{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["de Barrios O"],"funding":["Instituto de Salud Carlos III","European Research Council","Agencia Estatal de Investigación","Ministerio de Ciencia e Innovación","José Carreras Leukämie-Stiftung","Fundación Científica Asociación Española Contra el Cáncer","Fight Kids Cancer Funding Programme"],"pagination":["99"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12305908"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(1)"],"pubmed_abstract":["Background
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.Methods
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-ba"],"journal":["Biomarker research"],"pubmed_title":["HDAC7 induction combined with standard-of-care chemotherapy provides a therapeutic advantage in t(4;11) infant B-cell acute lymphoblastic leukemia."],"pmcid":["PMC12305908"],"funding_grant_id":["957466","POSTD20024DEBA","RYC2021-031197-I","PRE2018-083183","Cure2MLL","DJCLS/07R/2022","PI21/01451","PI20/00822","MICINN, EUR2019-103835","101100665"],"pubmed_authors":["Ocon-Gabarro I","Schneider P","Parra M","Martinez-Moreno A","Tejedor JR","Romecin PA","de Barrios O","Marschalek R","Bueno C","Gusi-Vives M","Meler A","Stam RW","Menendez P","Cazzaniga G","Fraga MF","Bardini M","Collazo O"],"additional_accession":[]},"is_claimable":false,"name":"HDAC7 induction combined with standard-of-care chemotherapy provides a therapeutic advantage in t(4;11) infant B-cell acute lymphoblastic leukemia.","description":"Background
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.Methods
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-ba","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Jul","modification":"2026-03-27T16:51:53.284Z","creation":"2025-08-27T03:11:10.59Z"},"accession":"S-EPMC12305908","cross_references":{"pubmed":["40722046"],"doi":["10.1186/s40364-025-00810-1"]}}