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Clonal origin and development of high hyperdiploidy in childhood acute lymphoblastic leukaemia

EL. Woodward, M. Yang, LH. Moura-Castro, H. van den Bos, R. Gunnarsson, L. Olsson-Arvidsson, DCJ. Spierings, A. Castor, N. Duployez, M. Zaliova, J. Zuna, B. Johansson, F. Foijer, K. Paulsson

. 2023 ; 14 (1) : 1658. [pub] 20230325

Language English Country England, Great Britain

Document type Journal Article

Persistent link   https://www.medvik.cz/link/bmc23003750

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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$a High hyperdiploid acute lymphoblastic leukemia (HeH ALL), one of the most common childhood malignancies, is driven by nonrandom aneuploidy (abnormal chromosome numbers) mainly comprising chromosomal gains. In this study, we investigate how aneuploidy in HeH ALL arises. Single cell whole genome sequencing of 2847 cells from nine primary cases and one normal bone marrow reveals that HeH ALL generally display low chromosomal heterogeneity, indicating that they are not characterized by chromosomal instability and showing that aneuploidy-driven malignancies are not necessarily chromosomally heterogeneous. Furthermore, most chromosomal gains are present in all leukemic cells, suggesting that they arose early during leukemogenesis. Copy number data from 577 primary cases reveals selective pressures that were used for in silico modeling of aneuploidy development. This shows that the aneuploidy in HeH ALL likely arises by an initial tripolar mitosis in a diploid cell followed by clonal evolution, in line with a punctuated evolution model.
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$a Yang, Minjun $u Department of Laboratory Medicine, Division of Clinical Genetics, Lund University, Lund, Sweden $1 https://orcid.org/0000000233241498
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$a Moura-Castro, Larissa H $u Department of Laboratory Medicine, Division of Clinical Genetics, Lund University, Lund, Sweden $1 https://orcid.org/0000000190635592
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$a van den Bos, Hilda $u European Research Institute for the Biology of Ageing (ERIBA), University of Groningen, University Medical Center Groningen, Groningen, The Netherlands
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$a Gunnarsson, Rebeqa $u Department of Laboratory Medicine, Division of Clinical Genetics, Lund University, Lund, Sweden
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$a Olsson-Arvidsson, Linda $u Department of Laboratory Medicine, Division of Clinical Genetics, Lund University, Lund, Sweden $u Department of Clinical Genetics, Pathology, and Molecular Diagnostics, Office for Medical Services, Region Skåne, Lund, Sweden
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$a Spierings, Diana C J $u European Research Institute for the Biology of Ageing (ERIBA), University of Groningen, University Medical Center Groningen, Groningen, The Netherlands $1 https://orcid.org/000000018403474X
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$a Castor, Anders $u Department of Pediatrics, Skåne University Hospital, Lund University, Lund, Sweden
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$a Zaliova, Marketa $u Department of Pediatric Hematology and Oncology, Second Faculty of Medicine, Charles University/University Hospital Motol, Prague, Czech Republic $u Childhood Leukaemia Investigation Prague (CLIP), Prague, Czech Republic $1 https://orcid.org/0000000216397124 $7 xx0074371
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$a Johansson, Bertil $u Department of Laboratory Medicine, Division of Clinical Genetics, Lund University, Lund, Sweden $u Department of Clinical Genetics, Pathology, and Molecular Diagnostics, Office for Medical Services, Region Skåne, Lund, Sweden $1 https://orcid.org/0000000188294813
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$a Foijer, Floris $u European Research Institute for the Biology of Ageing (ERIBA), University of Groningen, University Medical Center Groningen, Groningen, The Netherlands $1 https://orcid.org/0000000309893127
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$a Paulsson, Kajsa $u Department of Laboratory Medicine, Division of Clinical Genetics, Lund University, Lund, Sweden. kajsa.paulsson@med.lu.se $1 https://orcid.org/000000017950222X
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