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Specifically, we define a sequence-specific regulatory element engaged by \u03b2-catenin only upon interaction with TCF7L2, revealing that partner choice, independent of\n                    <jats:italic toggle=\"yes\">CTNNB1<\/jats:italic>\n                    mutational status, ultimately determines cell fate. Our findings, validated across multiple tumor models and patient tissues, offer a framework for understanding how differential \u03b2-catenin-TCF\/LEF interaction orchestrates context-specific Wnt signaling outcomes.\n                  <\/jats:p>","DOI":"10.1073\/pnas.2528450123","type":"journal-article","created":{"date-parts":[[2026,6,10]],"date-time":"2026-06-10T17:38:23Z","timestamp":1781113103000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":2,"title":["Differential Wnt\/\u03b2-catenin signaling via TCF7L2\/LEF1 binding specificity shapes cellular and tumor phenotypes"],"prefix":"10.1073","volume":"123","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2224-480X","authenticated-orcid":false,"given":"Thomas A.","family":"Kluiver","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/02aj7yc53","id-type":"ROR","asserted-by":"publisher"}],"name":"Princess M\u00e1xima Center for Pediatric 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