biostudies-literaturede Barrios OInstituto de Salud Carlos IIIEuropean Research CouncilAgencia Estatal de InvestigaciónMinisterio de Ciencia e InnovaciónJosé Carreras Leukämie-StiftungFundación Científica Asociación Española Contra el CáncerFight Kids Cancer Funding Programme99https://www.ebi.ac.uk/biostudies/studies/S-EPMC12305908biostudies-literatureUnknown13(1)<h4>Background</h4>Infants diagnosed with B cell acute lymphoblastic leukemia (B-ALL) and t(4;11) chromosomal rearrangement display poor therapeutic response, associated to the low expression of B lymphocyte factor HDAC7. This study was conceived to identify a therapeutic strategy for t(4;11) B-ALL that restores optimal HDAC7 expression.<h4>Methods</h4>A multiomics approach in a large infant pro-B-ALL cohort was employed to identify HDAC7's repression mechanism. These data, combined with cell culture assays in a variety of pro-B-ALL cell lines with differential HDAC7 levels, led us to define a novel combination therapy. Murine leukemia models and ex vivo assays using patient-derived xenografts (PDX) were employed to assess the benefits of this therapy when incorporated to glucocorticoid-baBiomarker researchHDAC7 induction combined with standard-of-care chemotherapy provides a therapeutic advantage in t(4;11) infant B-cell acute lymphoblastic leukemia.PMC12305908957466POSTD20024DEBARYC2021-031197-IPRE2018-083183Cure2MLLDJCLS/07R/2022PI21/01451PI20/00822MICINN, EUR2019-103835101100665Ocon-Gabarro ISchneider PParra MMartinez-Moreno ATejedor JRRomecin PAde Barrios OMarschalek RBueno CGusi-Vives MMeler AStam RWMenendez PCazzaniga GFraga MFBardini MCollazo OfalseHDAC7 induction combined with standard-of-care chemotherapy provides a therapeutic advantage in t(4;11) infant B-cell acute lymphoblastic leukemia.<h4>Background</h4>Infants diagnosed with B cell acute lymphoblastic leukemia (B-ALL) and t(4;11) chromosomal rearrangement display poor therapeutic response, associated to the low expression of B lymphocyte factor HDAC7. This study was conceived to identify a therapeutic strategy for t(4;11) B-ALL that restores optimal HDAC7 expression.<h4>Methods</h4>A multiomics approach in a large infant pro-B-ALL cohort was employed to identify HDAC7's repression mechanism. These data, combined with cell culture assays in a variety of pro-B-ALL cell lines with differential HDAC7 levels, led us to define a novel combination therapy. Murine leukemia models and ex vivo assays using patient-derived xenografts (PDX) were employed to assess the benefits of this therapy when incorporated to glucocorticoid-ba2025-01-01T00:00:00Z2025 Jul2026-03-27T16:51:53.284Z2025-08-27T03:11:10.59ZS-EPMC123059084072204610.1186/s40364-025-00810-1