{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Barrett JE"],"funding":["Austrian Science Fund FWF","Forskningsrådet om Hälsa, Arbetsliv och Välfärd (Swedish Research Council for Health, Working Life and Welfare)","European Research Council"],"pagination":["97"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11965489"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["5(1)"],"pubmed_abstract":["<h4>Background</h4>In order to advance personalized primary cancer prevention, surrogate endpoint biomarkers in distant, easy to access tissues (i.e., field defect indicators) reflecting field cancerization in the organ at risk are essential.<h4>Methods</h4>Here we utilized medroxyprogesterone acetate and 7,12-dimethylbenzanthracene to induce mammary gland cancers in mice. We assessed epigenetic signatures reflective of carcinogen exposure, cell-type composition, mitotic age, and methylation at progesterone receptor binding sites in both, the tissue at risk (normal mammary gland; field cancerization) and distant non-at-risk organs (cervix, oviduct, and blood; field defect indicators), in mice that did and did not develop mammary gland cancers.<h4>Results</h4>We demonstrate that the anti-pr"],"journal":["Communications medicine"],"pubmed_title":["Epigenetic signatures in surrogate tissues are able to assess cancer risk and indicate the efficacy of preventive measures."],"pmcid":["PMC11965489"],"funding_grant_id":["742432","P 31228-B33","2021-02974"],"pubmed_authors":["Kofler B","Ishaq Parveen I","Gemzell-Danielsson K","Weber DD","Stefan VE","Felder TK","Tevini J","Alkasalias T","Redl E","Catalano L","Barrett JE","Aminzadeh-Gohari S","Widschwendter M","Rotharmel J","Herzog CM","Lang R","Obrist P"],"additional_accession":[]},"is_claimable":false,"name":"Epigenetic signatures in surrogate tissues are able to assess cancer risk and indicate the efficacy of preventive measures.","description":"<h4>Background</h4>In order to advance personalized primary cancer prevention, surrogate endpoint biomarkers in distant, easy to access tissues (i.e., field defect indicators) reflecting field cancerization in the organ at risk are essential.<h4>Methods</h4>Here we utilized medroxyprogesterone acetate and 7,12-dimethylbenzanthracene to induce mammary gland cancers in mice. We assessed epigenetic signatures reflective of carcinogen exposure, cell-type composition, mitotic age, and methylation at progesterone receptor binding sites in both, the tissue at risk (normal mammary gland; field cancerization) and distant non-at-risk organs (cervix, oviduct, and blood; field defect indicators), in mice that did and did not develop mammary gland cancers.<h4>Results</h4>We demonstrate that the anti-pr","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Apr","modification":"2026-06-01T05:39:48.554Z","creation":"2025-07-01T03:05:40.386Z"},"accession":"S-EPMC11965489","cross_references":{"pubmed":["40175633"],"doi":["10.1038/s43856-025-00779-w"]}}