ArticleBlood cancer discovery2022
Integrated Genomic Analysis Identifies UBTF Tandem Duplications as a Recurrent Lesion in Pediatric Acute Myeloid Leukemia.
Article in Blood cancer discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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64 citing papers in PubMed, 93 citations in OpenAlex.
- Clinical impact of minimal residual disease in blood and bone marrow of children with acute myeloid leukemia.Blood advances · 2023Trial
- Menin inhibition in pediatric UBTF-TD myelodysplastic syndrome: molecular rationale and clinical observation.Molecular and cellular pediatrics · 2026Article
- A New Paradigm for Pediatric AML: Improving the Pipeline for Treatments Targeting Cytogenetic and Molecular Alterations.Cancers · 2026Review
- Beyond nuclear export: chromatin-bound XPO1/CRM1 as a transcriptional scaffold.International journal of hematology · 2026Review
- Article
- Venetoclax in combination with cytarabine with or without idarubicin or azacitidine in children, adolescents, and young adults with relapsed or refractory acute myeloid leukaemia (VENAML): a multicentre, phase 1 expansion study.The Lancet. Haematology · 2026Article
- Dysregulation of the inside-out signaling pathway in CNS-infiltrated pediatric T-cell acute lymphoblastic leukemia.Research square · 2026Article
- The Mutational Landscape of Acute Myeloid Leukemia and Its Impact.International journal of molecular sciences · 2026Review
- Uncovering a role for METTL13 in malignant transformation of human hematopoietic stem cells and in the progression of pediatric leukemia.Cell death & disease · 2026Article
- Pancancer Analysis and the Oncogenic Role ofInternational journal of molecular sciences · 2026Article
- Ontogeny Dictates Oncogenic Potential, Lineage Hierarchy, and Therapy Response in Pediatric Leukemia.Cancer discovery · 2026Article
- Tandem Duplications in UBTF Create XPO1-Dependent Nuclear Export Signals that Reveal a Leukemic Therapeutic Dependency.Blood cancer discovery · 2026Article
- Genetic landscape of pediatric acute myeloid leukemia in Taiwan.Scientific reports · 2026Article
- CanID: A Robust and Accurate RNA-seq Expression-based Diagnostic Classification Scheme for Pediatric Malignancies.Genomics, proteomics & bioinformatics · 2025Article
- Thrombopoietin increases susceptibility for EVI1 + KMT2A-MLLT3-driven AML expressing stem cell genes linked to poor outcome.Nature communications · 2025Article
- Fast and sensitive detection of targeted gene fusions using frequency minimizers and fuzzy pattern matching with Fuzzion2.Cell reports methods · 2025Article
- Review
- Clonal Evolution of Pediatric Acute Myeloid Leukemia and Its Contribution to Disease Relapse.medRxiv : the preprint server for health sciences · 2025Article
- Loss of STAT3 in acute myeloid leukemia favors tissue infiltration linked to CXCR4 signaling.Blood neoplasia · 2025Article
- Uncovering a role for METTL13 in malignant transformation of human hematopoietic stem cells and in the progression of pediatric leukemia.Research square · 2025Article
4 more citing papers are in PubMed but not listed here.
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48 authors at 6 institutions in 2 countries.
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Abstract
The genetics of relapsed pediatric acute myeloid leukemia (AML) has yet to be comprehensively defined. Here, we present the spectrum of genomic alterations in 136 relapsed pediatric AMLs. We identified recurrent exon 13 tandem duplications (TD) in upstream binding transcription factor (UBTF) in 9% of relapsed AML cases. UBTF-TD AMLs commonly have normal karyotype or trisomy 8 with cooccurring WT1 mutations or FLT3-ITD but not other known oncogenic fusions. These UBTF-TD events are stable during disease progression and are present in the founding clone. In addition, we observed that UBTF-TD AMLs account for approximately 4% of all de novo pediatric AMLs, are less common in adults, and are associated with poor outcomes and MRD positivity. Expression of UBTF-TD in primary hematopoietic cells is sufficient to enhance serial clonogenic activity and to drive a similar transcriptional program to UBTF-TD AMLs. Collectively, these clinical, genomic, and functional data establish UBTF-TD as a new recurrent mutation in AML. SIGNIFICANCE: We defined the spectrum of mutations in relapsed pediatric AML and identified UBTF-TDs as a new recurrent genetic alteration. These duplications are more common in children and define a group of AMLs with intermediate-risk cytogenetic abnormalities, FLT3-ITD and WT1 alterations, and are associated with poor outcomes. See related commentary by Hasserjian and Nardi, p. 173. This article is highlighted in the In This Issue feature, p. 171.
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