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http://dx.doi.org/10.1002/jha2.107 | DOI Listing |
Int J Lab Hematol
January 2025
Department of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Introduction: NUP98 rearrangements are rare in acute leukemias and portend a poor prognosis.
Methods: This study explored clinicopathologic and molecular features of five patients with NUP98 rearranged (NUP98-r) acute leukemias, including three females and two males with a median age of 34 years.
Results: NUP98 fusion partners were associated with distinctive leukemia characteristics and biology.
Blood
January 2025
Memorial Sloan Kettering Cancer Center, New York, New York, United States.
A mixed phenotype is characteristic of de novo Mixed Phenotype Acute Leukemia (MPAL) but can also be seen in other leukemias. It poses substantial classification and management dilemmas. Herein, we report a large cohort of acute leukemia with a mixed phenotype and define Acute Myeloid Leukemia with Mixed Phenotype (AML-MP) and MPAL as two distinct groups by characterizing the clinical, genetic, and transcriptomic features.
View Article and Find Full Text PDFInt Cancer Conf J
January 2025
Department of Hematology, Uwajima City Hospital, Goten-Machi, Uwajima, Ehime 798-8510 Japan.
Mixed-phenotype acute leukemia (MPAL) with fusion is a rare leukemia subtype exhibiting both myeloid and lymphoid traits. Standard treatment involves chemotherapy with a tyrosine kinase inhibitor (TKI). However, establishing the optimal treatment strategy for elderly patients with MPAL with fusion is challenging due to their intolerance to intensive chemotherapy.
View Article and Find Full Text PDFPediatr Blood Cancer
March 2025
Departments of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Rearrangements of cytokine receptor-like factor 2 gene (CRLF2) are present in ∼50% of B-lymphoblastic leukemia/lymphoma (B-ALL) with BCR::ABL1-like features. Herein, we report three patients with CRLF2-rearranged mixed phenotype acute leukemia (MPAL). All three cases were B/myeloid MPAL in young patients harboring P2RY8::CRLF2 or IGH::CRLF2 with additional genomic alterations in signaling (JAK and RAS) and cell cycle (CDKN2A/B) pathways, a genomic profile similar to that in BCR::ABL1-like B-ALL.
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