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oai:repisalud.isciii.es:20.500.12105/160672025-04-04T14:39:21Zcom_20.500.12105_2052com_20.500.12105_2051com_20.500.12105_15322col_20.500.12105_19608col_20.500.12105_16977col_20.500.12105_16990

00925njm 22002777a 4500 dc Lahera, Antonio author López-Nieva, Pilar author Alarcón, Hernán author Marín-Rubio, José L author Cobos-Fernández, María Ángeles author Fernandez-Navarro, Pablo L author Fernandez, Agustín F author Vela-Martín, Laura author Sastre, Isabel author Ruiz-García, Sara author Llamas, Pilar author López-Lorenzo, José L author Cornago, Javier author Santos, Javier author Fernández-Piqueras, José author Villa-Morales, María author 2023-05 Despite 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. Br J Haematol. 2023 May;201(4):718-724. 10.1111/bjh.18694 1365-2141 British journal of haematology 36786170 http://hdl.handle.net/20.500.12105/16067 JAK/STAT pathway SOCS3 Precursor T-cell neoplasms (T-ALL/LBL) SOCS3 deregulation contributes to aberrant activation of the JAK/STAT pathway in precursor T-cell neoplasms