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An extra chromosome 9 derived from either a normal chromosome 9 or a derivative chromosome 9 in a patient with acute myeloid leukemia positive for t(9;11)(p21.3;q23.3): A case report

Authors
Gao, ManPang, HuiKim, Young MiLu, XianglanWang, XianfuLee, JiyunWang, MingweiMeng, FanzhengLi, Shibo
Issue Date
12월-2019
Publisher
SPANDIDOS PUBL LTD
Keywords
acute myeloid leukemia; trisomy 9; t(9; 11)(p21; 3; q23; 3); disease progression
Citation
ONCOLOGY LETTERS, v.18, no.6, pp.6725 - 6731
Indexed
SCIE
SCOPUS
Journal Title
ONCOLOGY LETTERS
Volume
18
Number
6
Start Page
6725
End Page
6731
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/61485
DOI
10.3892/ol.2019.11035
ISSN
1792-1074
Abstract
Translocation (9;11)(p21.3;q23.3) is one of the most common lysine methyltransferase 2A (KMT2A)-rearrangements in de novo and therapy-related acute myeloid leukemia (AML). Numerous in vitro and in vivo studies have demonstrated that the KMT2A/MLLT3 super elongation complex subunit (MLLT3) fusion gene on the derivative chromosome 11 serves a crucial role in leukemogenesis. Trisomy 9 as a secondary chromosome change in patients with t(9;11) is relatively rare. The present study reported a unique case of AML with a chromosome 9 trisomy secondary to t(9;11)(p21.3;q23.3) through the cytogenetic analysis of leukemic blood and bone marrow. Further characterization with fluorescence in situ hybridization and array comparative genomic hybridization analysis revealed that this extra chromosome 9 was either a copy of normal chromosome 9 or a derivative chromosome 9. Conversely with the previously reported favorable outcome of AML patients with t(9;11)(p21.3;q23.3), in the present study, the cells with only translocation persisted, whereas the cells with an extra chromosome 9 disappeared following initial chemotherapy. With this unique case, the present study hypothesized that the extra chromosome 9 could serve a crucial role in AML disease progression and contribute to cellular sensitivity to chemotherapy.
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