From 1983, standardized therapeutic protocols for pediatric acute myeloid leukemia (AML) based on the BFM group experience were introduced in Poland. We retrospectively analyzed the results of pediatr Show more
From 1983, standardized therapeutic protocols for pediatric acute myeloid leukemia (AML) based on the BFM group experience were introduced in Poland. We retrospectively analyzed the results of pediatric AML treatment in Poland from 1983 to 2019 (excluding promyelocytic, therapy-related, biphenotypic, and Down syndrome AML). The study included 899 children suffering from AML treated with the following: AML-PPPLBC 83 (1983-1993, The probability of three-year overall survival was 0.34 ± 0.03, 0.37 ± 0.05, 0.54 ± 0.04, 0.67 ± 0.03, and 0.75 ± 0.05; event-free survival was 0.31 ± 0.03, 0.34 ± 0.05, 0.44 ± 0.04, 0.53 ± 0.03, and 0.67 ± 0.05; and relapse-free survival was 0.52 ± 0.03, 0.65 ± 0.05, 0.58 ± 0.04, 0.66 ± 0.03, and 0.78 ± 0.05, respectively, in the subsequent periods. A systematic reduction of early deaths and deaths in remission was achieved, while the percentage of relapses decreased only in the last therapeutic period. Surprisingly good results were obtained in the group of patients treated with AML-BFM 2012 with unfavorable genetic abnormalities like KMT2A-MLLT10/t(10;11)(p12;q23) and DEK-NUP214/t(6;9)(p23;q24), while unsatisfactory outcomes were found in the patients with FLT3-ITD. The use of standardized, systematically modified therapeutic protocols, with the successive consideration of genetic prognostic factors, and advances in supportive care led to a significant improvement in AML treatment outcomes over the last 40 years. Show less
The first paper concerning hair nicotine determination was published in 1983 by Ishiyama et al. Since then, examining hair nicotine content has become a valuable tool facilitating assessment of exposu Show more
The first paper concerning hair nicotine determination was published in 1983 by Ishiyama et al. Since then, examining hair nicotine content has become a valuable tool facilitating assessment of exposure to tobacco smoke in various groups of people (active and passive smokers or even neonates and fetus). The present article describes briefly recent research studies on the use of hair nicotine as a biomarker. Furthermore, the paper describes various determination techniques related to nicotine in hair, as well as advantages and disadvantages of hair nicotine as a biomarker. Show less
Toxic tobacco smoke exposure to human organism is strictly related to progress of atherosclerosis changes. One of the mechanisms of these effects is a change of blood lipoprotein fraction concentratio Show more
Toxic tobacco smoke exposure to human organism is strictly related to progress of atherosclerosis changes. One of the mechanisms of these effects is a change of blood lipoprotein fraction concentrations. The concentrations of the lipid profile parameters (TCL, HDL, LDL, TG) and the chosen biomarkers (urine cotinine and 1-hydroxypyrene and blood carboxyhaemoglobine) were determined. It was studied whether the procedure of the groups determination (nonsmokers, passive and active smokers) affect the calculated average values of lipid profile parameters. The role of the applied biomarkers for the detection of the effects related to the tobacco smoke exposure is also discussed. It is concluded that there is no difference among the lipid profiles of passive smokers and nonsmokers. Cigarette smoking increases and lowers the TG and HDL concentrations, respectively. Urine cotinine seems to be the best indicator of tobacco smoke exposure among three chosen biomarkers. Study subjects were 300 male and female volunteers. Show less