Trial reportScientific reports2019
Integrated analysis of relapsed B-cell precursor Acute Lymphoblastic Leukemia identifies subtype-specific cytokine and metabolic signatures.
Trial report in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed.
- Article
- Proteomic Profiling of Bone Marrow Aspirates from Patients with Methotrexate- and Vincristine-Resistant B-Cell Acute Lymphoblastic Leukemia: A Retrospective Analysis.Pharmaceuticals (Basel, Switzerland) · 2026Article
- An integrative molecular map of pediatric B-cell precursor acute lymphoblastic leukemia.Communications medicine · 2026Article
- B-cell acute lymphoblastic leukemia following myelodysplastic syndromes: a case report and literature review.Journal of hematopathology · 2026Review
- Review
- Dynamic evolution of TCF3-PBX1 leukemias at the single-cell level under chemotherapy pressure.HemaSphere · 2025Article
- A machine learning and deep learning-based integrated multi-omics technique for leukemia prediction.Heliyon · 2024Article
- Advances in next-generation sequencing for relapsed pediatric acute lymphoblastic leukemia: current insights and future directions.Frontiers in genetics · 2024Review
- Targetable lesions and proteomes predict therapy sensitivity through disease evolution in pediatric acute lymphoblastic leukemia.Nature communications · 2023Article
- Article
- Article
- Pharmacologic Inhibition of NT5C2 Reverses Genetic and Nongenetic Drivers of 6-MP Resistance in Acute Lymphoblastic Leukemia.Cancer discovery · 2022Article
- An alternative CYB5A transcript is expressed in aneuploid ALL and enriched in relapse.BMC genomic data · 2022Article
- Synergistic apoptotic effect of Mcl-1 inhibition and doxorubicin on B-cell precursor acute lymphoblastic leukemia cells.Molecular biology reports · 2022Article
- Elucidating minimal residual disease of paediatric B-cell acute lymphoblastic leukaemia by single-cell analysis.Nature cell biology · 2022Article
- Adipocytes disrupt the translational programme of acute lymphoblastic leukaemia to favour tumour survival and persistence.Nature communications · 2021Article
- Gene Fusions Create Partner and Collateral Dependencies Essential to Cancer Cell Survival.Cancer research · 2021Article
- Frequency and prognostic impact of ZEB2 H1038 and Q1072 mutations in childhood B-other acute lymphoblastic leukemia.Haematologica · 2021Article
- Review
- Mutational and functional genetics mapping of chemotherapy resistance mechanisms in relapsed acute lymphoblastic leukemia.Nature cancer · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
31 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent efforts reclassified B-Cell Precursor Acute Lymphoblastic Leukemia (BCP-ALL) into more refined subtypes. Nevertheless, outcomes of relapsed BCP-ALL remain unsatisfactory, particularly in adult patients where the molecular basis of relapse is still poorly understood. To elucidate the evolution of relapse in BCP-ALL, we established a comprehensive multi-omics dataset including DNA-sequencing, RNA-sequencing, DNA methylation array and proteome MASS-spec data from matched diagnosis and relapse samples of BCP-ALL patients (n = 50) including the subtypes DUX4, Ph-like and two aneuploid subtypes. Relapse-specific alterations were enriched for chromatin modifiers, nucleotide and steroid metabolism including the novel candidates FPGS, AGBL and ZNF483. The proteome expression analysis unraveled deregulation of metabolic pathways at relapse including the key proteins G6PD, TKT, GPI and PGD. Moreover, we identified a novel relapse-specific gene signature specific for DUX4 BCP-ALL patients highlighting chemotaxis and cytokine environment as a possible driver event at relapse. This study presents novel insights at distinct molecular levels of relapsed BCP-ALL based on a comprehensive multi-omics integrated data set including a valuable proteomics data set. The relapse specific aberrations reveal metabolic signatures on genomic and proteomic levels in BCP-ALL relapse. Furthermore, the chemokine expression signature in DUX4 relapse underscores the distinct status of DUX4-fusion BCP-ALL.
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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.