| Summary: | Acute myeloid leukemia (AML) is a heterogeneous disease. A significant proportion of AML patients is refractory to clinical treatment or relapses. Our aim is to determine new potential AML clinical treatment prognosis markers. We investigated various cell fate and epigenetic regulation important gene level differences between refractory and responsive AML patient groups at diagnosis stage and after clinical treatment using RT-qPCR. We demonstrated that oncogenic <i>MYC</i> and <i>WT1</i> and metabolic <i>IDH1</i> gene expression was significantly higher and cell cycle inhibitor <i>CDKN1A (p21)</i> gene expression was significantly lower in refractory patients’ bone marrow cells compared to treatment responsive patients both at diagnosis and after clinical treatment. Moreover, we determined that, compared to clinical treatment responsive patients, refractory patients possess a significantly higher gene expression of histone deacetylase 2 (<i>HDAC2</i>) and epigenetic DNA modulator <i>TET1</i> and a significantly lower gene expression of lysine acetyltransferase 6A (<i>KAT6A</i>) and nucleosome remodeling and deacetylase (NuRD) complex component <i>GATAD2A</i>. We suggest that <i>MYC</i>, <i>WT1</i>, <i>IDH1</i>, <i>CDKN1A</i>, <i>HDAC2</i>, <i>TET1</i>, <i>KAT6A</i> and <i>GATAD2A</i> gene expression changes might characterize refractory AML. Thus, they might be useful for AML prognosis. Additionally, we suggest that epigenetic modulation might be beneficial in combination with standard treatment.
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