{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T15:54:36Z","timestamp":1792166076369,"version":"4.4.0"},"reference-count":75,"publisher":"American Society for Clinical Investigation","issue":"8","license":[{"start":{"date-parts":[[2024,4,15]],"date-time":"2024-04-15T00:00:00Z","timestamp":1713139200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100002428","name":"Fonds zur F\u00f6rderung der wissenschaftlichen Forschung","doi-asserted-by":"crossref","award":["SFB-F61,SFB-F47"],"award-info":[{"award-number":["SFB-F61,SFB-F47"]}],"id":[{"id":"10.13039\/501100002428","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100002341","name":"Academy of Finland","doi-asserted-by":"crossref","award":["326238,340141,345803,344698"],"award-info":[{"award-number":["326238,340141,345803,344698"]}],"id":[{"id":"10.13039\/501100002341","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,4,15]]},"abstract":"<jats:p>\n                    T cell acute lymphoblastic leukemia (T-ALL) is an aggressive immature T cell cancer. Mutations in\n                    <jats:italic>IL7R<\/jats:italic>\n                    have been analyzed genetically, but downstream effector functions such as STAT5A and STAT5B hyperactivation are poorly understood. Here, we studied the most frequent and clinically challenging STAT5B\n                    <jats:sup>N642H<\/jats:sup>\n                    driver in T cell development and immature T cell cancer onset and compared it with STAT5A hyperactive variants in transgenic mice. Enhanced STAT5 activity caused disrupted T cell development and promoted an early T cell progenitor\u2013ALL phenotype, with upregulation of genes involved in T cell receptor (TCR) signaling, even in absence of surface TCR. Importantly, TCR pathway genes were overexpressed in human T-ALL and mature T cell cancers and activation of TCR pathway kinases was STAT5 dependent. We confirmed STAT5 binding to these genes using ChIP-Seq analysis in human T-ALL cells, which were sensitive to pharmacologic inhibition by dual STAT3\/5 degraders or ZAP70 tyrosine kinase blockers in vitro and in vivo. We provide genetic and biochemical proof that STAT5A and STAT5B hyperactivation can initiate T-ALL through TCR pathway hijacking and suggest similar mechanisms for other T cell cancers. Thus, STAT5 or TCR component blockade are targeted therapy options, particularly in patients with chemoresistant clones carrying STAT5B\n                    <jats:sup>N642H<\/jats:sup>\n                    .\n                  <\/jats:p>","DOI":"10.1172\/jci168536","type":"journal-article","created":{"date-parts":[[2024,4,14]],"date-time":"2024-04-14T14:00:36Z","timestamp":1713103236000},"source":"Crossref","is-referenced-by-count":16,"title":["Hyperactive STAT5 hijacks T cell receptor signaling and drives immature T cell acute lymphoblastic leukemia"],"prefix":"10.1172","volume":"134","author":[{"given":"Tobias","family":"Suske","sequence":"first","affiliation":[{"name":"Institute of Animal Breeding and Genetics and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Helena","family":"Sorger","sequence":"additional","affiliation":[{"name":"Institute of Animal Breeding and Genetics 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