{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,14]],"date-time":"2026-09-14T22:52:25Z","timestamp":1789426345893,"version":"build-2803163510"},"reference-count":38,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2025,6,11]],"date-time":"2025-06-11T00:00:00Z","timestamp":1749600000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Intl Journal of Cancer"],"published-print":{"date-parts":[[2025,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p><jats:italic>TP53<\/jats:italic> is included in most cancer predisposition multigene panels, especially those exploring Hereditary Breast and Ovarian Cancer (HBOC) predisposition. The purpose of this study was to define the contribution of <jats:italic>TP53<\/jats:italic> pathogenic variants (PV) to the HBOC phenotype by collecting genotypes and phenotypes of 398 patients harboring a <jats:italic>TP53<\/jats:italic> variant identified by 53,085 HBOC panel sequencing in 15 French laboratories. Heterozygous <jats:italic>TP53<\/jats:italic> variants were identified in 0.44% of HBOC panels, evenly distributed between PV and VUS. Breast cancers associated with <jats:italic>TP53<\/jats:italic> were predominantly triple positive, particularly Her2+ breast cancer, in situ cancer, or phyllodes tumors (<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.0001 for both). Interestingly, <jats:italic>TP53<\/jats:italic> PV were identified across all ages in breast cancer patients, with enrichment before 36y. We demonstrated that null variants were linked with the HBOC phenotype, and missense variants, especially with a dominant negative effect, with the LFS phenotype (<jats:italic>p<\/jats:italic>\u2009=\u20090.0096). Patients with breast cancer harboring null variants displayed an earlier age of onset compared to missense (<jats:italic>p<\/jats:italic>\u2009=\u20090.0030). Surprisingly, we identified, in late\u2010onset cancer patients, <jats:italic>TP53<\/jats:italic> hotspot PV usually identified in classic LFS, which underlines variable penetrance. Thus, this study suggests the existence of two phenotypic entities associated with <jats:italic>TP53<\/jats:italic> PV: clinical LFS and <jats:italic>TP53<\/jats:italic>\u2010related breast cancer. The type of <jats:italic>TP53<\/jats:italic> variant, as well as modifying factors reflected in family history, may influence these phenotypes, and both should be considered to define the clinical follow\u2010up of patients and relatives.<\/jats:p>","DOI":"10.1002\/ijc.35475","type":"journal-article","created":{"date-parts":[[2025,6,12]],"date-time":"2025-06-12T02:09:49Z","timestamp":1749694189000},"page":"897-907","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Deciphering dual clinical entities associated with <scp><i>TP53<\/i><\/scp> pathogenic variants: Insights from 53,085 <scp>HBOC<\/scp> panel analyses in French laboratories"],"prefix":"10.1002","volume":"157","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1699-0670","authenticated-orcid":false,"given":"Edwige","family":"Kasper","sequence":"first","affiliation":[{"name":"Department of Genetics Univ Rouen Normandie, Normandie Univ, Inserm U1245, and CHU 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