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Complex and monosomal karyotype are distinct cytogenetic entities with an adverse prognostic impact in paediatric acute myeloid leukaemia. A NOPHO-DBH-AML study.

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Authors
Bager, Ninna
Juul-Dam, Kristian L
Sandahl, Julie D
Abrahamsson, Jonas
Beverloo, Berna
de Bont, Eveline S J M
Ha, Shau-Yin
Jahnukainen, Kirsi
Jónsson, Ólafur G
Kaspers, Gertjan L
Kovalova, Zhanna
Lausen, Birgitte
De Moerloose, Barbara
Noren-Nyström, Ulrika
Palle, Josefine
Saks, Kadri
Zeller, Bernward
Kjeldsen, Eigil
Hasle, Henrik
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Issue Date
2018-11-01

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Complex and monosomal karyotype are distinct cytogenetic entities with an adverse prognostic impact in paediatric acute myeloid leukaemia. A NOPHO-DBH-AML study. 2018, 183(4):618-628 Br J Haematol
Abstract
Data on occurrence, genetic characteristics and prognostic impact of complex and monosomal karyotype (CK/MK) in children with acute myeloid leukaemia (AML) are scarce. We studied CK and MK in a large unselected cohort of childhood AML patients diagnosed and treated according to Nordic Society for Paediatric Haematology and Oncology (NOPHO)-AML protocols 1993-2015. In total, 800 patients with de novo AML were included. CK was found in 122 (15%) and MK in 41 (5%) patients. CK and MK patients were young (median age 2·1 and 3·3 years, respectively) and frequently had FAB M7 morphology (24% and 22%, respectively). Refractory disease was more common in MK patients (15% vs. 4%) and stem cell transplantation in first complete remission was more frequent (32% vs. 19%) compared with non-CK/non-MK patients. CK showed no association with refractory disease but was an independent predictor of an inferior event-free survival (EFS; hazard ratio [HR] 1·43, P = 0·03) and overall survival (OS; HR 1·48, P = 0·01). MK was associated with a poor EFS (HR 1·57, P = 0·03) but did not show an inferior OS compared to non-MK patients (HR 1·14, P = 0·62). In a large paediatric cohort, we characterized AML with non-recurrent abnormal karyotype and unravelled the adverse impact of CK and MK on prognosis.
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https://onlinelibrary.wiley.com/doi/full/10.1111/bjh.15587
ae974a485f413a2113503eed53cd6c53
10.1111/bjh.15587
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