ArticleBlood advances2018
Mutational dynamics of early and late relapsed childhood ALL: rapid clonal expansion and long-term dormancy.
Article in Blood advances, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- Genetic evolution and relapse-associated mutations in adult T-cell acute lymphoblastic leukemia patients treated in PETHEMA trials.HemaSphere · 2025Article
- PU.1 eviction at lymphocyte-specific chromatin domains mediates glucocorticoid response in acute lymphoblastic leukemia.Nature communications · 2024Article
- Gene expression prognostic of early relapse risk in low-risk B-cell acute lymphoblastic leukaemia in children.EJHaem · 2024Article
- Therapy-Acquired Clonal Mutations in Thiopurine Drug-Response Genes Drive Majority of Early Relapses in Pediatric B-Cell Precursor Acute Lymphoblastic Leukemia.Diagnostics (Basel, Switzerland) · 2023Article
- Accumulation of STR-Loci Aberrations in Subclones of Jurkat Cell Line as a Model of Tumor Clonal Evolution.Genes · 2023Article
- Mutational patterns and clonal evolution from diagnosis to relapse in pediatric acute lymphoblastic leukemia.Scientific reports · 2021Article
- When dormancy fuels tumour relapse.Communications biology · 2021Review
- Article
- Review
- Prognostic Impact of Somatic Copy Number Alterations in Childhood B-Lineage Acute Lymphoblastic Leukemia.Current oncology reports · 2020Review
- Loss of glucocorticoid receptor expression mediates in vivo dexamethasone resistance in T-cell acute lymphoblastic leukemia.Leukemia · 2020Article
- Mutational landscape and patterns of clonal evolution in relapsed pediatric acute lymphoblastic leukemia.Blood cancer discovery · 2020Article
- Single-cell analysis of childhood leukemia reveals a link between developmental states and ribosomal protein expression as a source of intra-individual heterogeneity.Scientific reports · 2020Article
- [Prognostic significance and risk factors of minimal residual disease ≥1% on 19th day of induction chemotherapy in children with acute lymphoblastic leukemia].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020Article
- Upfront Treatment Influences the Composition of Genetic Alterations in Relapsed Pediatric B-Cell Precursor Acute Lymphoblastic Leukemia.HemaSphere · 2020Article
- PIK3CA-CDKN2A clonal evolution in metastatic breast cancer and multiple points cell-free DNA analysis.Cancer cell international · 2019Article
- A rare subgroup of leukemia stem cells harbors relapse-inducing potential in acute lymphoblastic leukemia.Experimental hematology · 2019Review
- Establishment and characterization of a novel childhood acute lymphoblastic leukemia cell line, HXEX-ALL1, with chromosome 9p and 17p deletions.Cancer cell international · 2019Article
- Global efforts toward the cure of childhood acute lymphoblastic leukaemia.The Lancet. Child & adolescent health · 2018Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Childhood acute lymphoblastic leukemia (cALL) is the most frequent pediatric cancer. Refractory/relapsed cALL presents a survival rate of ∼45% and is still one of the leading causes of death by disease among children. Mechanisms, such as clonal competition and evolutionary adaptation, govern treatment resistance. However, the underlying clonal dynamics leading to multiple relapses and differentiating early (<36 months postdiagnosis) from late relapse events remain elusive. Here, we use an integrative genome-based analysis combined with serial sampling of relapsed tumors (from primary tumor to ≤4 relapse events) from 19 pre-B-cell cALL patients (8 early and 11 late relapses) to assess the fitness of somatic mutations and infer their ancestral relationships. By quantifying both general clonal dynamics and newly acquired subclonal diversity, we show that 2 distinct evolutionary patterns govern early and late relapse: on one hand, a highly dynamic pattern, sustained by a putative defect of DNA repair processes, illustrating the quick emergence of fitter clones, and on the other hand, a quasi-inert evolution pattern, suggesting the escape from dormancy of leukemia stem cells likely spared from initial cytoreductive therapy. These results offer new insights into cALL relapse mechanisms and highlight the pressing need for adapted treatment strategies to circumvent resistance mechanisms.
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