Acute monocytic leukemia with KMT2A::LASP1 developed 9 months after diagnosis of acute megakaryoblastic leukemia in a 2-year-old boy.


Journal

International journal of hematology
ISSN: 1865-3774
Titre abrégé: Int J Hematol
Pays: Japan
ID NLM: 9111627

Informations de publication

Date de publication:
Oct 2023
Historique:
received: 30 01 2023
accepted: 24 05 2023
revised: 23 05 2023
medline: 23 10 2023
pubmed: 14 6 2023
entrez: 14 6 2023
Statut: ppublish

Résumé

Acute myeloid leukemia (AML) is known as one of the subsequent malignant neoplasms that can develop after cancer treatment, but it is difficult to distinguish from relapse when the preceding cancer is leukemia. We report a 2-year-old boy who developed acute megakaryoblastic leukemia (AMKL, French-American-British classification [FAB]: M7) at 18 months of age and achieved complete remission with multi-agent chemotherapy without hematopoietic stem cell transplantation. Nine months after diagnosis and 4 months after completing treatment for AMKL, he developed acute monocytic leukemia (AMoL) with the KMT2A::LASP1 chimeric gene (FAB: M5b). The second complete remission was achieved using multi-agent chemotherapy and he underwent cord blood transplantation 4 months after AMoL was diagnosed. He is currently alive and disease free at 39 and 48 months since his AMoL and AMKL diagnoses, respectively. Retrospective analysis revealed that the KMT2A::LASP1 chimeric gene was detected 4 months after diagnosis of AMKL. Common somatic mutations were not detected in AMKL or AMoL and no germline pathogenic variants were detected. Since the patient's AMoL was different from his primary leukemia of AMKL in terms of morphological, genomic, and molecular analysis, we concluded that he developed a subsequent leukemia rather than a relapse of his primary leukemia.

Identifiants

pubmed: 37314622
doi: 10.1007/s12185-023-03622-x
pii: 10.1007/s12185-023-03622-x
doi:

Substances chimiques

Adaptor Proteins, Signal Transducing 0
Cytoskeletal Proteins 0
LASP1 protein, human 0
LIM Domain Proteins 0
KMT2A protein, human 0
Histone-Lysine N-Methyltransferase EC 2.1.1.43
Oncogene Proteins, Fusion 0

Types de publication

Case Reports Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

514-518

Informations de copyright

© 2023. Japanese Society of Hematology.

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Auteurs

Takashi Fujita (T)

Department of, Pediatrics, University of Tsukuba Hospital, Tsukuba, Japan.

Hiroko Fukushima (H)

Department of, Pediatrics, University of Tsukuba Hospital, Tsukuba, Japan. fkhiroko@md.tsukuba.ac.jp.
Department of Child Health, Faculty of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki, 305-8575, Japan. fkhiroko@md.tsukuba.ac.jp.

Toru Nanmoku (T)

Department of Clinical Laboratory, University of Tsukuba Hospital, Tsukuba, Japan.

Yuki Arakawa (Y)

Department of Hematology and Oncology, Saitama Children's Medical Center, Saitama, Japan.

Takao Deguchi (T)

Division of Cancer Immunodiagnostics, Children's Cancer Center, National Center for Child Health and Development, Tokyo, Japan.

Ryoko Suzuki (R)

Department of, Pediatrics, University of Tsukuba Hospital, Tsukuba, Japan.
Department of Child Health, Faculty of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki, 305-8575, Japan.

Yuni Yamaki (Y)

Department of, Pediatrics, University of Tsukuba Hospital, Tsukuba, Japan.

Sho Hosaka (S)

Department of, Pediatrics, University of Tsukuba Hospital, Tsukuba, Japan.

Hidetoshi Takada (H)

Department of, Pediatrics, University of Tsukuba Hospital, Tsukuba, Japan.
Department of Child Health, Faculty of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki, 305-8575, Japan.

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