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ArticleInternational journal of hematology2025

KMT2A-CBL fusion gene in the first reported case of T-cell acute lymphoblastic leukemia associated with Wiedemann-Steiner syndrome.

Akihiro Nishimura, Akihiro Tamura, Tomoko Fujikawa, Shotaro Inoue, Naoko Nakatani, Kandai Nozu, Nobuyuki Yamamoto

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Article in International journal of hematology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

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7 authors.

Akihiro NishimuraDepartment of Pediatrics, Kobe University Graduate School of Medicine, 7-5-1 Kusunokicho Chuo-ku, Kobe, Hyogo, 650-0017, Japan.
Akihiro TamuraDepartment of Pediatrics, Kobe University Graduate School of Medicine, 7-5-1 Kusunokicho Chuo-ku, Kobe, Hyogo, 650-0017, Japan. atamura@med.kobe-u.ac.jp.ORCID http://orcid.org/0000-0001-7710-827X
Tomoko FujikawaDepartment of Pediatrics, Kobe University Graduate School of Medicine, 7-5-1 Kusunokicho Chuo-ku, Kobe, Hyogo, 650-0017, Japan.
Shotaro InoueDepartment of Pediatrics, Kobe University Graduate School of Medicine, 7-5-1 Kusunokicho Chuo-ku, Kobe, Hyogo, 650-0017, Japan.
Naoko NakataniDepartment of Pediatrics, Kobe University Graduate School of Medicine, 7-5-1 Kusunokicho Chuo-ku, Kobe, Hyogo, 650-0017, Japan.
Kandai NozuDepartment of Pediatrics, Kobe University Graduate School of Medicine, 7-5-1 Kusunokicho Chuo-ku, Kobe, Hyogo, 650-0017, Japan.
Nobuyuki YamamotoDepartment of Pediatrics, Kobe University Graduate School of Medicine, 7-5-1 Kusunokicho Chuo-ku, Kobe, Hyogo, 650-0017, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Wiedemann-Steiner syndrome (WSS) is a congenital malformation syndrome characterized by intellectual disability, developmental delay, and distinctive facial features, caused by germline mutations in the KMT2A gene. Despite the key role of KMT2A in hematopoiesis, leukemia has not been previously reported in WSS patients. This report presents the first documented case of acute lymphoblastic leukemia (ALL) in a WSS patient. A 16-year-old boy with developmental delay, distinct facial features, and genital abnormalities was diagnosed with WSS following the identification of a heterozygous frameshift mutation in KMT2A. At age 17, he developed T-cell ALL harboring the KMT2A-CBL fusion gene, of which only nine cases have been reported so far. cDNA sequence analysis of the KMT2A-CBL transcript at the site of the germline KMT2A pathogenic variant revealed a wild-type sequence, indicating that the KMT2A-CBL fusion occurred on the wild-type allele. While this observation suggests a potential cooperative role of the KMT2A-CBL chimeric gene and the germline KMT2A pathogenic mutation in leukemogenesis, the rarity of leukemia in WSS underscores the need for cautious interpretation. This case provides preliminary insights into a possible mechanism of leukemogenesis in WSS, but further studies are required to clarify the relationship between WSS and ALL.

Indexed as

Abnormalities, MultipleHistone-Lysine N-MethyltransferaseIntellectual DisabilityMyeloid-Lymphoid Leukemia ProteinOncogene Proteins, FusionPrecursor T-Cell Lymphoblastic Leukemia-LymphomaProto-Oncogene Proteins c-cblAdolescentFrameshift MutationHumansMaleCBL protein, humanHistone-Lysine N-MethyltransferaseKMT2A protein, humanMyeloid-Lymphoid Leukemia ProteinOncogene Proteins, FusionProto-Oncogene Proteins c-cblAcute lymphoblastic leukemiaKMT2A-CBWiedemann-Steiner syndrome

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.