{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Lahera A"],"funding":["Comunidad de Madrid","Ministerio de Economía y Competitividad (Ministry of Economy and Competitiveness)"],"pagination":["152"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11271448"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["8(1)"],"pubmed_abstract":["Precursor T-cell neoplasms (T-ALL/LBL) are aggressive hematological malignancies that arise from the malignant transformation of immature thymocytes. Despite the JAK/STAT pathway is recurrently altered in these neoplasms, there are not pharmacological inhibitors officially approved for the treatment of T-ALL/LBL patients that present oncogenic JAK/STAT pathway mutations. In the effort to identify potential therapeutic targets for those patients, we followed an alternative approach and focused on their transcriptional profile. We combined the analysis of molecular data from T-ALL/LBL patients with the generation of hematopoietic cellular models to reveal that JAK/STAT pathway mutations are associated with an aberrant transcriptional profile. Specifically, we demonstrate that JAK/STAT pathwa"],"journal":["NPJ precision oncology"],"pubmed_title":["PIM1 is a potential therapeutic target for the leukemogenic effects mediated by JAK/STAT pathway mutations in T-ALL/LBL."],"pmcid":["PMC11271448"],"funding_grant_id":["SAF2015-70561-R","B2017/BMD-3778; LINFOMAS-CM"],"pubmed_authors":["Lahera A","Llamas P","Vela-Martin L","Cornago J","Fernandez-Piqueras J","Fernandez-Navarro P","Lopez-Lorenzo JL","Santos J","Villa-Morales M"],"additional_accession":[]},"is_claimable":false,"name":"PIM1 is a potential therapeutic target for the leukemogenic effects mediated by JAK/STAT pathway mutations in T-ALL/LBL.","description":"Precursor T-cell neoplasms (T-ALL/LBL) are aggressive hematological malignancies that arise from the malignant transformation of immature thymocytes. Despite the JAK/STAT pathway is recurrently altered in these neoplasms, there are not pharmacological inhibitors officially approved for the treatment of T-ALL/LBL patients that present oncogenic JAK/STAT pathway mutations. In the effort to identify potential therapeutic targets for those patients, we followed an alternative approach and focused on their transcriptional profile. We combined the analysis of molecular data from T-ALL/LBL patients with the generation of hematopoietic cellular models to reveal that JAK/STAT pathway mutations are associated with an aberrant transcriptional profile. Specifically, we demonstrate that JAK/STAT pathwa","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jul","modification":"2026-06-02T23:34:19.261Z","creation":"2025-04-19T13:12:13.153Z"},"accession":"S-EPMC11271448","cross_references":{"pubmed":["39033228"],"doi":["10.1038/s41698-024-00638-2"]}}