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fusion gene in hematological neoplasms: clinical features, current practices, and prognoses.
Hematology
December 2024
Bone Marrow Transplantation Center of The First Affiliated Hospital & Liangzhu Laboratory, Zhejiang University School of Medicine, Hangzhou, People's Republic of China.
Introduction: -, formerly , is a rarely reported fusion gene in hematological malignancies, especially in Asian people.
Case Presentations: Six patients with fusion gene were identified at the First Affiliated Hospital, Zhejiang University School of Medicine, China between October 2019 and October 2023, with a median age of 25 years. Clinical diagnoses included acute myeloid leukemia (AML) in 2 patients, acute lymphoblastic leukemia (ALL) in 3, and mixed phenotype acute leukemia (MPAL) in 1.
An unusual presentation of a pediatric patient with mixed phenotypic acute leukemia with gene rearrangement.
Pediatr Hematol Oncol
October 2023
Department of Pathology, University of Texas, Dell Children's Medical Center, Austin, Texas, USA.
Mixed phenotype leukemia (MPAL) is a rare type of acute leukemia with blasts that co-express antigens of more than one lineage on the same cell or that have separate populations of blasts of different lineages. Here, we report a five-year-old male with inguinal lymphadenopathy diagnosed with MPAL-T/Myeloid MPAL-T/M. The clone demonstrated lineage and immunophenotypically distinct blast populations in the bone marrow and lymph nodes.
View Article and Find Full Text PDFMOZ/ENL complex is a recruiting factor of leukemic AF10 fusion proteins.
Nat Commun
April 2023
Tsuruoka Metabolomics Laboratory, National Cancer Center, Tsuruoka, Yamagata, 997-0052, Japan.
Changes in the transcriptional machinery cause aberrant self-renewal of non-stem hematopoietic progenitors. AF10 fusions, such as CALM-AF10, are generated via chromosomal translocations, causing malignant leukemia. In this study, we demonstrate that AF10 fusion proteins cause aberrant self-renewal via ENL, which binds to MOZ/MORF lysine acetyltransferases (KATs).
View Article and Find Full Text PDFThe role of the PZP domain of AF10 in acute leukemia driven by AF10 translocations.
Nat Commun
July 2021
Department of Pharmacology, University of Colorado School of Medicine, Aurora, CO, USA.
Article Synopsis
- Chromosomal translocations of the AF10 gene are linked to acute leukemias, and its PZP domain is crucial for preventing malignant transformation.
- Functional AF10 can counteract the harmful effects of the CALM-AF10 fusion, stopping leukemia development in stem cells both in the lab and in animal models.
- AF10 interacts with chromatin and influences gene expression, and its loss in the CALM-AF10 fusion leads to cancer transformation, while retaining AF10 can reverse this process.
A JAK/STAT-mediated inflammatory signaling cascade drives oncogenesis in AF10-rearranged AML.
Blood
June 2021
Tumor Initiation and Maintenance Program, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA.
Leukemias bearing fusions of the AF10/MLLT10 gene are associated with poor prognosis, and therapies targeting these fusion proteins (FPs) are lacking. To understand mechanisms underlying AF10 fusion-mediated leukemogenesis, we generated inducible mouse models of acute myeloid leukemia (AML) driven by the most common AF10 FPs, PICALM/CALM-AF10 and KMT2A/MLL-AF10, and performed comprehensive characterization of the disease using transcriptomic, epigenomic, proteomic, and functional genomic approaches. Our studies provide a detailed map of gene networks and protein interactors associated with key AF10 fusions involved in leukemia.
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