ArticleLeukemia2019
Genetic mechanisms of primary chemotherapy resistance in pediatric acute myeloid leukemia.
Article in Leukemia, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
83 citing papers in PubMed, 1 synthesis or guideline pooled it, 130 citations in OpenAlex.
- DNA methylation in monozygotic twins discordant for acute lymphoblastic leukemia: a case report and systematic review.Clinical epigenetics · 2025Pooled it
- Genomic landscape of patients with FLT3-mutated acute myeloid leukemia (AML) treated within the CALGB 10603/RATIFY trial.Leukemia · 2022Trial
- Quantitative molecular cartography of emergency myelopoiesis reveals conserved modules of hematopoietic activation.Cell stem cell · 2026Article
- Methylome profiling reveals context-dependent chemo-resistance mechanisms and enhances risk stratification in AML.Cancer cell international · 2026Article
- LIN28A-Dependent Kinome and Phosphoproteome Reprogramming Promotes Imatinib Resistance.Molecular & cellular proteomics : MCP · 2026Article
- Ontogeny Dictates Oncogenic Potential, Lineage Hierarchy, and Therapy Response in Pediatric Leukemia.Cancer discovery · 2026Article
- Natural bioactive molecules and chemotherapeutics synergism for enhanced cancer therapy.Nutrition & metabolism · 2026Review
- Osimertinib activates a TGF-β2-dependent secretory program that drives lung adenocarcinoma progression.The Journal of clinical investigation · 2026Article
- Sequence-dependent splicing dysregulation drives therapy resistance in pediatric AML.Cell reports. Medicine · 2026Article
- CanID: A Robust and Accurate RNA-seq Expression-based Diagnostic Classification Scheme for Pediatric Malignancies.Genomics, proteomics & bioinformatics · 2025Article
- The miRNA Landscape of Leukemia - Cellular Actions to Therapy through Molecular Mechanisms.Cell biochemistry and biophysics · 2025Review
- ASAH1-mediated sphingolipid metabolic reprogramming in venetoclax resistance of AML: beyond the monocytic phenotypes.BMC cancer · 2025Article
- Fusion oncoproteins and cooperating mutations define disease phenotypes in NUP98-rearranged leukemia.Blood · 2025Article
- Characteristics and prognosis of paediatric normal karyotype acute myeloid leukaemia: A NOPHO-DBH AML study.British journal of haematology · 2025Article
- High-grade gliomas derived from an ovarian mature teratoma: clonal dynamics and genetic insights.International cancer conference journal · 2025Article
- Image-based drug screening combined with molecular profiling identifies signatures and drivers of therapy resistance in pediatric AML.Cell reports. Medicine · 2025Article
- The RNA-binding protein CELF1 targets ATG5 to regulate autophagy and promote drug resistance in acute myeloid leukemia.Cell death & disease · 2025Article
- Review
- Transcriptional and epigenetic rewiring by the NUP98::KDM5A fusion oncoprotein directly activates CDK12.Nature communications · 2025Article
- Multiplex gene editing models of del(7q) reveal combinedBlood neoplasia · 2025Article
23 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
18 authors at 8 institutions in 2 countries.
Funding
Abstract
Acute myeloid leukemias (AML) are characterized by mutations of tumor suppressor and oncogenes, involving distinct genes in adults and children. While certain mutations have been associated with the increased risk of AML relapse, the genomic landscape of primary chemotherapy-resistant AML is not well defined. As part of the TARGET initiative, we performed whole-genome DNA and transcriptome RNA and miRNA sequencing analysis of pediatric AML with failure of induction chemotherapy. We identified at least three genetic groups of patients with induction failure, including those with NUP98 rearrangements, somatic mutations of WT1 in the absence of apparent NUP98 mutations, and additional recurrent variants including those in KMT2C and MLLT10. Comparison of specimens before and after chemotherapy revealed distinct and invariant gene expression programs. While exhibiting overt therapy resistance, these leukemias nonetheless showed diverse forms of clonal evolution upon chemotherapy exposure. This included selection for mutant alleles of FRMD8, DHX32, PIK3R1, SHANK3, MKLN1, as well as persistence of WT1 and TP53 mutant clones, and elimination of FLT3, PTPN11, and NRAS mutant clones. These findings delineate genetic mechanisms of primary chemotherapy resistance in pediatric AML, which should inform improved approaches for its diagnosis and therapy.
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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.