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Ploidy and clinical characteristics of childhood acute myeloid leukemia: A NOPHO-AML study.

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Authors
Sandahl, Julie Damgaard
Kjeldsen, Eigil
Abrahamsson, Jonas
Ha, Shau-Yin
Heldrup, Jesper
Jahnukainen, Kirsi
Jónsson, Olafur G
Lausen, Birgitte
Palle, Josefine
Zeller, Bernward
Forestier, Erik
Hasle, Henrik
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Issue Date
2014-08

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Citation
Genes Chromosomes Cancer 2014, 53 (8):667-75
Abstract
We report the first large series (n = 596) of pediatric acute myeloid leukemia (AML) focusing on modal numbers (MN) from the population-based NOPHO-AML trials. Abnormal karyotypes were present in 452 cases (76%) and numerical aberrations were present in 40% (n = 237) of all pediatric AML. Among patients with an abnormal karyotype, the MN 46 was most common (n = 251; 56%) of which 36 (8%) were pseudodiploid with numerical aberrations, followed by MN 47 (n = 80; 18%) and MN 43-45 (n = 48; 8%). No cases had MN less than 43. Hyperdiploid AML with MN 48-65 comprised 11% of all cases and was associated with early onset (median age 2 years), female sex (57%), and a dominance of acute megakaryoblastic leukemia (AMKL) (29%). Hypodiploidy constituted 8% of all AML and was associated with older age (median age 9 years), male predominance (60%), FAB M2 (56%), and t(8;21)(q22;q22) (56%) with loss of sex chromosomes. Inferior outcome was observed for hypodiploid cases (5-year event-free survival 40% and 5-year overall survival 40%) but did not reach statistical significance. Chromosomes were gained in a nonrandom pattern, where chromosomes 8, 21, 19, and 6 were the most commonly gained. In conclusion, based on MNs, two cytogenetic subgroups with characteristic clinical features are described; hypodiploidy found in 8% and associated with high median age, male sex, t(8;21)(q22;q22), and FAB M2 and possibly associated with inferior outcome (P = 0.13), and hyperdiploidy with MN 48-65 in 11% associated with early onset, female sex, and AMKL.
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http://onlinelibrary.wiley.com/doi/10.1002/gcc.22177/epdf
http://dx.doi.org/10.1002/gcc.22177
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Archived with thanks to Genes, chromosomes & cancer
ae974a485f413a2113503eed53cd6c53
10.1002/gcc.22177
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