{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Casado-Garcia A"],"funding":["MCIU/AEI/FEDER","MINECO/FEDER","Ayuda para Contratos predoctorales para la formación de doctores","FEDER","Fundación Científica de la Asociación Española contra el Cáncer","NCI NIH HHS","American Lebanese Syrian Associated","FEDER MINECO","Miguel Servet Grant"],"pagination":["1098-1109"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9359729"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["82(6)"],"pubmed_abstract":["Preventing development of childhood B-cell acute lymphoblastic leukemia (B-ALL), a disease with devastating effects, is a longstanding and unsolved challenge. Heterozygous germline alterations in the PAX5 gene can lead to B-ALL upon accumulation of secondary mutations affecting the JAK/STAT signaling pathway. Preclinical studies have shown that this malignant transformation occurs only under immune stress such as exposure to infectious pathogens. Here we show in Pax5+/- mice that transient, early-life administration of clinically relevant doses of ruxolitinib, a JAK1/2 inhibitor, significantly mitigates the risk of B-ALL following exposure to infection; 1 of 29 animals treated with ruxolitinib developed B-ALL versus 8 of 34 untreated mice. Ruxolitinib treatment preferentially targeted Pax5"],"journal":["Cancer research"],"pubmed_title":["Transient Inhibition of the JAK/STAT Pathway Prevents B-ALL Development in Genetically Predisposed Mice."],"pmcid":["PMC9359729"],"funding_grant_id":["R01 CA241452","SAF2015-64420-R","CPII19/00024","PRE2019-088887","CSI021-19","UIC-017","CSI067-18","SAF2017-83061-R","PRYCO211305SANC","CSI144P20","CSI001U16","RTI2018-093314-B-I00","CSI234P18","AES 2017-2020","R01CA241452","9659122185-122185-4-21"],"pubmed_authors":["Alonso-Lopez D","Raboso-Gallego J","Blanco O","Aleman-Arteaga S","Garcia Criado FJ","Orfao A","Riesco S","Sanchez-Garcia I","Yang JJ","Vicente-Duenas C","Nichols KE","Mayado A","Oak N","Ramirez-Orellana M","Martinez-Cano J","Prieto-Matos P","Mann-Ran C","Buhles A","Gonzalez-Murillo A","Sterker D","Casado-Garcia A","Weiss A","Garcia Cenador MB","Radimerski T","Sanchez EG","Cobaleda C","Isidro-Hernandez M","De Las Rivas J"],"additional_accession":[]},"is_claimable":false,"name":"Transient Inhibition of the JAK/STAT Pathway Prevents B-ALL Development in Genetically Predisposed Mice.","description":"Preventing development of childhood B-cell acute lymphoblastic leukemia (B-ALL), a disease with devastating effects, is a longstanding and unsolved challenge. Heterozygous germline alterations in the PAX5 gene can lead to B-ALL upon accumulation of secondary mutations affecting the JAK/STAT signaling pathway. Preclinical studies have shown that this malignant transformation occurs only under immune stress such as exposure to infectious pathogens. Here we show in Pax5+/- mice that transient, early-life administration of clinically relevant doses of ruxolitinib, a JAK1/2 inhibitor, significantly mitigates the risk of B-ALL following exposure to infection; 1 of 29 animals treated with ruxolitinib developed B-ALL versus 8 of 34 untreated mice. Ruxolitinib treatment preferentially targeted Pax5","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Mar","modification":"2026-05-28T03:45:24.595Z","creation":"2025-04-06T00:52:45.007Z"},"accession":"S-EPMC9359729","cross_references":{"pubmed":["35131871"],"doi":["10.1158/0008-5472.CAN-21-3386"]}}