{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Carr T"],"funding":["NIAID NIH HHS","NCI NIH HHS","National Institutes of Health"],"pagination":["845488"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8971981"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13"],"pubmed_abstract":["T lymphocyte acute lymphoblastic leukemia (T-ALL) is a heterogeneous disease affecting T cells at multiple stages of their development and is characterized by frequent genomic alterations. The transcription factor LEF1 is inactivated through mutation in a subset of T-ALL cases but elevated LEF1 expression and activating mutations have also been identified in this disease. Here we show, in a murine model of T-ALL arising due to <i>E2a</i> inactivation, that the developmental timing of <i>Lef1</i> mutation impacts its ability to function as a cooperative tumor suppressor or oncogene. T cell transformation in the presence of LEF1 allows leukemic cells to become addicted to its presence. In contrast, deletion prior to transformation both accelerates leukemogenesis and results in leukemic cells"],"journal":["Frontiers in immunology"],"pubmed_title":["Oncogenic and Tumor Suppressor Functions for Lymphoid Enhancer Factor 1 in <i>E2a<sup>-/-</sup></i> T Acute Lymphoblastic Leukemia."],"pmcid":["PMC8971981"],"funding_grant_id":["R01 AI079213","R21 AI096530","R21 AI119894","P30 CA014599"],"pubmed_authors":["Xue HH","Carr T","Dias S","Sigvardsson M","Le Beau MM","Kee BL","McGregor S","Verykokakis M","Bartom ET"],"additional_accession":[]},"is_claimable":false,"name":"Oncogenic and Tumor Suppressor Functions for Lymphoid Enhancer Factor 1 in <i>E2a<sup>-/-</sup></i> T Acute Lymphoblastic Leukemia.","description":"T lymphocyte acute lymphoblastic leukemia (T-ALL) is a heterogeneous disease affecting T cells at multiple stages of their development and is characterized by frequent genomic alterations. The transcription factor LEF1 is inactivated through mutation in a subset of T-ALL cases but elevated LEF1 expression and activating mutations have also been identified in this disease. Here we show, in a murine model of T-ALL arising due to <i>E2a</i> inactivation, that the developmental timing of <i>Lef1</i> mutation impacts its ability to function as a cooperative tumor suppressor or oncogene. T cell transformation in the presence of LEF1 allows leukemic cells to become addicted to its presence. In contrast, deletion prior to transformation both accelerates leukemogenesis and results in leukemic cells","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022","modification":"2026-04-08T18:06:55.955Z","creation":"2025-04-05T22:19:38.995Z"},"accession":"S-EPMC8971981","cross_references":{"pubmed":["35371057"],"doi":["10.3389/fimmu.2022.845488"]}}