{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T18:07:03Z","timestamp":1791223623883,"version":"4.1.0"},"reference-count":51,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2026,4,18]],"date-time":"2026-04-18T00:00:00Z","timestamp":1776470400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,4,18]],"date-time":"2026-04-18T00:00:00Z","timestamp":1776470400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Intl Journal of Cancer"],"published-print":{"date-parts":[[2026,9,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Basal\u2010like breast cancer (BLBC) is characterized as the most aggressive and poorly understood breast cancer (BC) subtype. Next to surgery, conventional chemotherapy and immunotherapy, radiotherapy (RT) represents one of the primary treatment options. Transcriptional plasticity is largely responsible for BLBC's ability to rapidly adapt to genotoxic stress, enabling cell survival, tumor repopulation, and disease progression. Our research group has recently shown that chemotherapy primarily elicits the epithelial\u2010to\u2010mesenchymal transition (EMT) transcriptomic program by epigenetically derepressing the expression of several important EMT\u2010promoting factors, which are crucial for drug tolerance and disease relapse. However, the induced transcriptomic programs upon RT in BLBC have been elusively addressed. To fill this gap, we leveraged high\u2010throughput bulk and spatial transcriptomic data in a syngeneic mouse model of BLBC, corroborated by publicly available patient\u2010derived bulk transcriptomic data and combined with an in\u00a0vitro 3D BLBC model approach. Contrary to our expectations, we found that irradiated basal\u2010like breast cancer (BLBC) tumors shifted their epithelial\/mesenchymal hybrid state toward a stronger epithelial gene expression program, ultimately driving MUC1 (Mucin 1) expression as a key mediator of cell survival following RT. Altogether, our study uncovers a new aspect of the BLBC transcriptional plasticity elicited by RT, leading to a distinct hybrid phenotypic state from that upon chemotherapy. Concluding, these data underscore the potential clinical value of MUC1 as a therapeutic target or prognostic marker to optimize BLBC patients\u2019 response to RT.<\/jats:p>","DOI":"10.1002\/ijc.70487","type":"journal-article","created":{"date-parts":[[2026,4,18]],"date-time":"2026-04-18T09:59:30Z","timestamp":1776506370000},"page":"1296-1310","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["<scp>MUC1<\/scp>\n                    as a Survival Effector of Radiotherapy\u2010Induced Epithelial Hybrid States in Basal\u2010Like Breast Cancer"],"prefix":"10.1002","volume":"159","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1954-4919","authenticated-orcid":false,"given":"Garyfallia","family":"Pantelaiou\u2010Prokaki","sequence":"first","affiliation":[{"name":"Translational Molecular Imaging Max Planck Institute for Multidisciplinary Sciences  G\u00f6ttingen Germany"},{"name":"Department of Gynecology and Obstetrics 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