Ernesto Diaz-Flores

TL;DR: Both near-haploid and low-hypodiploid leukemic cells show activation of Ras-signaling and phosphoinositide 3-kinase (PI3K)-signaling pathways and are sensitive to PI3K inhibitors, indicating that these drugs should be explored as a new therapeutic strategy for this aggressive form of leukemia.

TL;DR: Using flow cytometry, a specific evoked STAT5 signaling signature was observed in a subset of samples from patients suspected of having juvenile myelomonocytic leukemia, suggesting a critical role of this pathway in the biological mechanism of this disorder and indicating potential targets for future therapies.

TL;DR: Drug profiling captures disease-relevant features and unexpected sensitivity to relevant drugs, which warrants further exploration of this functional assay in the context of clinical trials to develop drug repurposing strategies for patients with urgent medical needs.

TL;DR: It is shown that p53 inactivation strongly cooperates with oncogenic Kras(G12D) to induce aggressive AML, while both lesions on their own induce T-cell malignancies with long latency, establishing an efficient new strategy for interrogating oncogene cooperation and providing strong evidence that the ability of p53 to limit aberrant self-renewal contributes to its tumor suppressor activity.

TL;DR: It is shown that MEK inhibitors are ineffective in MPD, but induce objective regression of many Nf1-deficient AMLs, which represents a robust strategy for identifying genes and pathways that modulate how primary cancer cells respond to targeted therapeutics and for probing mechanisms of de novo and acquired resistance.