ArticleCommunications biology2023
Deep genomic characterization highlights complexities and prognostic markers of pediatric acute myeloid leukemia.
Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- Genomic Profiling, Induction Response, and Transplant Outcomes in Pediatric Acute Myeloid Leukemia: A Single-Center Retrospective Cohort Study.International journal of molecular sciences · 2026Article
- [Allogeneic hematopoietic stem cell transplantation for pediatric acute leukemia harboring theZhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2025Article
- Review
- Patterns and variations of copy number alterations in acute myeloid leukemia: insights from the LeukAtlas database.Leukemia · 2025Article
- G3BP1::CSF1R: a new and actionable gene fusion in acute megakaryoblastic leukemia.Blood advances · 2025Article
- Case Report: Pediatric AML withFrontiers in oncology · 2025Article
- Insights into the Clinical, Biological and Therapeutic Impact of Copy Number Alteration in Cancer.International journal of molecular sciences · 2024Review
- Genetically Distinct Acute Megakaryoblastic Leukemia following Low Hypodiploid B-Lymphoblastic Leukemia linked byPediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology SocietyArticle
Corrections and comments
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pediatric acute myeloid leukemia (AML) is an uncommon but aggressive hematological malignancy. The poor outcome is attributed to inadequate prognostic classification and limited treatment options. A thorough understanding on the genetic basis of pediatric AML is important for the development of effective approaches to improve outcomes. Here, by comprehensively profiling fusion genes as well as mutations and copy number changes of 141 myeloid-related genes in 147 pediatric AML patients with subsequent variant functional characterization, we unveil complex mutational patterns of biological relevance and disease mechanisms including MYC deregulation. Also, our findings highlight TP53 alterations as strong adverse prognostic markers in pediatric AML and suggest the core spindle checkpoint kinase BUB1B as a selective dependency in this aggressive subgroup. Collectively, our present study provides detailed genomic characterization revealing not only complexities and mechanistic insights into pediatric AML but also significant risk stratification and therapeutic strategies to tackle the disease.
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