Impact of mutations inFLT3, PTPN11andRASgenes on the overall survival of pediatric B cell precursor acute lymphoblastic leukemia in Brazil
Autor: | Camilla Andrade, Bruno Almeida Lopes, Maria S. Pombo-de-Oliveira, Francianne Gomes Andrade, Thayana Conceição Barbosa, Mariana Emerenciano, Marcela B. Mansur |
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Rok vydání: | 2014 |
Předmět: |
Male
Neuroblastoma RAS viral oncogene homolog Cancer Research Oncogene Proteins Fusion Protein Tyrosine Phosphatase Non-Receptor Type 11 Gene mutation medicine.disease_cause Precursor B-Cell Lymphoblastic Leukemia-Lymphoma Odds Ratio Humans Medicine Child B cell Univariate analysis business.industry Infant Newborn Infant Hematology Odds ratio Prognosis PTPN11 Genes ras medicine.anatomical_structure fms-Like Tyrosine Kinase 3 Oncology Child Preschool Mutation Immunology Cancer research Female Hyperdiploidy KRAS business Brazil |
Zdroj: | Leukemia & Lymphoma. 55:1501-1509 |
ISSN: | 1029-2403 1042-8194 |
DOI: | 10.3109/10428194.2013.847934 |
Popis: | 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. |
Databáze: | OpenAIRE |
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