@misc{Książek_Teofila_Assessment_2015, author={Książek, Teofila}, address={Kraków}, howpublished={online}, year={2015}, school={Wydział Lekarski}, language={pol}, abstract={Acute myeloid leukemia (AML) is a heterogeneous group of hematologic malignancies. The most relevant prognostic factors in AML are chromosomal abnormalities and gene mutations. However, no clear guidelines for the methods of minimal residual disease (MRD) diagnostics are available until now. Definitive clinical benefits in this field are still under investigation in children with AML.In the present study, the value of molecular markers for the detection of MRD in children with AML has been assessed. The study group included 188 children below 18 years of age with de novo AML treated according to AML-BFM 2004 Interim in 15 Polish oncology centers. The expression of selected fusion genes and WT1 gene was determined by RT-qPCR in bone marrow and blood samples. The incidence of fusion genes was 14.4% (27) for RUNX1(AML1)-RUNX1T1(ETO), 5.9% (11) for PML-RARA, and 4.2% (8) for CBFB-MYH11 and MLL-MLLT3 (MLL-AF9). WT1 overexpression before treatment was present in 80.5% patients. Quantitative analysis revealed different levels of normalized copy number (NCN) of fusion gene transcript at the time of diagnosis, but also their systematic decrease in the following treatment stages. In the case of RUNX1(AML1)-RUNX1T1(ETO), the best predictive value for treatment failure was observed for samples collected at 21st–28th day of treatment. When it comes to gene WT1, a strong relationship between}, abstract={NCN(WT1) on the 15th day of treatment and the incidence of treatment failure was shown.Molecular detection of minimal residual disease in AML still remains a very important scientific issue, and all conducted research can contribute to the treatment improvement.}, title={Assessment of selected molecular markers for determination of minimal residual disease in children with acute myeloid leukemia}, type={Praca doktorska}, keywords={minimal residual disease, children, acute myeloid leukemia, fusion genes, gene WT1}, }