ArticleCancer discovery2022
Elevated Mutational Age in Blood of Children Treated for Cancer Contributes to Therapy-Related Myeloid Neoplasms.
Article in Cancer discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Risk for second primary malignancies in patients with multiple myeloma: a systematic review and meta-analysis.Frontiers in oncology · 2026Pooled it
- Therapy-Related Mutational Signatures in Subsequent Neoplasms among Survivors of Childhood Cancer.Cancer discovery · 2026Article
- Clonal hematopoiesis in patients with cancer and cancer survivors: From clonal burden to cardiovascular diseases.Cancer · 2026Review
- Reconstructing the lifelong history of cells and tissues via somatic mutation analysis.Cellular and molecular life sciences : CMLS · 2025Review
- Posttransplantation clonal dynamics of hematopoietic stem cells carrying prenatal and early-lifeHemaSphere · 2025Article
- Treatment-related mutagenic processes in acute lymphoblastic leukemia.Haematologica · 2025Review
- High-plex imaging of hepatoblastoma and adjacent liver in pediatric patients reveals a predominant myeloid infiltrate expressing immune-checkpoints.Cancer immunology, immunotherapy : CII · 2025Article
- Mutagenic Impact and Evolutionary Influence of Chemoradiotherapy in Hematologic Malignancies.Blood cancer discovery · 2025Article
- Clonal Hematopoiesis in Cancer and Cardiovascular Disease: JACC: CardioOncology State-of-the-Art Review.JACC. CardioOncology · 2025Review
- The long-term effects of chemotherapy on normal blood cells.Nature genetics · 2025Article
- Chemotherapy and the somatic mutation burden of sperm.JCI insight · 2025Article
- Unraveling mutagenic processes influencing the tumor mutational patterns of individuals with constitutional mismatch repair deficiency.Nature communications · 2025Article
- Prenatal Exposure to Chemotherapy Increases the Mutation Burden in Human Neonatal Hematopoietic Stem Cells.Cancer discovery · 2025Article
- Genetic and epigenetic bases of long-term adverse effects of childhood cancer therapy.Nature reviews. Cancer · 2025Review
- Antineoplastic therapy affects the in vitro phenotype and functionality of healthy human bone marrow-derived mesenchymal stromal cells.Archives of toxicology · 2025Article
- Mutagenic impact and evolutionary influence of radiotherapy in hematologic malignancies.bioRxiv : the preprint server for biology · 2024Article
- Distinct landscape and clinical implications of therapy-related clonal hematopoiesis.The Journal of clinical investigation · 2024Review
- Single-cell RNA sequencing of pediatric Hodgkin lymphoma to study the inhibition of T cell subtypes.HemaSphere · 2024Article
- Transient Differentiation-State Plasticity Occurs during Acute Lymphoblastic Leukemia Initiation.Cancer research · 2024Article
- Selective pressures of platinum compounds shape the evolution of therapy-related myeloid neoplasms.Nature communications · 2024Article
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13 authors at 2 institutions in 1 country.
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Abstract
Childhood cancer survivors are confronted with various chronic health conditions like therapy-related malignancies. However, it is unclear how exposure to chemotherapy contributes to the mutation burden and clonal composition of healthy tissues early in life. Here, we studied mutation accumulation in hematopoietic stem and progenitor cells (HSPC) before and after cancer treatment of 24 children. Of these children, 19 developed therapy-related myeloid neoplasms (t-MN). Posttreatment HSPCs had an average mutation burden increase comparable to what treatment-naïve cells accumulate during 16 years of life, with excesses up to 80 years. In most children, these additional mutations were induced by clock-like processes, which are also active during healthy aging. Other patients harbored mutations that could be directly attributed to treatments like platinum-based drugs and thiopurines. Using phylogenetic inference, we demonstrate that most t-MN in children originate after the start of treatment and that leukemic clones become dominant during or directly after chemotherapy exposure. SIGNIFICANCE: Our study shows that chemotherapy increases the mutation burden of normal blood cells in cancer survivors. Only few drugs damage the DNA directly, whereas in most patients, chemotherapy-induced mutations are caused by processes similar to those present during normal aging. This article is highlighted in the In This Issue feature, p. 1825.
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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.