ArticleNature communications2015
Rise and fall of subclones from diagnosis to relapse in pediatric B-acute lymphoblastic leukaemia.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 216 papers.
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Who cites it
216 citing papers in PubMed, 358 citations in OpenAlex.
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- Status of IKZF1 Deletions in Diagnose and Relapsed Pediatric B-ALL Patients.Biochemical genetics · 2026Article
- Unraveling Research Trends and Hotspots of Genetic Variants in Acute Leukemias: A Web of Science and Scopus-Based Bibliometric Study.International journal of medical sciences · 2026Article
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- Relapse in childhood B-cell precursor acute lymphoblastic leukemia: insights from transcriptomic signatures of diagnostic bone marrow.Frontiers in oncology · 2026Review
- Single-cell transcriptome analysis defines novel molecular subtypes and reveals therapeutic implications of T/myeloid mixed-phenotype acute leukemia.Genome medicine · 2025Article
- Leveraging genomic diagnostics for prognostics and therapeutics in pediatric acute leukemia.HemaSphere · 2025Article
- Comprehensive Epigenome-Wide Profiling Reveals Distinctive DNA Methylation Signatures and Potential Prognostic Biomarkers in Mexican Pediatric B-ALL.International journal of molecular sciences · 2025Article
- Treatment-related mutagenic processes in acute lymphoblastic leukemia.Haematologica · 2025Review
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- A clinical solution for tracking clonal evolution of acute myeloid leukemia after allogeneic transplantation using bulk next generation sequencing.Bone marrow transplantation · 2025Article
- Genome-level selection in tumors as a universal marker of resistance to therapy.Nature communications · 2025Article
- Genetic evolution and relapse-associated mutations in adult T-cell acute lymphoblastic leukemia patients treated in PETHEMA trials.HemaSphere · 2025Article
- Tumor microenvironment as a novel therapeutic target for lymphoid leukemias.Annals of hematology · 2025Review
156 more citing papers are in PubMed but not listed here.
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Authors and funding
29 authors at 9 institutions in 1 country.
Funding
Abstract
There is incomplete understanding of genetic heterogeneity and clonal evolution during cancer progression. Here we use deep whole-exome sequencing to describe the clonal architecture and evolution of 20 pediatric B-acute lymphoblastic leukaemias from diagnosis to relapse. We show that clonal diversity is comparable at diagnosis and relapse and clonal survival from diagnosis to relapse is not associated with mutation burden. Six pathways were frequently mutated, with NT5C2, CREBBP, WHSC1, TP53, USH2A, NRAS and IKZF1 mutations enriched at relapse. Half of the leukaemias had multiple subclonal mutations in a pathway or gene at diagnosis, but mostly with only one, usually minor clone, surviving therapy to acquire additional mutations and become the relapse founder clone. Relapse-specific mutations in NT5C2 were found in nine cases, with mutations in four cases being in descendants of the relapse founder clone. These results provide important insights into the genetic basis of treatment failure in ALL and have implications for the early detection of mutations driving relapse.
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