Anna Reister Schultz

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: Together, these findings suggest that combined BCR-ABL1 kinase inhibition and protein degradation may represent a strategy to address B CR-ABl1-dependent drug resistance, and warrants further investigation into the eradication of persistent leukemic stem cells, which rely on neither the presence nor the activity of the BCR/F3 protein for survival.

TL;DR: It is demonstrated that combining asciminib with ATP site TKIs enhances target inhibition and suppression of resistant outgrowth in Ph+ clinical isolates and cell lines and restores ponatinib's effectiveness against currently untreatable compound mutants at clinically achievable concentrations.

TL;DR: Exome sequencing of samples from patients treated with the FLT3 inhibitor, crenolanib, is performed to show that resistance occurs due to diverse molecular mechanisms, not primarily due to secondaryFLT3 mutations.

TL;DR: Ruxolitinib was well tolerated and demonstrated an estimated response rate of 32%, and patients with a diagnosis of CNL and/or harboring CSF3R-T618I were most likely to respond.