{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,18]],"date-time":"2025-12-18T20:08:15Z","timestamp":1766088495503,"version":"3.48.0"},"reference-count":44,"publisher":"American Society of Hematology","issue":"25","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2025,12,18]]},"abstract":"<jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>T-cell acute lymphoblastic leukemia (T-ALL) represents a group of aggressive hematological malignancies characterized by unfavorable prognosis, urging the need for innovative therapeutic strategies. LEF1 is a member of the lymphoid enhancer factor (LEF)\/T-cell factor family of DNA-binding transcription factors, known for their interaction with nuclear \u03b2-catenin in the context of the Wnt signaling pathway. Although the implication of LEF1 in colon cancer is well documented, its clinical relevance and functional consequences remain elusive in T-ALL. In this study, we provide valuable insights into the prevalence and significance of LEF1 alterations in a comprehensive cohort of 474 pediatric and adult patients with T-ALL enrolled in the FRALLE-2000 (French group for childhood ALL) and GRAALL 2003-2005 (Group for Research on Adult Acute Lymphoblastic Leukemia) trials, respectively. LEF1 alterations were detected in 63 cases (13%), including 9 point mutations (14.3%), 18 large deletions (28.6%), and, strikingly, 36 focal deletions (57.1%), which emerge as the most recurrent subtype. LEF1-altered cases were associated with increased central nervous system involvement and improved initial treatment response. Importantly, we unveil the existence of a previously undescribed dominant-negative LEF1 isoform resulting from focal deletions of the exons 2-3. This novel truncated protein, previously unreported in the literature, is associated with the disruption of the Wnt pathway and T-cell receptor signaling, which can be exploited as a therapeutic strategy to enhance chemosensitivity in LEF1-deleted T-ALL cases. The trials were registered at www.clinicaltrials.gov as #NCT00222027 (GRAALL 2003) and #NCT00327678 (GRAALL 2005); FRALLE2000T protocol (FRALLE-2000).<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1182\/blood.2025030161","type":"journal-article","created":{"date-parts":[[2025,8,26]],"date-time":"2025-08-26T20:04:03Z","timestamp":1756238643000},"page":"3036-3049","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":1,"title":["<i>LEF1<\/i>\n                    intragenic deletion induces a dominant-negative isoform and unveils a Wnt\/\u03b2-catenin vulnerability in T-ALL"],"prefix":"10.1182","volume":"146","author":[{"ORCID":"https:\/\/orcid.org\/0009-0002-8440-7299","authenticated-orcid":false,"given":"Manon","family":"Delafoy","sequence":"first","affiliation":[{"name":"1Institut Necker Enfants Malades, INSERM Unit\u00e9 1151, Paris, France"},{"name":"2Facult\u00e9 de M\u00e9decine, Universit\u00e9 Paris Cit\u00e9, Paris, 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