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Zhang, Yingchi; Gao, Yufeng; Zhang, Hui; Zhang, Jingliao; He, Fuhong; Hnízda, Aleš; Qian, Maoxiang; Liu, Xiaoming; Gocho, Yoshihiro; Pui, Ching-Hon; Cheng, Tao; Wang, Qianfei; Yang, Jun J.; Zhu, Xiaofan; Liu, Xin
Blood, 05/2018, Letnik: 131, Številka: 20Journal Article
Philadelphia chromosome (Ph)-like acute lymphoblastic leukemia (ALL) comprises ∼10% to 15% of childhood ALL cases, many of which respond exquisitely to tyrosine kinase inhibitors (TKIs), for example, imatinib in PDGFRB-rearranged ALL. However, some cases developed drug resistance to TKIs and the mechanisms are poorly understood. In this study, we identified a novel PDGFRB fusion gene, namely AGGF1-PDGFRB, and functionally characterized its oncogenic potential in vitro. Further genomic profiling of longitudinally collected samples during treatment revealed the emergence of a mutation, PDGFRBC843G, which directly conferred resistance to all generations of ABL TKIs, including imatinib, dasatinib, nilotinib, and ponatinib. PDGFRB-mutant leukemia cells are highly sensitive to multitarget kinase inhibitor CHZ868, suggesting potential therapeutic options for some patients resistant to ABL TKIs. In summary, we describe a complex clonal evolution pattern in Ph-like ALL and identified a novel PDGFRB point mutation that drives leukemia relapse after ABL TKI treatment. •AGGF1-PDGFRB is a novel oncogenic fusion gene in Ph-like ALL.•Genomic profiling and functional studies identified a novel PDGFRB mutation directly related to TKI resistance.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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