Age-specific transcriptional responses to Flt3-ITD and cooperating Flt3/Runx1 mutations cause hematopoietic stem cell depletion and myeloid progenitor expansion during adult, but not fetal/neonatal, stages of development.

Acute myeloid leukemia-specific predictive logic models reveal new therapeutic targets involved in cancer resistance mechanisms paving the way for personalized precision medicine.

FLT3-ITD/STAT5A signaling is more sensitive to Dot1L inhibition than the canonical MLL-fusion activated drivers of leukemogenesis, providing a potential therapeutic avenue for one of the most frequent lesions in leukemia.

Cellular and molecular analyses of human AML cells reveal a novel pathway activated by the bone marrow microenvironment that confers resistance to FLT3 inhibition and can be exploited to improve the efficacy of FLT3 inhibitor therapy for AML.

Integrated analyses of acute myeloid leukemia genetics and epigenetics demonstrate that epigenetic evolution occurs in a convergent manner in the absence of DNA mutations at relapse post-chemotherapy.

Neutrophil extracellular traps are an immunogenic source of leukemia antigens in dendritic cell-based vaccination and are able to instruct antileukemia CD8 T-cell responses.

The inhibitory or deletion effect of MELK does not impair the proliferation of basal-like breast cancer cell lines.

Inhibiting PRMT1 enzymatic activity promotes megakaryocyte terminal differentiation via RBM15-mediated RNA metabolism, which is dysregulated in hematological malignancies.