<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Barrett JE</submitter><funding>Austrian Science Fund FWF</funding><funding>Forskningsrådet om Hälsa, Arbetsliv och Välfärd (Swedish Research Council for Health, Working Life and Welfare)</funding><funding>European Research Council</funding><pagination>97</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11965489</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>5(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/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.&lt;h4>Methods&lt;/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.&lt;h4>Results&lt;/h4>We demonstrate that the anti-pr</pubmed_abstract><journal>Communications medicine</journal><pubmed_title>Epigenetic signatures in surrogate tissues are able to assess cancer risk and indicate the efficacy of preventive measures.</pubmed_title><pmcid>PMC11965489</pmcid><funding_grant_id>742432</funding_grant_id><funding_grant_id>P 31228-B33</funding_grant_id><funding_grant_id>2021-02974</funding_grant_id><pubmed_authors>Kofler B</pubmed_authors><pubmed_authors>Ishaq Parveen I</pubmed_authors><pubmed_authors>Gemzell-Danielsson K</pubmed_authors><pubmed_authors>Weber DD</pubmed_authors><pubmed_authors>Stefan VE</pubmed_authors><pubmed_authors>Felder TK</pubmed_authors><pubmed_authors>Tevini J</pubmed_authors><pubmed_authors>Alkasalias T</pubmed_authors><pubmed_authors>Redl E</pubmed_authors><pubmed_authors>Catalano L</pubmed_authors><pubmed_authors>Barrett JE</pubmed_authors><pubmed_authors>Aminzadeh-Gohari S</pubmed_authors><pubmed_authors>Widschwendter M</pubmed_authors><pubmed_authors>Rotharmel J</pubmed_authors><pubmed_authors>Herzog CM</pubmed_authors><pubmed_authors>Lang R</pubmed_authors><pubmed_authors>Obrist P</pubmed_authors></additional><is_claimable>false</is_claimable><name>Epigenetic signatures in surrogate tissues are able to assess cancer risk and indicate the efficacy of preventive measures.</name><description>&lt;h4>Background&lt;/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.&lt;h4>Methods&lt;/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.&lt;h4>Results&lt;/h4>We demonstrate that the anti-pr</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Apr</publication><modification>2026-06-01T05:39:48.554Z</modification><creation>2025-07-01T03:05:40.386Z</creation></dates><accession>S-EPMC11965489</accession><cross_references><pubmed>40175633</pubmed><doi>10.1038/s43856-025-00779-w</doi></cross_references></HashMap>