Evidence map›Paper›PMID 42852916›Full record

ReviewCancer reports (Hoboken, N.J.)2026

Myelodysplastic Syndromes-Transformed Acute Myeloid Leukemia With Concurrent DEK::CAN Fusion Gene Positivity and WT1 Overexpression: A Case Report and Literature Review.

Wanxiu Mao, Tengmin Zhou, Xi Xu, Sheng Luo, Songfu Jiang, Zhijie Yu

Abstract readCase ReportsReview
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In one paragraph

Review in Cancer reports (Hoboken, N.J.), 2026. 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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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Wanxiu MaoZhejiang Chinese Medical University, Hangzhou, China.ORCID https://orcid.org/0009-0005-6777-6393
Tengmin ZhouDepartment of Rehabilitation Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Xi XuDepartment of Hematology, Wenzhou Key Laboratory of Hematology Research, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Sheng LuoDepartment of Hematology, Wenzhou Key Laboratory of Hematology Research, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Songfu JiangDepartment of Hematology, Wenzhou Key Laboratory of Hematology Research, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.ORCID https://orcid.org/0000-0002-2039-4233
Zhijie YuDepartment of Hematology, Wenzhou Key Laboratory of Hematology Research, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.ORCID https://orcid.org/0000-0003-3442-4066

Funding

Basic public welfare research projects of Wenzhou Science and Technology Bureau Y20240969
6 · The paper itself

Abstract

backgroundMyelodysplastic syndromes (MDS) are a group of clonal hematopoietic stem cell disorders with a risk of progression to acute myeloid leukemia (AML). MDS-transformed AML (MDS-AML) has a poor prognosis. The concurrent presence of DEK::CAN fusion gene positivity and WT1 overexpression is extremely rare and likely denotes a highly aggressive disease. CASE: A 57-year-old Han Chinese female with a 5-year history of MDS (DEK::CAN status at initial diagnosis unknown) presented with fatigue and pancytopenia. Bone marrow blasts accounted for 81% (AML-M5), and karyotype showed t(6;9)(p23;q34). Real-time quantitative PCR (qPCR) revealed a DEK::CAN/ABL ratio of 188.21% and a WT1/ABL ratio of 52.90%; next-generation sequencing identified a U2AF1 mutation (p.Arg156His). The patient received IA regimen induction followed by intermediate-dose cytarabine consolidation. Complete remission (CR) was achieved after induction; after the first consolidation cycle, a transient CR with incomplete hematologic recovery (CRi) occurred, and CR was re-established at the final evaluation. Severe infections occurred repeatedly during treatment. Although the patient achieved CR after induction chemotherapy, recurrent infections and cumulative chemotherapy-related cytopenias prevented timely allogeneic hematopoietic stem cell transplantation (allo-HSCT). She died approximately 1 month after the last chemotherapy cycle; the cause was clinically suspected to be fatal hemorrhage, though autopsy was not performed.

conclusionMDS-AML with concurrent DEK::CAN and WT1 mRNA overexpression is a highly aggressive entity. Although chemotherapy can induce remission, treatment-related complications often preclude transplantation. Early molecular screening is recommended, and once any form of remission (CR or CRi) is achieved, prompt bridging to allo-HSCT should be pursued. Targeted therapy should also be explored.

Indexed as

Chromosomal Proteins, Non-HistoneLeukemia, Myeloid, AcuteMyelodysplastic SyndromesOncogene ProteinsOncogene Proteins, FusionPoly-ADP-Ribose Binding ProteinsWT1 ProteinsAntineoplastic Combined Chemotherapy ProtocolsFemaleHumansMiddle AgedChromosomal Proteins, Non-HistoneDEK protein, humanOncogene ProteinsOncogene Proteins, FusionPoly-ADP-Ribose Binding ProteinsWT1 protein, humanWT1 Proteinscase reportDEK::CAN fusion geneMDS‐transformed acute myeloid leukemiamyelodysplastic syndromesWT1 overexpression

Identifiers

PMID42852916

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