ArticleScience (New York, N.Y.)2008
Genomic analysis of the clonal origins of relapsed acute lymphoblastic leukemia.
Article in Science (New York, N.Y.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 427 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
427 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Vaccination and the Risk of Childhood Cancer-A Systematic Review and Meta-Analysis.Frontiers in oncology · 2020Pooled it
- Association of the independent polymorphisms in CDKN2A with susceptibility of acute lymphoblastic leukemia.Bioscience reports · 2018Pooled it
- Randomized, Parallel Group, Open-Label Bioequivalence Trial of Intramuscular Pegaspargase in Patients With Relapsed Acute Lymphoblastic Leukemia.JCO global oncology · 2020Trial
- Integrated analysis of relapsed B-cell precursor Acute Lymphoblastic Leukemia identifies subtype-specific cytokine and metabolic signatures.Scientific reports · 2019Trial
- Next-Generation Sequencing in Adult B Cell Acute Lymphoblastic Leukemia Patients.Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation · 2017Trial
- CREB1 and GSK3 Isoforms as Potential Adaptive Signaling Nodes in PI3K/Akt/mTOR Inhibitor Treated Philadelphia Chromosome-Positive B-ALL.International journal of molecular sciences · 2026Article
- A genomic and epigenomic lens into the biology of acute lymphoblastic leukaemia.Nature reviews. Cancer · 2026Review
- Antigen Pressure, Clonal Evolution, and Lineage Plasticity in B-Cell Acute Lymphoblastic Leukemia: Resistance Biology in the Immunotherapy Era.Current hematologic malignancy reports · 2026Review
- Article
- Chromatin regulatorsChinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2026Article
- Incidental Detection of Acute Leukemia During Genetic Evaluation of Neurodevelopmental Disorder in a Pediatric Clinic: A Case Report.Case reports in pediatrics · 2026Article
- Leveraging genomic diagnostics for prognostics and therapeutics in pediatric acute leukemia.HemaSphere · 2025Article
- The Inositol-5-Phosphatase SHIP1: Expression, Regulation and Role in Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2025Review
- Genetic evolution and relapse-associated mutations in adult T-cell acute lymphoblastic leukemia patients treated in PETHEMA trials.HemaSphere · 2025Article
- Review
- Targeting LMO2-induced autocrine FLT3 signaling to overcome chemoresistance in early T-cell precursor acute lymphoblastic leukemia.Leukemia · 2025Article
- Review
- Article
- Cancer liquid biopsies by Oxford Nanopore Technologies sequencing of cell-free DNA: from basic research to clinical applications.Molecular cancer · 2024Review
- Determinants of survival after first relapse of acute lymphoblastic leukemia: a Children's Oncology Group study.Leukemia · 2024Article
367 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
7 authors.
Funding
Abstract
Most children with acute lymphoblastic leukemia (ALL) can be cured, but the prognosis is dismal for the minority of patients who relapse after treatment. To explore the genetic basis of relapse, we performed genome-wide DNA copy number analyses on matched diagnosis and relapse samples from 61 pediatric patients with ALL. The diagnosis and relapse samples typically showed different patterns of genomic copy number abnormalities (CNAs), with the CNAs acquired at relapse preferentially affecting genes implicated in cell cycle regulation and B cell development. Most relapse samples lacked some of the CNAs present at diagnosis, which suggests that the cells responsible for relapse are ancestral to the primary leukemia cells. Backtracking studies revealed that cells corresponding to the relapse clone were often present as minor subpopulations at diagnosis. These data suggest that genomic abnormalities contributing to ALL relapse are selected for during treatment, and they point to new targets for therapeutic intervention.
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What OpenQuestion holds
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.