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Mutations of FLT3, NRAS, KRAS, and PTPN11 are frequent and possibly mutually exclusive in high hyperdiploid childhood acute lymphoblastic leukemia by Kajsa Paulsson; Andrea Horvat; Bodil Strömbeck; Fredrik Nilsson; Jesper Heldrup; Mikael Behrendtz; Erik Forestier; Anna Andersson; Thoas Fioretos; Bertil Johansson is a Medicine article available to read on EtoBox.

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## Abstract Although it has been suggested that mutations of the __FLT3__, __NRAS__, __KRAS__, and __PTPN11__ genes are particularly frequent in high hyperdiploid (>50 chromosomes) pediatric acute lymphoblastic leukemias (ALLs), this has as yet not been confirmed in a large patient cohort. Furthermore, it is unknown whether mutations of these genes coexist in hyperdiploid cases. We performed mutation analyses of __FLT3__, __NRAS__, __KRAS__, and __PTPN11__ in a consecutive series of 78 high hyperdiploid ALLs. Twenty‐six (33%) of the cases harbored a mutation, comprising six activating point mutations and one internal tandem duplication of __FLT3__ (7/78 cases; 9.0%), eight codon 12, 13, or 61 __NRAS__ mutations (8/78 cases; 10%), five codon 12 or 13 __KRAS__ mutations (5/78 cases, 6.4%), and seven exon 3 or 13 __PTPN11__ mutations (7/78 cases; 9.0%). No association was seen between the presence of a mutation in __FLT3__, __NRAS__, __KRAS__, or __PTPN11__ and gender, age, white blood cell count, or relapse, suggesting that they do not confer a negative prognostic impact. Only one case harbored mutations in two different genes, suggesting that mutations of these four genes are genera

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Author
Kajsa Paulsson; Andrea Horvat; Bodil Strömbeck; Fredrik Nilsson; Jesper Heldrup; Mikael Behrendtz; Erik Forestier; Anna Andersson; Thoas Fioretos; Bertil Johansson
Publisher
John Wiley and Sons; Wiley (John Wiley & Sons); Wiley-Liss Inc; Wiley (ISSN 1045-2257)
Published
2007
Language
EN
Field
Medicine (Life Sciences)

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