ArticleNature genetics2022
The genomic landscape of pediatric acute lymphoblastic leukemia.
Article in Nature genetics, 2022. 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 259 papers.
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
259 citing papers in PubMed, 369 citations in OpenAlex.
- Trial
- PTEN-loss confers dependence on the guanylate synthesis enzyme IMPDH in T-cell acute lymphoblastic leukemia.EMBO molecular medicine · 2026Article
- A genomic and epigenomic lens into the biology of acute lymphoblastic leukaemia.Nature reviews. Cancer · 2026Review
- Plasticity under pressure: biology and detection of lineage switch in acute leukemia.Leukemia · 2026Review
- Association of Childhood Acute Leukemia With Autoimmune Diseases.International journal of cancer · 2026Article
- Tisa-cel and axi-cel CAR structure influences the development of resistance to CD19-CAR-T therapy.Leukemia · 2026Article
- Measurable residual disease detected by next-generation sequencing in T-cell acute lymphoblastic leukemia.Nature communications · 2026Article
- Pitfalls and Challenges in the Detection of ZNF384 Rearrangements by Fluorescence in Situ Hybridization.Genes, chromosomes & cancer · 2026Article
- Article
- Selective sensitivity of Ph-like B-cell acute lymphoblastic leukemia to BRG1 inhibition identifies a therapeutic vulnerability.Leukemia · 2026Article
- Biological and pathogenic roles of major genes harbored in intrachromosomal amplification of chromosome 21 in childhood acute lymphoblastic leukemia (Review).Oncology letters · 2026Review
- Article
- clinTALL: machine learning-driven multimodal subtype classification and treatment outcome prediction in pediatric T-ALL.Genome medicine · 2026Article
- The clinical relevance of RAS pathway gene mutations in childhood B-cell acute lymphoblastic leukemia.Annals of hematology · 2026Article
- Personalized reference genome-based pipeline reveals comprehensive haplotype-resolved views of cancer genomes.bioRxiv : the preprint server for biology · 2026Article
- Clinical features and initial treatment outcomes of pediatric B-cell acute lymphoblastic leukemia with P2RY8::CRLF2 fusion positivity: a case series.Translational pediatrics · 2026Article
- Chromosome 15q deletions confer inferior outcomes among children with ETV6::RUNX1 B-cell acute lymphoblastic leukemia.Blood advances · 2026Article
- Hyperleukocytosis and outcomes in pediatric B-cell acute lymphoblastic leukemia: A report from the REDIAL Consortium.medRxiv : the preprint server for health sciences · 2026Article
- A Greek Case-Control Replication Study ofGenes · 2026Article
- Deep learning based individualized cross-platform molecular subtype classification of B-lineage acute lymphoblastic leukemia.NPJ precision oncology · 2026Article
199 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
77 authors at 20 institutions in 1 country.
Funding
Abstract
Acute lymphoblastic leukemia (ALL) is the most common childhood cancer. Here, using whole-genome, exome and transcriptome sequencing of 2,754 childhood patients with ALL, we find that, despite a generally low mutation burden, ALL cases harbor a median of four putative somatic driver alterations per sample, with 376 putative driver genes identified varying in prevalence across ALL subtypes. Most samples harbor at least one rare gene alteration, including 70 putative cancer driver genes associated with ubiquitination, SUMOylation, noncoding transcripts and other functions. In hyperdiploid B-ALL, chromosomal gains are acquired early and synchronously before ultraviolet-induced mutation. By contrast, ultraviolet-induced mutations precede chromosomal gains in B-ALL cases with intrachromosomal amplification of chromosome 21. We also demonstrate the prognostic significance of genetic alterations within subtypes. Intriguingly, DUX4- and KMT2A-rearranged subtypes separate into CEBPA/FLT3- or NFATC4-expressing subgroups with potential clinical implications. Together, these results deepen understanding of the ALL genomic landscape and associated outcomes.
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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.