 12 for N, n = 12 for ADJ and n = 22 forT groups) . Lower microbial alpha diversity measures were observed in ADJ/T groups relative to N group and associated with higher mean Z score DNA methylation of candidate genes. Specific genera (n = 16) with significant change between ADJ/T groups relative to N group occurred mostly in ADJ group (13/16) and half of them (8/16) were associated with DNA methylation status. Integrated MAM and genome-wide methylation analysis demonstrated that hyper-methylated sites, associated with lower alpha diversity measures dominantly occurred within near the transcription start site, codifying genes were involved in metabolic processes. Our result shows that microbial dysbiosis in EAC mostly occurs in adjacent BE and such dysbiosis was associated with DNA methylation status, offering support for a pathogenic role of interaction between host genotoxic changes and MAM in this tumor type.  \nKeywords Barrett’s esophagus, Esophageal adenocarcinoma, Mucosa-associated microbiome, DNA methylation, RRBS, Telomere shortening  \n*Correspondence: Tomomitsu Tahara [taharatm@takii.kmu.ac.jp](taharatm@takii.kmu.ac.jp)  \nFull list of author information is available at the end of the article  \n© The Author(s) 2024. Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit [http://creativecommons.org/licenses/by-nc-nd/4.0/](http://creativecommons.org/licenses/by-nc-nd/4.0/.)[.](http://creativecommons.org/licenses/by-nc-nd/4.0/.)  \nShijimaya et al. Clinical Epigenetics (2024) 16:184  \nIntroduction  \nEsophageal adenocarcinoma (EAC) accounts for more than half of esophageal cancers in western countries [1–3] and its incidence is gradually increasing in Japan [4, 5]. Ba","cbCaid5DXitb85tF","https://ap.wps.com/l/cbCaid5DXitb85tF","pdf",1555883,11,"English","# Abstract\n# Introduction\n## Host genotoxic changes in EAC and BE\n## Microbiome dysbiosis and reported host-microbe links\n# Results","[{\"question\":\"What tissue groups were compared in the study of MAM and EAC progression?\",\"answer\":\"The study analyzed three biopsy groups: nonneoplastic Barrett’s esophagus without cancer (N), biopsies from adjacent areas associated with EAC (ADJ), and biopsies from EAC tumor tissues (T).\"},{\"question\":\"How were MAM and host genotoxic changes measured?\",\"answer\":\"MAM was profiled using 16S rRNA gene sequencing, while host genotoxic changes were assessed via TP53 mutation status, telomere length, and DNA methylation of candidate genes and genome-wide DNA methylation using RRBS.\"},{\"question\":\"What key association did the integrated analysis reveal?\",\"answer\":\"Hyper-methylated genome sites were associated with lower microbial alpha diversity and were enriched near transcription start sites, with genes involved in metabolic processes.\"}]","Distinct microbiome dysbiosis and epigenetic anomaly in esophageal adenocarcinoma and its underlying Barrett’s esophagus | PDF",1789994442,28]