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Título
SOCS3 deregulation contributes to aberrant activation of the JAK/STAT pathway in precursor T-cell neoplasms
Autor(es)
Lahera, Antonio | López-Nieva, Pilar | Alarcón, Hernán | Marín-Rubio, José L | Cobos-Fernández, María Á | Fernandez-Navarro, Pablo L ISCIII | Fernández, Agustín F | Vela-Martín, Laura | Sastre, Isabel | Ruiz-García, Sara | Llamas, Pilar | López-Lorenzo, José L | Cornago, Javier | Santos, Javier | Fernández-Piqueras, José | Villa-Morales, María
Fecha de publicación
2023-05
Cita
Br J Haematol. 2023 May;201(4):718-724.
Idioma
Inglés
Tipo de documento
journal article
Resumen
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.
Palabras clave
MESH
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma | Leukemia-Lymphoma, Adult T-Cell | Humans | Janus Kinases | Signal Transduction | Suppressor of Cytokine Signaling 3 Protein | STAT Transcription Factors | STAT3 Transcription Factor | Suppressor of Cytokine Signaling Proteins | T-Lymphocytes
Versión en línea
DOI
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