Abstract
Patients with normal karyotype represent the single largest cytogenetic group of acute myeloid leukemia (AML), with highly heterogeneous clinical and molecular characteristics. In this study, we sought to determine new prognostic biomarkers in cytogenetically normal (CN)-AML patients. A gene expression (GE)-based risk score was built, summing up the prognostic value of 22 genes whose expression is associated with a bad prognosis in a training cohort of 163 patients. GE-based risk score allowed identifying a high-risk group of patients (53.4%) in two independent cohorts of CN-AML patients. GE-based risk score and EVI1 gene expression remained independent prognostic factors using multivariate Cox analyses. Combining GE-based risk score with EVI1 gene expression allowed the identification of three clinically different groups of patients in two independent cohorts of CN-AML patients. Thus, GE-based risk score is powerful to predict clinical outcome for CN-AML patients and may provide potential therapeutic advances.
Highlights
Acute myeloid leukemia (AML) is a cytogenetically and molecularly heterogeneous disease characterized by accumulation of a variety of somatically acquired genetic aberrations in myeloid precursors, resulting in their clonal proliferation and maturation arrest
We designed a GEbased risk score incorporating the prognostic information of 22 genes associated with poor overall survival (OS) in cytogenetically normal (CN)-acute myeloid leukemia (AML) patients
Besides the powerful prognostic value of this gene expression (GE)-based risk score, our current study highlights some pathways that could be involved in poor prognostic CNAML
Summary
Acute myeloid leukemia (AML) is a cytogenetically and molecularly heterogeneous disease characterized by accumulation of a variety of somatically acquired genetic aberrations in myeloid precursors, resulting in their clonal proliferation and maturation arrest. These genetic alterations are found in bone marrow or blood cells of approximately 55% of previously-untreated adults with AML and have long been recognized as independent predictors for clinical outcome, allowing the classification of patients into favorable, intermediate, and unfavorable prognostic groups [1]. No genetic aberrations have been identified in 45% of adult AML patients yet. Twenty-four % of CN-AML patients show none of the aforementioned mutations, underlining the biological and clinical heterogeneity of this disease [5]
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