SOCS3 deregulation contributes to aberrant activation of the JAK/STAT pathway in precursor T‐cell neoplasms.

Summary: 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. [ABSTRACT FROM AUTHOR]