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
One hallmark of pediatric tumors is their low mutational burden, which contrasts with adult tumors, where cancer-causing mutations often accumulate over decades of DNA replication and environmental exposure. This raises the question of how such mutations arise in young patients. We have proposed that developmental mu...
Helen S. Mueller, Kaisha Garvin, Sophia Rha et al.· Cancer Research· 0 citations
DNA-proximal phosphorylation of MYB is identified as a critical regulatory mechanism required for MYB oncogenesis through cooperative organization of transcription factors and nominated MYB N-terminal phosphorylation and its upstream kinases as candidate therapeutic targets for MYB-dependent leukemia.
Shu-Yuan Cheng, Katarzyna Kulej, Masahiro Uni et al.· Cancer Research· 0 citations
A recurrent AML dark proteome is defined and a framework for the discovery of tumor-specific non-canonical proteins for mechanistic and therapeutic studies is established.
L. Schmalbrock, Asher Preska Steinberg, Katarzyna Kulej et al.· bioRxiv· 0 citations
Findings identify failure to accumulate H3K27 acetylation as a hallmark of resistance to EZH2 inhibition-based treatment, and show that pharmacological HDAC inhibition can restore this chromatin transition and re-sensitize resistant tumors, providing a rationale for combined epigenetic targeting strategies in INI1-defi...
N. Arrighetti, C. Soffientini, V. Zuco et al.· bioRxiv· 1 citation
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