ArticleJournal of hematology & oncology2017
Transcriptome sequencing in pediatric acute lymphoblastic leukemia identifies fusion genes associated with distinct DNA methylation profiles.
Article in Journal of hematology & oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed.
- Article
- An integrative molecular map of pediatric B-cell precursor acute lymphoblastic leukemia.Communications medicine · 2026Article
- The GF-NEO discovery platform unveils a [KQE][DG] sequence motif within fusion neoantigens in pediatric cancer.iScience · 2026Article
- Review
- A Decade of Transformation in the Management of Childhood Acute Lymphoblastic Leukemia: From Conventional Chemotherapy to Precision Medicine.Pediatric reports · 2025Review
- Rapid Identification ofEJHaem · 2025Article
- Ex vivo drug responses and molecular profiles of 597 pediatric acute lymphoblastic leukemia patients.HemaSphere · 2025Article
- Molecular characterization and biomarker identification in paediatric B-cell acute lymphoblastic leukaemia.Journal of cellular and molecular medicine · 2024Article
- A multiomic characterization of the leukemia cell line REH using short- and long-read sequencing.Life science alliance · 2024Article
- Decoding the genetic symphony: Profiling protein-coding and long noncoding RNA expression in T-acute lymphoblastic leukemia for clinical insights.PNAS nexus · 2024Article
- From early methods for DNA diagnostics to genomes and epigenomes at high resolution during four decades - a personal perspective.Upsala journal of medical sciences · 2024Review
- Multimodal classification of molecular subtypes in pediatric acute lymphoblastic leukemia.NPJ precision oncology · 2023Article
- DUX4-r exerts a neomorphic activity that depends on GTF2I in acute lymphoblastic leukemia.Science advances · 2023Article
- Pediatric Acute Lymphoblastic Leukemia Emerging Therapies-From Pathway to Target.International journal of molecular sciences · 2023Review
- Feasibility to use whole-genome sequencing as a sole diagnostic method to detect genomic aberrations in pediatric B-cell acute lymphoblastic leukemia.Frontiers in oncology · 2023Article
- Treatment for a primary multidrug-resistant B-cell acute lymphoblastic leukemia patient carrying a SSBP2-CSF1R fusion gene: a case report.Frontiers in oncology · 2023Article
- ZNF384 Fusion Oncoproteins Drive Lineage Aberrancy in Acute Leukemia.Blood cancer discovery · 2022Article
- Multi-Cohort Transcriptomic Subtyping of B-Cell Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2022Article
- The oncogenic fusion landscape in pediatric CNS neoplasms.Acta neuropathologica · 2022Review
- Analysis of DUX4 Expression in Bone Marrow and Re-Discussion of DUX4 Function in the Health and Disease.Turk patoloji dergisi · 2022Article
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Authors and funding
14 authors.
Funding
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Abstract
backgroundStructural chromosomal rearrangements that lead to expressed fusion genes are a hallmark of acute lymphoblastic leukemia (ALL). In this study, we performed transcriptome sequencing of 134 primary ALL patient samples to comprehensively detect fusion transcripts.
methodsWe combined fusion gene detection with genome-wide DNA methylation analysis, gene expression profiling, and targeted sequencing to determine molecular signatures of emerging ALL subtypes.
resultsWe identified 64 unique fusion events distributed among 80 individual patients, of which over 50% have not previously been reported in ALL. Although the majority of the fusion genes were found only in a single patient, we identified several recurrent fusion gene families defined by promiscuous fusion gene partners, such as ETV6, RUNX1, PAX5, and ZNF384, or recurrent fusion genes, such as DUX4-IGH. Our data show that patients harboring these fusion genes displayed characteristic genome-wide DNA methylation and gene expression signatures in addition to distinct patterns in single nucleotide variants and recurrent copy number alterations.
conclusionOur study delineates the fusion gene landscape in pediatric ALL, including both known and novel fusion genes, and highlights fusion gene families with shared molecular etiologies, which may provide additional information for prognosis and therapeutic options in the future.
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