RUNX1::CBFA2T2 rearranged acute myeloid leukemia transformed from JAK2 V617F mutated primary myelofibrosis
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Updated: Jun 4, 2025

Transduction-Transplantation Mouse Model of Myeloproliferative Neoplasm
Published on: December 22, 2016
Lina Han1, Prasad Koduru1, Miguel Cantu1
1Department of Pathology University of Texas Southwestern Medical Center Dallas Texas USA.
Abstract:
Acute myeloid leukemia (AML) with RUNX1::CBFA2T2 fusion is rare with largely unknown clinicopathological features and genomic characterization. We present one such case of AML transformed from JAK2 V617F mutated primary myelofibrosis and review the literature on this topic. The immunophenotype and the landscape of cooperative gene alterations in AML with RUNX1::CBFA2T2 resemble those of AML with RUNX1::RUNX1T1, including expression of CD19, cooperative gene alterations in signaling pathway (JAK2), epigenetic/chromatin and cell cycle regulation (TET2, SMC3, and CDKN2A/B), and additional chromosomal abnormalities (trisomies 8 and 15). This case study provides insights into the pathogenesis of this rare subtype of AML.
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