Oncogenic mutations in the NRAS gene are carried by 10-22% acute myeloid leukemia (AML) patients and represent one of the most commonly detected molecular aberrations in AML [1-6]. The mutations lead to increased activity of RAS pathway affecting cellular proliferation, survival, and differentiation [7].
NRAS mutations are mainly located in gene hotspots - codons 12, 13 (exon 2) and 61 (exon 3); mutations in other codons are detected rarely [1-5]. The hotspot mutations can be multiple and are often lost during disease progression [1,2,4,8,9].
Although NRAS alterations were first reported in AML more than 30 years ago, their prognostic impact as well as their contribution to malignant transformation remains disputed. The aim of this study was to determine the relevance of single and multiple point NRAS mutations in AML through detailed analysis of well molecularly characterized AML patients.