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The characterization of chromosomal abnormalities may provide significant insights into genetic mechanisms of malignant transformation in hematopoietic cells. However, T-ALL is genetically very heterogenous and driving mutations as well as clonal markers for the assessment of minimal residual disease are not always identifiable. Hence, there is a clinical need to further refine the genetic landscape of T-ALL including previously unrecognized fusion partners of commonly translocated genes in T-ALL of childhood.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      In this study, we screened\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u2009229\u00a0T-ALL cases by our targeted genomic capture high-throughput sequencing (gc-HTS) approach. In total, we identified\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200960 gene\u2013gene fusions, present in\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200957 (25%) of the patients. Nine rare or even unrecognized translocations were identified and validated. Furthermore, owing to its interesting chromosomal structure, we studied the oncogenic potential of the complex rearrangement of chromosome 2 and 12, found in a near-early T-cell progenitor (ETP) ALL that leads to the fusion events\n                      <jats:italic>PRKCE::ETV6<\/jats:italic>\n                      and\n                      <jats:italic>ETV6::INO80D<\/jats:italic>\n                      . Exogenous expression of\n                      <jats:italic>PRKCE::ETV6<\/jats:italic>\n                      in Ba\/F3 pro-B and D1 T-cells caused interleukin-independent proliferation and enhanced survival upon interleukin withdrawal, respectively.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      Our study underlines the heterogenous mutational landscape in T-ALL. The previously unrecognized\n                      <jats:italic>PRKCE::ETV6<\/jats:italic>\n                      resulting from a complex rearrangement involving chromosome 2 and 12 demonstrated transforming potential in cytokine-dependent cellular models support the notion of a driver mutation in near ETP-ALL. Our data reconfirm the relevance of ETV6-fusion proteins in the pathogenesis of undifferentiated T-ALL. Importantly, genomic breakpoints at the\n                      <jats:italic>ETV6<\/jats:italic>\n                      locus represent potentially robust MRD markers for (near) ETP-ALL that lack IG\/TR rearrangements.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s40348-025-00208-x","type":"journal-article","created":{"date-parts":[[2025,10,22]],"date-time":"2025-10-22T11:42:05Z","timestamp":1761133325000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Characterization of a PRKCE::ETV6 fusion as a potential oncogenic driver in T-cell acute lymphoblastic leukemia"],"prefix":"10.1186","volume":"12","author":[{"given":"Esther L.","family":"Monsees","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Udo","family":"zur Stadt","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julia","family":"Strauss","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sabrina","family":"Schuster","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nadja","family":"Kleist","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard T.","family":"Hauch","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Spohn","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gerrit","family":"Wolters-Eisfeld","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin A.","family":"Horstmann","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gabriele","family":"Escherich","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lena","family":"Behrmann","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,10,22]]},"reference":[{"issue":"9617","key":"208_CR1","doi-asserted-by":"publisher","first-page":"1030","DOI":"10.1016\/S0140-6736(08)60457-2","volume":"371","author":"CH Pui","year":"2008","unstructured":"Pui CH, Robison LL, Look AT (2008) Acute lymphoblastic leukaemia. 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