ArticleBlood advances2021
Genomic characterization of relapsed acute myeloid leukemia reveals novel putative therapeutic targets.
Article in Blood advances, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed, 2 syntheses or guidelines pooled it, 57 citations in OpenAlex.
- Molecular Landscape of Acute Myeloid Leukemia in Pediatric Patient-Age-Related Correlations: A Systematic Review.International journal of molecular sciences · 2025Pooled it
- Prognostic factors and outcomes in pediatric acute myeloid leukemia: a comprehensive bibliometric analysis of global research trends.Frontiers in oncology · 2025Pooled it
- The roles of chromatin remodeling and 3D genome organization in cancers: from mechanistic insights to emerging treatment options.Molecular cancer · 2026Review
- Rapid Transcription Dynamics Confers Cytarabine Resistance in Acute Myeloid Leukemia.Blood cancer discovery · 2026Article
- Gilteritinib response in acute myeloid leukemia harboring a rare FLT3 juxtamembrane domain mutation with subsequent clonal evolution.Annals of hematology · 2026Article
- MicroRNA-206 as a Novel Potential Prognostic Biomarker for Distinguishing Philadelphia Chromosome-Positive and Negative ALL Patients.International journal of hematology-oncology and stem cell research · 2026Article
- The LMO2-LDB1-TAL1 complex regulates transcription networks in acute myeloid leukemia.Blood neoplasia · 2026Article
- Immune monitoring for relapse of acute myeloid leukemia after allogeneic stem cell transplantation in clinical laboratories.Frontiers in immunology · 2026Review
- IL-1 signaling and inflammasomes in acute myeloid leukemia: mechanisms and therapeutic opportunities.Cellular and molecular life sciences : CMLS · 2025Review
- Clonal Evolution of Pediatric Acute Myeloid Leukemia and Its Contribution to Disease Relapse.medRxiv : the preprint server for health sciences · 2025Article
- Characteristics and prognosis of paediatric normal karyotype acute myeloid leukaemia: A NOPHO-DBH AML study.British journal of haematology · 2025Article
- Dendritic Cells of Leukemic Origin (DCCancers · 2025Article
- Novel classification system and high-risk categories of pediatric acute myeloid leukemia.Haematologica · 2025Review
- Nidogen-1, a Player in KMT2A-Rearranged Pediatric Acute Myeloid Leukemia.International journal of molecular sciences · 2025Article
- Epigenetic mechanisms of drug resistance in acute myeloid leukemia: advances in small-molecule targeted therapy.Frontiers in pharmacology · 2025Review
- Review
- Whole Exome Sequencing of Intermediate-Risk Acute Myeloid Leukemia without Recurrent Genetic Abnormalities Offers Deeper Insights into New Diagnostic Classifications.International journal of molecular sciences · 2024Article
- Article
- Combination therapy with novel agents for acute myeloid leukaemia: Insights into treatment of a heterogenous disease.British journal of haematology · 2024Review
- Identification ofGenes & diseases · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
20 authors at 8 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Relapse is the leading cause of death of adult and pediatric patients with acute myeloid leukemia (AML). Numerous studies have helped to elucidate the complex mutational landscape at diagnosis of AML, leading to improved risk stratification and new therapeutic options. However, multi-whole-genome studies of adult and pediatric AML at relapse are necessary for further advances. To this end, we performed whole-genome and whole-exome sequencing analyses of longitudinal diagnosis, relapse, and/or primary resistant specimens from 48 adult and 25 pediatric patients with AML. We identified mutations recurrently gained at relapse in ARID1A and CSF1R, both of which represent potentially actionable therapeutic alternatives. Further, we report specific differences in the mutational spectrum between adult vs pediatric relapsed AML, with MGA and H3F3A p.Lys28Met mutations recurrently found at relapse in adults, whereas internal tandem duplications in UBTF were identified solely in children. Finally, our study revealed recurrent mutations in IKZF1, KANSL1, and NIPBL at relapse. All of the mentioned genes have either never been reported at diagnosis in de novo AML or have been reported at low frequency, suggesting important roles for these alterations predominantly in disease progression and/or resistance to therapy. Our findings shed further light on the complexity of relapsed AML and identified previously unappreciated alterations that may lead to improved outcomes through personalized medicine.
Indexed as
Identifiers
What Socratic 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 Socratic graph.