Relapsed B-acute lymphoblastic leukemia (B-ALL) generally occurs due to the emergence of subclones resistant to therapy, leading to poor outcome. Here, we describe novel genomic alterations responsible for therapeutic resistance at a subtype level in a clinical trial (AALL1331) which randomized patients to blinatumomab...
Yuan Feng, Han-Xia Li, H. Mulder et al.· Blood· 0 citations
It is shown that genetic knockout of Brpf1 as well as Kat6a, Kat7, and a subset of other HAT complex members led to decreased cell fitness, and pharmacologic inhibition of KAT6A/7 using small molecule inhibitor PF9363 was effective in multiple preclinical models of NUP98-rearranged leukemia.
N. Michmerhuizen, Ella Monfort, Z. G. Soares et al.· Cancer Research· 0 citations
Findings define previously unrecognized interactions between CD38 and targetable pathways and genes in T-ALL and identify rational combinatorial strategies to enhance CD38-directed therapies and reduce relapse risk.
R. Shraim, Gong-Ping Shi, Yi-Zhen Li et al.· Blood· 0 citations
Functional validation using genetic and transplantation-based mouse models demonstrated that SOX11 cooperates with MYCN to accelerate T-ALL onset and establish a cooperative SOX11–MYCN oncogenic axis driving γδ-like T-ALL.
André Almeida, Igor Fijalkowski, K. Christensen et al.· bioRxiv· 0 citations
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