ArticleScientific reports2021
Mutational patterns and clonal evolution from diagnosis to relapse in pediatric acute lymphoblastic leukemia.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 14 citations in OpenAlex.
- TP53 isoform dysregulation in pediatric B-ALL: identifying markers of favorable prognosis and relapse-associated dynamic.Molecular biology reports · 2026Article
- An integrative molecular map of pediatric B-cell precursor acute lymphoblastic leukemia.Communications medicine · 2026Article
- T2T-CHM13 improves read mapping and detection of clinically relevant genetic variation in the Swedish population.Genome research · 2025Article
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- Review
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- Advances in next-generation sequencing for relapsed pediatric acute lymphoblastic leukemia: current insights and future directions.Frontiers in genetics · 2024Review
- 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
- Comprehensive detection ofFrontiers in molecular biosciences · 2024Article
- Multimodal classification of molecular subtypes in pediatric acute lymphoblastic leukemia.NPJ precision oncology · 2023Article
- 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
- Prognostic significance of copy number variation in B-cell acute lymphoblastic leukemia.Frontiers in oncology · 2022Review
Corrections and comments
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Authors and funding
16 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanisms driving clonal heterogeneity and evolution in relapsed pediatric acute lymphoblastic leukemia (ALL) are not fully understood. We performed whole genome sequencing of samples collected at diagnosis, relapse(s) and remission from 29 Nordic patients. Somatic point mutations and large-scale structural variants were called using individually matched remission samples as controls, and allelic expression of the mutations was assessed in ALL cells using RNA-sequencing. We observed an increased burden of somatic mutations at relapse, compared to diagnosis, and at second relapse compared to first relapse. In addition to 29 known ALL driver genes, of which nine genes carried recurrent protein-coding mutations in our sample set, we identified putative non-protein coding mutations in regulatory regions of seven additional genes that have not previously been described in ALL. Cluster analysis of hundreds of somatic mutations per sample revealed three distinct evolutionary trajectories during ALL progression from diagnosis to relapse. The evolutionary trajectories provide insight into the mutational mechanisms leading relapse in ALL and could offer biomarkers for improved risk prediction in individual patients.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.