Cody Coblentz

TL;DR: Analyses of samples from patients with acute myeloid leukaemia reveal that drug response is associated with mutational status and gene expression; the generated dataset provides a basis for future clinical and functional studies of this disease.

TL;DR: A large functional genomic resource is expanded, avenues for mechanistic exploration and drug development, and tools for predicting outcome in AML are revealed, including a single gene, PEAR1, which is found to be among the strongest predictors of patient survival.

TL;DR: Results demonstrate that combined inhibition of JAK/STAT signaling and LSD1 is a promising therapeutic strategy for CEBPA/CSF3R mutant AML.

TL;DR: It is shown that activating mutations in the granulocyte colony stimulating factor receptor (CSF3R) co-operate with loss-of-function mutations of CEBPA to promote AML development through an enhancer-dependent mechanism.

TL;DR: Cumulatively, the regions of the CSF3R extracellular and transmembrane domains in which missense mutations exhibit leukemogenic capacity are expanded and the mechanistic underpinnings that underlie altered CSf3R expression, dimerization, and signaling activation are elucidated.