Nagy L, Kao HY, Chakravarti D, et al. Nuclear receptor repression mediated by a complex containing SMRT, mSin3A, and histone deacetylase. Cell. 1997;89(3):373-80.
Zhou F, Liu Y, Rohde C, et al. AML1-ETO requires enhanced C/D box snoRNA/RNP formation to induce self-renewal and leukaemia. Nat Cell Biol. 2017;19(7):844-855. doi:10.1038/ncb3563.
Banerji V, Frumm SM, Ross KN, et al. The intersection of genetic and chemical genomic screens identifies GSK-3α as a target in human acute myeloid leukemia. J Clin Invest. 2012;122(3):935-47. doi:10.1172/JCI46465.
Christian S, Merz C, Evans L, et al. The novel dihydroorotate dehydrogenase (DHODH) inhibitor BAY 2402234 triggers differentiation and is effective in the treatment of myeloid malignancies. Leukemia. 2019;33(10):2403-2415. doi:10.1038/s41375-019-0461-5.
Bester AC, Lee JD, Chavez A, et al. An Integrated Genome-wide CRISPRa Approach to Functionalize lncRNAs in Drug Resistance. Cell. 2018;173(3):649-664.e20. doi:10.1016/j.cell.2018.03.052.
Hahn CK, Berchuck JE, Ross KN, et al. Proteomic and genetic approaches identify Syk as an AML target. Cancer Cell. 2009;16(4):281-94. doi:10.1016/j.ccr.2009.08.018.
Pizzirani D, Roberti M, Grimaudo S, et al. Identification of biphenyl-based hybrid molecules able to decrease the intracellular level of Bcl-2 protein in Bcl-2 overexpressing leukemia cells. J Med Chem. 2009;52(21):6936-40. doi:10.1021/jm900907s.
Tam WF, Gu T-L, Chen J, et al. Id1 is a common downstream target of oncogenic tyrosine kinases in leukemic cells. Blood. 2008;112(5):1981-92. doi:10.1182/blood-2007-07-103010.
Peck D, Crawford ED, Ross KN, Stegmaier K, Golub TR, Lamb J. A method for high-throughput gene expression signature analysis. Genome Biol. 2006;7(7):R61. doi:10.1186/gb-2006-7-7-r61.
Stegmaier K, Ross KN, Colavito SA, O'Malley S, Stockwell BR, Golub TR. Gene expression-based high-throughput screening(GE-HTS) and application to leukemia differentiation. Nat Genet. 2004;36(3):257-63. doi:10.1038/ng1305.