ArticlePloS one2015
Characterization of LEF1 High Expression and Novel Mutations in Adult Acute Lymphoblastic Leukemia.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 57 citations in OpenAlex.
- Distribution of molecular subtypes in a Colombian cohort of patients with acute lymphoblastic leukemia using whole-transcriptome analysis.Frontiers in oncology · 2026Article
- Targeting Wnt Signaling in Acute Lymphoblastic Leukemia.Cancers · 2025Review
- Tumor microenvironment as a novel therapeutic target for lymphoid leukemias.Annals of hematology · 2025Review
- Melatonin antagonizes bone loss induced by mechanical unloading via IGF2BP1-dependent mCellular and molecular life sciences : CMLS · 2025Article
- Correction: Characterization of LEF1 High Expression and Novel Mutations in Adult Acute Lymphoblastic Leukemia.PloS one · 2024Article
- Effects of S-Adenosylhomocysteine Hydrolase Downregulation on Wnt Signaling Pathway in SW480 Cells.International journal of molecular sciences · 2023Article
- Single-cell RNA sequencing of solid pseudopapillary neoplasms of the pancreas in children.Cancer science · 2023Article
- Characterization of Philadelphia-like Pre-B Acute Lymphoblastic Leukemia: Experiences in Mexican Pediatric Patients.International journal of molecular sciences · 2022Article
- Oncogenic and Tumor Suppressor Functions for Lymphoid Enhancer Factor 1 inFrontiers in immunology · 2022Article
- E Protein Transcription Factors as Suppressors of T Lymphocyte Acute Lymphoblastic Leukemia.Frontiers in immunology · 2022Review
- CRLF2 and IKZF1 abnormalities in Mexican children with acute lymphoblastic leukemia and recurrent gene fusions: exploring surrogate markers of signaling pathways.The journal of pathology. Clinical research · 2021Article
- Article
- Wnt Signaling in Leukemia and Its Bone Marrow Microenvironment.International journal of molecular sciences · 2020Review
- The Role Played by Wnt/β-Catenin Signaling Pathway in Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2020Review
- WNT Signaling in Hematological Malignancies.Frontiers in oncology · 2020Review
- MicroRNA-6852 suppresses glioma A172 cell proliferation and invasion by targeting LEF1.Experimental and therapeutic medicine · 2019Article
- Aberrant ARID5B expression and its association with Ikaros dysfunction in acute lymphoblastic leukemia.Oncogenesis · 2018Article
- c-Myc is a novelThe Journal of biological chemistry · 2018Article
- Plant homeodomain finger protein 2 as a novel IKAROS target in acute lymphoblastic leukemia.Epigenomics · 2018Article
- Ikaros regulation of the BCL6/BACH2 axis and its clinical relevance in acute lymphoblastic leukemia.Oncotarget · 2017Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Aberrant activation of the Wnt pathway plays a pathogenetic role in tumors and has been associated with adverse outcome in acute lymphoblastic leukemia (ALL). Lymphoid enhancer binding factor 1 (LEF1), a key mediator of Wnt signaling, has been linked to leukemic transformation, and LEF1 mutations have been identified in T-ALL. Here we found LEF1 is highly expressed in 25.0% adult ALL patients and LEF1 high expression was associated with high-risk leukemia factors (high WBC, Philadelphia chromosome positive, complex karyotype), shorter event-free survival (EFS), and high relapse rates in patients with B-ALL. LEF1 high expression is also associated with high mutation rate of Notch1 and JAK1 in T-ALL. We identified 2 novel LEF1 mutations (K86E and P106L) in 4 of 131 patients with ALL, and those patients with high-risk ALL (high WBC, complex karyotype). These results suggest a role for LEF1 mutations in leukemogenesis. We further explored the effect of the mutations on cell proliferation and found both mutations significantly promoted the proliferation of ALL cells. We also observed the effect of LEF1 and its mutations on the transcription of its targets, c-MYC and Cyclin D1. We found LEF1 increased the promoter activity of its targets c-MYC and Cyclin D1, and LEF1 K86E and P106L mutants further significantly enhanced this effect. We also observed that the c-MYC and Cyclin D1 mRNA levels were significantly increased in patients with LEF1 high expression compared with those with low expression. Taken together, our findings indicate high LEF1 expression and mutation are associated with high-risk leukemia and our results also revealed that LEF1 high expression and/or gain-of-function mutations are involved in leukemogenesis of ALL.
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