Prognostic impact of co-occurring FLT3 mutations across molecular subgroups in intensively treated acute myeloid leukemia: insights from real-world genomic data

Blood Cancer Journal 2026 Open access

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Authors: Yu-Sung Chang, Feng‐Ming Tien, Y. Wang, Yao Chi-yuan, Xavier Cheng-Hong Tsai, Sao‐Chih Ni, Min-Yen Lo, Wan-Hsuan Lee, Chien‐Chin Lin, Yuan‐Yeh Kuo, Yen‐Ling Peng, Mei-Hsuan Tseng
+5 more Bor-Sheng Ko, Ming Yao, Hwei‐Fang Tien, Hsin-An Hou, Wen‐Chien Chou
DOI: 10.1038/s41408-025-01438-y
Cited by: 1
References: 12

Abstract

FMS-like tyrosine kinase 3 ( FLT3 ), a class III receptor tyrosine kinase that activates RAS/MAPK, STAT5, and PI3K/Akt pathways [ 1 , 2 ], is among the most frequently mutated genes in acute myeloid leukemia (AML), with internal tandem duplication ( FLT3 ITD ) in 20–25% of cases, and tyrosine kinase domain point mutations ( FLT3 TKD ) in 5–10% [ 3 , 4 , 5 ]. As FLT3 mutations ( FLT3 MUT ) are often subclonal rather than founding events [ 6 , 7 ], their prognostic impact is best evaluated across genetically defined AML subtypes rather than solely within co-mutation contexts. While FLT3 MUT activate oncogenic signaling cascades [ 8 ], their impact on global gene expression and transcriptional networks in AML remains unclear. Elucidating how these clones disrupt transcriptional homeostasis may uncover key pathways driving leukemogenesis and therapeutic resistance.

Fields of Study & Subjects

Acute Myeloid Leukemia Research Chronic Myeloid Leukemia Treatments Genomics and Rare Diseases

Publication details

Journal / source
Blood Cancer Journal
Publisher
Springer Science and Business Media LLC
Volume
16
Issue
1
Pages
3–3
Publication date
6 January 2026
Language
EN