ArticleLeukemia2024
Mutational mechanisms in multiply relapsed pediatric acute lymphoblastic leukemia.
Article in Leukemia, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- A complex mutational signature generated by cytarabine resistance.NAR cancer · 2026Article
- Integrated Genomic Profiling of Pediatric Acute Lymphoblastic Leukemia: Genomic Landscape, Risk Stratification and Association of RAS Pathway Mutations with Early Treatment Response.International journal of molecular sciences · 2026Article
- LC-MS/MS quantification of 6-methylthio-2'-deoxyguanosine and 6-thio-2'-deoxyguanosine in genomic DNA with enzymatically synthesized isotope-labelled internal standards.Analytical and bioanalytical chemistry · 2026Article
- The Mutational Epidemiology of Childhood Cancer.Clinical chemistry · 2025Review
- The genomic landscape of relapsed infant and childhood KMT2A-rearranged acute leukemia.Nature communications · 2025Article
- Treatment-related mutagenic processes in acute lymphoblastic leukemia.Haematologica · 2025Review
- Human Placental Genomic Instability Predicts Adverse Pregnancy Outcomes.Research square · 2025Article
- A Thiopurine-like Mutagenic Process Defines TGCT Subtypes.bioRxiv : the preprint server for biology · 2025Article
- Mutational signatures and kataegis in pediatric B-cell precursor acute lymphoblastic leukemia.HemaSphere · 2025Article
- Unraveling the Genetic Heterogeneity of Acute Lymphoblastic Leukemia Based on NGS Applications.Cancers · 2024Review
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Pediatric acute lymphoblastic leukemia (ALL) is marked by low mutational load at initial diagnosis, which increases at relapse. To determine which processes are active in (relapsed) ALL and how they behave during disease progression before and after therapy, we performed whole genome sequencing on 97 tumor samples of 29 multiply relapsed ALL patients. Mutational load increased upon relapse in 28 patients and upon every subsequent relapse in 22 patients. In addition to two clock-like mutational processes, we identified UV-like damage, APOBEC activity, reactive oxygen species, thiopurine-associated damage and an unknown therapy component as drivers of mutagenesis. Mutational processes often affected patients over longer time periods, but could also occur in isolated events, suggesting the requirement of additional triggers. Thiopurine exposure was the most prominent source of new mutations in relapse, affecting over half of the studied patients in first and/or later relapse and causing potential relapse-driving mutations in multiple patients. Our data demonstrate that multiple mutational processes frequently act in parallel as prominent secondary drivers with dynamic activity during ALL development and progression.
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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.