ArticleBlood2020
Therapy-induced mutations drive the genomic landscape of relapsed acute lymphoblastic leukemia.
Article in Blood, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06882057 (Chinese Children's Cancer Group-2025 Protocol for Newly Diagnosed Low Risk Childhood B-cell Acute Lymphoblastic Leukemia), which is not on this map. Cited by 181 papers, 1 of them a synthesis that pooled it.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Chinese Children's Cancer Group-2025 Protocol for Newly Diagnosed Low Risk Childhood B-cell Acute Lymphoblastic Leukemia
Who cites it
181 citing papers in PubMed, 1 synthesis or guideline pooled it, 293 citations in OpenAlex.
- Association ofHaematologica · 2024Pooled it
- Comparative efficacy and long-term survival of CD19/22 versus CD19 CAR-T immunotherapy in Relapsed/Refractory B-ALL with TP53 alterations.Journal of translational medicine · 2026Trial
- DNA-thioguanine nucleotide as a treatment marker in acute lymphoblastic leukemia patients with NUDT15 variant genotypes.PloS one · 2021Trial
- Impact of p53 Target Genes on Drug Resistance in TP53-Mutated B-Cell Precursor Acute Lymphoblastic Leukemia.Cancer medicine · 2026Article
- Genomic profiling of Mexican patients with B-cell precursor acute lymphoblastic leukemia reveals clinically significant somatic and potential germline variants.The journal of pathology. Clinical research · 2026Article
- Plasticity under pressure: biology and detection of lineage switch in acute leukemia.Leukemia · 2026Review
- A complex mutational signature generated by cytarabine resistance.NAR cancer · 2026Article
- Article
- Therapy-Related Mutational Signatures in Subsequent Neoplasms among Survivors of Childhood Cancer.Cancer discovery · 2026Article
- Targeting the NR3C1-ACSL4 Axis Triggers Ferroptosis to Overcome Radioresistance in Prostate Cancer.Cancer science · 2026Article
- CNR1 and CNR2 Cannabinoid Receptor Mutations in Cancer Cells.Current issues in molecular biology · 2026Article
- Deep learning based individualized cross-platform molecular subtype classification of B-lineage acute lymphoblastic leukemia.NPJ precision oncology · 2026Article
- The landscape of structural variation in pediatric cancer.Cancer cell · 2026Article
- Epigenetic Inhibitor 5-Azacytidine Triggers DIM-2/DIM-5-Dependent Mutagenesis in H3K9me3-Enriched Regions ofJournal of fungi (Basel, Switzerland) · 2026Article
- Therapy-associated mutagenesis at CTCF binding sites is shaped by chromatin context and DNA repair capacity.bioRxiv : the preprint server for biology · 2026Article
- Article
- Cancer evolution and multi-omic profile of relapsed colorectal liver metastases after treatment.Genome medicine · 2026Article
- Analysis of error profiles of indels and structural variants in deep-sequencing data.Cell genomics · 2026Article
- Article
- Relapse in childhood B-cell precursor acute lymphoblastic leukemia: insights from transcriptomic signatures of diagnostic bone marrow.Frontiers in oncology · 2026Review
121 more citing papers are in PubMed but not listed here.
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Authors and funding
47 authors at 11 institutions in 3 countries.
Funding
Abstract
To study the mechanisms of relapse in acute lymphoblastic leukemia (ALL), we performed whole-genome sequencing of 103 diagnosis-relapse-germline trios and ultra-deep sequencing of 208 serial samples in 16 patients. Relapse-specific somatic alterations were enriched in 12 genes (NR3C1, NR3C2, TP53, NT5C2, FPGS, CREBBP, MSH2, MSH6, PMS2, WHSC1, PRPS1, and PRPS2) involved in drug response. Their prevalence was 17% in very early relapse (<9 months from diagnosis), 65% in early relapse (9-36 months), and 32% in late relapse (>36 months) groups. Convergent evolution, in which multiple subclones harbor mutations in the same drug resistance gene, was observed in 6 relapses and confirmed by single-cell sequencing in 1 case. Mathematical modeling and mutational signature analysis indicated that early relapse resistance acquisition was frequently a 2-step process in which a persistent clone survived initial therapy and later acquired bona fide resistance mutations during therapy. In contrast, very early relapses arose from preexisting resistant clone(s). Two novel relapse-specific mutational signatures, one of which was caused by thiopurine treatment based on in vitro drug exposure experiments, were identified in early and late relapses but were absent from 2540 pan-cancer diagnosis samples and 129 non-ALL relapses. The novel signatures were detected in 27% of relapsed ALLs and were responsible for 46% of acquired resistance mutations in NT5C2, PRPS1, NR3C1, and TP53. These results suggest that chemotherapy-induced drug resistance mutations facilitate a subset of pediatric ALL relapses.
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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.