Trisomy 8 in pediatric acute myeloid leukemia: A NOPHO-AML study.
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Authors
Laursen, Anne Cathrine LundSandahl, Julie Damgaard
Kjeldsen, Eigil
Abrahamsson, Jonas
Asdahl, Peter
Ha, Shau-Yin
Heldrup, Jesper
Jahnukainen, Kirsi
Jónsson, Ólafur G
Lausen, Birgitte
Palle, Josefine
Zeller, Bernward
Forestier, Erik
Hasle, Henrik
Issue Date
2016-09
Metadata
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Trisomy 8 in pediatric acute myeloid leukemia: A NOPHO-AML study. 2016, 55 (9):719-26 Genes Chromosomes CancerAbstract
Trisomy 8 (+8) is a common cytogenetic aberration in acute myeloid leukemia (AML); however, the impact of +8 in pediatric AML is largely unknown. We retrospectively investigated 609 patients from the NOPHO-AML database to determine the clinical and cytogenetic characteristics of +8 in pediatric AML and to investigate its prognostic impact. Complete cytogenetic data were available in 596 patients (98%) aged 0-18 years, diagnosed from 1993 to 2012, and treated according to the NOPHO-AML 1993 and 2004 protocols in the Nordic countries and Hong Kong. We identified 86 patients (14%) with +8. Trisomy 8 was combined with other cytogenetic aberrations in 68 patients (11%) (+8 other) and in 18 patients (3%), it was the sole abnormality (+8 alone). Trisomy 8 was associated with FAB M5 (36%) but otherwise clinically comparable with non-trisomy 8 patients. Trisomy 8 was favorable in patients of young age and with t(9;11). Trisomy 8 alone was associated with older age (median age 10.1 years), FAB M2 (33%), and FLT3-ITD mutations (58%). The 5-year event-free survival for patients with +8 alone was 50% and 5-year overall survival was 75%. In conclusion, +8 is one of the most common cytogenetic aberrations in pediatric AML. Trisomy 8 positive AML is a heterogeneous group and the majority of cases have additional cytogenetic aberrations. Patients with +8 alone differed from patients with +8 other and were associated with older age, FAB M2, and FLT3-ITD aberrations. There were no differences in survival despite the more frequent occurrence of FLT3-ITD in +8 alone. © 2016 Wiley Periodicals, Inc.Description
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http://dx.doi.org/ 10.1002/gcc.22373Rights
Archived with thanks to Genes, chromosomes & cancerae974a485f413a2113503eed53cd6c53
10.1002/gcc.22373
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