Lahera, AntonioLópez-Nieva, PilarAlarcón, HernánMarín-Rubio, José LCobos-Fernández, María ÁngelesFernandez-Navarro, Pablo LFernandez, Agustín FVela-Martín, LauraSastre, IsabelRuiz-García, SaraLlamas, PilarLópez-Lorenzo, José LCornago, JavierSantos, JavierFernández-Piqueras, JoséVilla-Morales, María2023-05-172023-05-172023-05Br J Haematol. 2023 May;201(4):718-724.http://hdl.handle.net/20.500.12105/16067Despite the Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway being frequently altered in T-ALL/LBL, no specific therapy has been approved for T-ALL/LBL patients with constitutive signalling by JAK/STAT, so there is an urgent need to identify pathway members that may be potential therapeutic targets. In the present study, we searched for JAK/STAT pathway members potentially modulated through aberrant methylation and identified SOCS3 hypermethylation as a recurrent event in T-ALL/LBL. Additionally, we explored the implications of SOCS3 deregulation in T-ALL/LBL and demonstrated that SOCS3 counteracts the constitutive activation of the JAK/STAT pathway through different molecular mechanisms. Therefore, SOCS3 emerges as a potential therapeutic target in T-ALL/LBL.engVoRhttp://creativecommons.org/licenses/by-nc/4.0/JAK/STAT pathwaySOCS3Precursor T-cell neoplasms (T-ALL/LBL)Precursor T-Cell Lymphoblastic Leukemia-LymphomaLeukemia-Lymphoma, Adult T-CellHumansJanus KinasesSignal TransductionSuppressor of Cytokine Signaling 3 ProteinSTAT Transcription FactorsSTAT3 Transcription FactorSuppressor of Cytokine Signaling ProteinsT-LymphocytesAtribución-NoComercial 4.0 Internacional367861702014718-72410.1111/bjh.186941365-2141British journal of haematologyopen access