Masato Murakami

TL;DR: It is demonstrated that large studies of acute leukemia PDXs that mimic human randomized clinical trials can characterize drug efficacy and generate transcriptional, functional, and proteomic biomarkers in both treatment-naive and relapsed/refractory disease.

TL;DR: It is demonstrated that JAK-STAT3-mediated cytokine production from malignant and nonmalignant cells contributes to MPN pathogenesis and thatJAK inhibition in both populations is required for therapeutic efficacy, providing novel insight into the mechanisms by which JAK kinase inhibition achieves therapeutic efficacy in MPNs.

TL;DR: Combined PI3K/mTOR and JAK2 inhibition synergistically reduced cancer cell number and tumor growth, decreased tumor seeding and metastasis, and also increased overall survival of the animals.

TL;DR: Hsp90 inhibition in B cell acute lymphoblastic leukemia overcomes resistance to JAK2 inhibitors and induces apoptotic cell death in mice treated with these inhibitors.

TL;DR: Type II JAK inhibition is a viable therapeutic approach for MPN patients after significant activity in murine MPN models and induced reductions in mutant allele burden not observed with type I JAK inhibitors.