De novo acute myeloid leukemia harboring concomitant t(8;21)(q22;q22);RUNX1::RUNX1T1 and BCR::ABL1 (p190 minor transcript)
Samo za registrovane korisnike
2022
Autori
Jaković, LjubomirFekete, Marija Dencic
Virijević, Marijana
Kraguljac Kurtović, Nada
Todorić-Zivanović, Biljana
Stamatović, Dragana
Karan-Đurašević, Teodora
Pavlović, Sonja
Leković, Danijela
Bogdanović, Andrija
Članak u časopisu (Objavljena verzija)
Metapodaci
Prikaz svih podataka o dokumentuApstrakt
De novo AMLs with typical nonrandom chromosomal abnormalities are often associated with specific morphology subtypes. The t(8;21) is one of the most prominent recurrent cytogenetic aberrations (RCA) in AML, frequently associated with AML with maturation, and is characterized as a good prognostic marker. On the contrary, BCR::ABL1 rearrangement is rarely observed in AMLs, without specific morphology, carrying poor prognosis. Its distinction from blastic transformation of chronic myeloid leukemia has been a matter of long debate. The revised WHO classification (2016) recognized AML with BCR::ABL1(+) as a provisional entity. The occurrence of additional cytogenetic aberrations in AML RCA within the same leukemic clone has been detected, albeit rare cases of BCR::ABL1(+) were reported, mainly as subclones. Those additional cytogenetic and molecular findings seem to significantly affect patient prognosis. Conventional cytogenetic analysis, fluorescent in situ hybridization (FISH), and polym...erase chain reaction (PCR) were applied at presentation and during the follow-up of the patient. We present a 34-year-old male patient with de novo AML harboring concomitant t(8;21) and t(9;22) in a single clone. The presence of both t(8;21) and Philadelphia chromosome (Ph+) in the same metaphases but in less than 100% of the analyzed cells, the p190 BCR::ABL transcript type, and absence of splenomegaly support that additional BCR::ABL1(+) is a part of the main leukemic clone. These findings, accompanied with an encouraging outcome of continuous cytogenetic and molecular remission after induction therapy, support BCR::ABL1 being a secondary genetic event in AML with t(8;21).
Ključne reči:
Translocations / Philadelphia chromosome / Acute leukemia / AberrationsIzvor:
Journal of Hematopathology, 2022, 15, 3, 191-195Izdavač:
- Heidelberg : Springer
DOI: 10.1007/s12308-022-00509-4
ISSN: 1868-9256
WoS: 000833454800001
Scopus: 2-s2.0-85137970915
Institucija/grupa
Institut za molekularnu genetiku i genetičko inženjerstvoTY - JOUR AU - Jaković, Ljubomir AU - Fekete, Marija Dencic AU - Virijević, Marijana AU - Kraguljac Kurtović, Nada AU - Todorić-Zivanović, Biljana AU - Stamatović, Dragana AU - Karan-Đurašević, Teodora AU - Pavlović, Sonja AU - Leković, Danijela AU - Bogdanović, Andrija PY - 2022 UR - https://imagine.imgge.bg.ac.rs/handle/123456789/1592 AB - De novo AMLs with typical nonrandom chromosomal abnormalities are often associated with specific morphology subtypes. The t(8;21) is one of the most prominent recurrent cytogenetic aberrations (RCA) in AML, frequently associated with AML with maturation, and is characterized as a good prognostic marker. On the contrary, BCR::ABL1 rearrangement is rarely observed in AMLs, without specific morphology, carrying poor prognosis. Its distinction from blastic transformation of chronic myeloid leukemia has been a matter of long debate. The revised WHO classification (2016) recognized AML with BCR::ABL1(+) as a provisional entity. The occurrence of additional cytogenetic aberrations in AML RCA within the same leukemic clone has been detected, albeit rare cases of BCR::ABL1(+) were reported, mainly as subclones. Those additional cytogenetic and molecular findings seem to significantly affect patient prognosis. Conventional cytogenetic analysis, fluorescent in situ hybridization (FISH), and polymerase chain reaction (PCR) were applied at presentation and during the follow-up of the patient. We present a 34-year-old male patient with de novo AML harboring concomitant t(8;21) and t(9;22) in a single clone. The presence of both t(8;21) and Philadelphia chromosome (Ph+) in the same metaphases