الفهرس 
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Abstract
Acute myeloid leukemia (AML) is a clinically and genetically heterogeneous disease that accounts for 20% and 70% of acute leukemia in children and adults respectively. The cytogentic finding was considered as the cardinal marker for AML risk stratification. The cytogenetically normal acute myeloid leukemia (CN-AML) is a large cytogenetic subgroup of AML, representing approximately 45% of adult patients with AML who are younger than 60 years. During the last decade, the prognostic stratification of CN-AML was based on several molecular marker including the nucleophosmin 1 (NPM1) gene, the fms-related tyrosine kinase 3 (FLT3) gene, the CCAAT/enhancer binding protein alpha (CEBPA) gene, the myeloid-lymphoid or mixed-lineage leukemia (MLL) gene, the neuroblastoma RAS viral oncogene homolog (NRAS) gene, the runt-related transcription factor 1 (RUNX1) gene and Wilms’ tumor gene (WT1).
This study aimed to assess the prognostic impact of Wilms’ tumor 1 (WT1) gene mutations in cytogenetically normal acute myeloid leukemia (CN-AML) among Egyptian patients.
Exons 7 of WT1 was screened for mutations in samples from 82 CN-AML patients out of 203 newly diagnosed AML patients, age range from 21-74 years, using a high-resolution capillary electrophoresis.
Seven patients out of 82 (8.3%) harbored WT1 mutations. There was no statistically significant difference between the WT1 mutant and wild type as regard age, sex, French-American-British subtypes and the prevalence of success of induction remission therapy (P = 0.97; 28.6% vs 29.3%). Patients with WT1 mutations had overall survival (OS) lower than the wild type one (HR= 1.38; 95% CI, 4.79 to 6.86; P = 0.004). In conclusion, CN-AML patients with WT1 gene mutation have poor clinical outcome. We recommend testing the WT1 mutations as part of molecularly based risk assessment and risk-adapted treatment stratification of patients with CN-AML.