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We analyzed mutations in four genes (FLT3, KRAS/NRAS and PTPN11) that might disrupt the RAS/mitogen activated protein kinase (MAPKinase) signaling pathway, to evaluate their prognostic value in children younger than 16 years old with B-cell precursor acute lymphoblastic leukemia (Bcp-ALL). The overall survival (OS) was determined with the Kaplan-Meier method. MAPKinase genes were mutated in 25.4% and 20.1% of childhood and infant Bcp-ALL, respectively. Children with hyperdiploidy were more prone to harboring a MAPKinase gene mutation (odds ratio [OR] 3.18; 95% confidence interval [CI] 1.07-9.49). The mean OS of all cases was 54.0 months. FLT3 and PTPN11 mutations had no impact on OS. K/NRAS mutations were strongly associated with MLL-AFF1 (OR 5.78; 95% CI 1.00-33.24), and conferred poorer OS (p = 0.034) in univariate analysis.

Original publication

DOI

10.3109/10428194.2013.847934

Type

Journal article

Journal

Leuk Lymphoma

Publication Date

07/2014

Volume

55

Pages

1501 - 1509

Keywords

Acute lymphoblastic leukemia, FLT3, K/NRAS, PTPN11, prognosis, Brazil, Child, Child, Preschool, Female, Genes, ras, Humans, Infant, Infant, Newborn, Male, Mutation, Odds Ratio, Oncogene Proteins, Fusion, Precursor B-Cell Lymphoblastic Leukemia-Lymphoma, Prognosis, Protein Tyrosine Phosphatase, Non-Receptor Type 11, fms-Like Tyrosine Kinase 3