but in less than 100% of the analyzed cells, the p190 BCR::ABL transcript type, and absence of splenomegaly support that additional BCR::ABL1(+) is a part of the main leukemic clone. These findings, accompanied with an encouraging outcome of continuous cytogenetic and molecular remission after induction therapy, support BCR::ABL1 being a secondary genetic event in AML with t(8;21). PB - Heidelberg : Springer T2 - Journal of Hematopathology T1 - De novo acute myeloid leukemia harboring concomitant t(8;21)(q22;q22);RUNX1::RUNX1T1 and BCR::ABL1 (p190 minor transcript) EP - 195 IS - 3 SP - 191 VL - 15 DO - 10.1007/s12308-022-00509-4 ER -
@article{ author = "Jaković, Ljubomir and Fekete, Marija Dencic and Virijević, Marijana and Kraguljac Kurtović, Nada and Todorić-Zivanović, Biljana and Stamatović, Dragana and Karan-Đurašević, Teodora and Pavlović, Sonja and Leković, Danijela and Bogdanović, Andrija", year = "2022", abstract = "De novo AMLs with typical nonrandom chromosomal abnormalities are often associated with specific morphology subtypes. The t(8;21) is one of the most prominent recurrent cytogenetic aberrations (RCA) in AML, frequently associated with AML with maturation, and is characterized as a good prognostic marker. On the contrary, BCR::ABL1 rearrangement is rarely observed in AMLs, without specific morphology, carrying poor prognosis. Its distinction from blastic transformation of chronic myeloid leukemia has been a matter of long debate. The revised WHO classification (2016) recognized AML with BCR::ABL1(+) as a provisional entity. The occurrence of additional cytogenetic aberrations in AML RCA within the same leukemic clone has been detected, albeit rare cases of BCR::ABL1(+) were reported, mainly as subclones. Those additional cytogenetic and molecular findings seem to significantly affect patient prognosis. Conventional cytogenetic analysis, fluorescent in situ hybridization (FISH), and polymerase chain reaction (PCR) were applied at presentation and during the follow-up of the patient. We present a 34-year-old male patient with de novo AML harboring concomitant t(8;21) and t(9;22) in a single clone. The presence of both t(8;21) and Philadelphia chromosome (Ph+) in the same metaphases but in less than 100% of the analyzed cells, the p190 BCR::ABL transcript type, and absence of splenomegaly support that additional BCR::ABL1(+) is a part of the main leukemic clone. These findings, accompanied with an encouraging outcome of continuous cytogenetic and molecular remission after induction therapy, support BCR::ABL1 being a secondary genetic event in AML with t(8;21).", publisher = "Heidelberg : Springer", journal = "Journal of Hematopathology", title = "De novo acute myeloid leukemia harboring concomitant t(8;21)(q22;q22);RUNX1::RUNX1T1 and BCR::ABL1 (p190 minor transcript)", pages = "195-191", number = "3", volume = "15", doi = "10.1007/s12308-022-00509-4" }
Jaković, L., Fekete, M. D., Virijević, M., Kraguljac Kurtović, N., Todorić-Zivanović, B., Stamatović, D., Karan-Đurašević, T., Pavlović, S., Leković, D.,& Bogdanović, A.. (2022). De novo acute myeloid leukemia harboring concomitant t(8;21)(q22;q22);RUNX1::RUNX1T1 and BCR::ABL1 (p190 minor transcript). in Journal of Hematopathology Heidelberg : Springer., 15(3), 191-195. https://doi.org/10.1007/s12308-022-00509-4
Jaković L, Fekete MD, Virijević M, Kraguljac Kurtović N, Todorić-Zivanović B, Stamatović D, Karan-Đurašević T, Pavlović S, Leković D, Bogdanović A. De novo acute myeloid leukemia harboring concomitant t(8;21)(q22;q22);RUNX1::RUNX1T1 and BCR::ABL1 (p190 minor transcript). in Journal of Hematopathology. 2022;15(3):191-195. doi:10.1007/s12308-022-00509-4 .
Jaković, Ljubomir, Fekete, Marija Dencic, Virijević, Marijana, Kraguljac Kurtović, Nada, Todorić-Zivanović, Biljana, Stamatović, Dragana, Karan-Đurašević, Teodora, Pavlović, Sonja, Leković, Danijela, Bogdanović, Andrija, "De novo acute myeloid leukemia harboring concomitant t(8;21)(q22;q22);RUNX1::RUNX1T1 and BCR::ABL1 (p190 minor transcript)" in Journal of Hematopathology, 15, no. 3 (2022):191-195, https://doi.org/10.1007/s12308-022-00509-4 . .