ArticleNature communications2023
Clonal origin and development of high hyperdiploidy in childhood acute lymphoblastic leukaemia.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- RNA Sequencing Technologies in Acute Lymphoblastic Leukemia: A Comparative Technical Review.Current issues in molecular biology · 2026Review
- Pervasive chromosomal instability drives the karyotypic evolution of hypodiploid tumours.Genome medicine · 2026Article
- Space-time clustering of childhood high hyperdiploid B-cell precursor acute lymphoblastic leukemia: a nationwide Swedish study.European journal of epidemiology · 2026Article
- Diagnostic performance of DNA index for detection of high hyperdiploidy in childhood B-cell acute lymphoblastic leukemia.PloS one · 2026Article
- Exploring Biochemical Characteristics of Pediatric Hyperdiploid Acute Lymphoblastic Leukemia by Raman Spectroscopy.Analytical chemistry · 2025Article
- Discovery of Cis-Regulatory Mechanisms via Non-Coding Mutations in Acute Lymphoblastic Leukemia.Genes, chromosomes & cancer · 2025Article
- Single-cell DNA and surface protein characterization of high hyperdiploid acute lymphoblastic leukemia at diagnosis and during treatment.HemaSphere · 2025Article
- Imaging Flow Cytometric Identification of Chromosomal Defects in Paediatric Acute Lymphoblastic Leukaemia.Cells · 2025Article
- Characterizing the allele-specific gene expression landscape in high hyperdiploid acute lymphoblastic leukemia with BASE.Scientific reports · 2024Article
- Insights into the Clinical, Biological and Therapeutic Impact of Copy Number Alteration in Cancer.International journal of molecular sciences · 2024Review
- Chromosomal instability in aneuploid acute lymphoblastic leukemia associates with disease progression.EMBO molecular medicine · 2024Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High hyperdiploid acute lymphoblastic leukemia (HeH ALL), one of the most common childhood malignancies, is driven by nonrandom aneuploidy (abnormal chromosome numbers) mainly comprising chromosomal gains. In this study, we investigate how aneuploidy in HeH ALL arises. Single cell whole genome sequencing of 2847 cells from nine primary cases and one normal bone marrow reveals that HeH ALL generally display low chromosomal heterogeneity, indicating that they are not characterized by chromosomal instability and showing that aneuploidy-driven malignancies are not necessarily chromosomally heterogeneous. Furthermore, most chromosomal gains are present in all leukemic cells, suggesting that they arose early during leukemogenesis. Copy number data from 577 primary cases reveals selective pressures that were used for in silico modeling of aneuploidy development. This shows that the aneuploidy in HeH ALL likely arises by an initial tripolar mitosis in a diploid cell followed by clonal evolution, in line with a punctuated evolution model.
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