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At present there has been more and more interest in studying gene mutations and gene expression to further classify Acute Myeloid Leukemia (AML). Furthermore, molecular abnormalities have been used as a prognostic tool and to aid treatment decisions for patients with AML. Attention has been focused on driver mutations in the Isocitrate Dehydrogenase 1 (IDH1). The prevalence of IDH mutations increases with age and IDH1 mutations have been associated with lower overall survival and disease free survival in CN-AML with NPM1 mutations and wildtype FLT3. Medinger et al. published a review on prognostic and therapeutic mutations in AML. Their report was published in Cancer Genomics and Proteomics in 2016.
In conclusion, the targeting of IDH mutations may provide therapeutic benefit for RR-AML with fewer side effects. In addition, the use of IDH1 inhibitors may improve current strategies for eliminating minimal residual disease after cytotoxic therapy.
Acute myeloid leukemia (AML) is a biologically complex and molecularly and clinically heterogeneous disease, and its incidence increases with age. Cytogenetics and mutation testing remain important prognostic tools for treatment after induction therapy. The post-induction treatment is dependent on risk stratification. Despite rapid advances in determination of gene mutations involved in the pathophysiology and biology of AML, and the rapid development of new drugs, treatment improvements changed slowly over the past 30 years, with the majority of patients eventually experiencing relapse and dying of their disease. Allogeneic hematopoietic stem cell transplantation remains the best chance of cure for patients with intermediate- or high-risk disease. This review gives an overview about advances in prognostic markers and novel treatment options for AML, focusing on new prognostic and probably therapeutic mutations, and novel drug therapies such as tyrosine kinase inhibitors.
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