High Frequency of Fusion Gene Transcript Resulting From t(10;11)(p12;q23) Translocation in Pediatric Acute Myeloid Leukemia in Poland

Książek, Teofila; Czogała, Małgorzata; Kaczówka, Przemysław; Sadowska, Beata; Pawińska-Wa̧sikowska, Katarzyna; Bik-Multanowski, Mirosław; Sikorska-Fic, Barbara; Matysiak, Michał; Skalska‐Sadowska, Jolanta; Wachowiak, Jacek; Rodziewicz-Konarska, Anna; Chybicka, Alicja; Muszyńska-Rosłan, Katarzyna; Krawczuk‐Rybak, Maryna; Grabowski, Dominik; Kowalczyk, Jerzy; Maciejka-Kemblowska, Lucyna; Adamkiewicz-Drożyńska, Elżbieta; Młynarski, Wojciech; Tomaszewska, Renata; Szczepański, Tomasz; J, Pohorecka; Karolczyk, Grażyna; Mizia‐Malarz, Agnieszka; Mycko, Katarzyna; Badowska, Wanda; Zielezińska, Karolina; Urasiński, Tomasz; Karpińska-Derda, Irena; Woszczyk, Mariola; Ciebiera, Małgorzata; Lejman, Monika; Skoczeń, Szymon; Balwierz, Walentyna

doi:10.3389/fped.2020.00278

Cited by 4 publications

(2 citation statements)

References 14 publications

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“…KMT2A-MLLT10/t(10;11)(p12;q23) was identified in almost 13% of patients in our cohort, while its occurrence is estimated as being 3% in large cohort studies [ 13 , 26 ]. Probability of five-year OS, EFS, and RFS in the group of patients with KMT2A -MLLT10 t(10;11)(p12;q23) in our research was 0.75 ± 0.09, 0.69 ± 0.09, and 0.84 ± 0.11, respectively.…”

Section: Discussionmentioning

confidence: 86%

Advances in the First Line Treatment of Pediatric Acute Myeloid Leukemia in the Polish Pediatric Leukemia and Lymphoma Study Group from 1983 to 2019

Czogała

Balwierz

Pawińska-Wa̧sikowska

et al. 2021

Cancers

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Background: 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). Methods: The study included 899 children suffering from AML treated with the following: AML-PPPLBC 83 (1983–1993, n = 187), AML-PPGLBC 94 (1994–1997, n = 74), AML-PPGLBC 98 (1998–2004, n = 151), AML-BFM 2004 Interim (2004–2015, n = 356), and AML-BFM 2012 (2015–2019, n = 131). Results: 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. Conclusions: 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.

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Section: Discussionmentioning

confidence: 86%

Advances in the First Line Treatment of Pediatric Acute Myeloid Leukemia in the Polish Pediatric Leukemia and Lymphoma Study Group from 1983 to 2019

Czogała

Balwierz

Pawińska-Wa̧sikowska

et al. 2021

Cancers

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“…Acute myeloid leukemia (AML) is a relatively rare heterogeneous group of hematologic malignancies in children, but it causes disproportionate mortality [1]. AML is associated with various molecular alterations in myeloid stem cells leading to rapid and uncontrolled growth and differentiation arrest of leukemic cells in bone marrow (BM) [2].…”

Section: Introductionmentioning

confidence: 99%

Straight to the Point—The Novel Strategies to Cure Pediatric AML

Lejman

Dziatkiewicz

Jurek

2022

IJMS

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Although the outcome has improved over the past decades, due to improved supportive care, a better understanding of risk factors, and intensified chemotherapy, pediatric acute myeloid leukemia remains a life-threatening disease, and overall survival (OS) remains near 70%. According to French-American-British (FAB) classification, AML is divided into eight subtypes (M0–M7), and each is characterized by a different pathogenesis and response to treatment. However, the curability of AML is due to the intensification of standard chemotherapy, more precise risk classification, improvements in supportive care, and the use of minimal residual disease to monitor response to therapy. The treatment of childhood AML continues to be based primarily on intensive, conventional chemotherapy. Therefore, it is essential to identify new, more precise molecules that are targeted to the specific abnormalities of each leukemia subtype. Here, we review abnormalities that are potential therapeutic targets for the treatment of AML in the pediatric population.

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Cytogenetics analysis as the central point of genetic testing in acute myeloid leukemia (AML): a laboratory perspective for clinical applications

et al. 2022

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High Frequency of Fusion Gene Transcript Resulting From t(10;11)(p12;q23) Translocation in Pediatric Acute Myeloid Leukemia in Poland

Cited by 4 publications

References 14 publications

Advances in the First Line Treatment of Pediatric Acute Myeloid Leukemia in the Polish Pediatric Leukemia and Lymphoma Study Group from 1983 to 2019

Advances in the First Line Treatment of Pediatric Acute Myeloid Leukemia in the Polish Pediatric Leukemia and Lymphoma Study Group from 1983 to 2019

Straight to the Point—The Novel Strategies to Cure Pediatric AML

Cytogenetics analysis as the central point of genetic testing in acute myeloid leukemia (AML): a laboratory perspective for clinical applications

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