Carles Codony-Servat

TL;DR: It is shown that resistant tumors display high Akt activation and that a combined treatment with AKT inhibitors causes synergistic tumour growth inhibition in vitro and in vivo.

TL;DR: The authors show AURKB activation to be associated with resistance in EGFR mutant lung cancer cells, and that AUR KB is a therapeutic target in resistant tumours that lack the p.T790M or other acquired mutations.

TL;DR: The data suggest that the combination of EGFR TKI with mTOR or PDE4 inhibitors could be adequate therapy for EGFR-mutant NSCLC patients with high pretreatment levels of BIM and mTOR.

TL;DR: The combination of afatinib with STAT3 inhibition cannot eliminate the potential problem of a remnant cancer stem cell population, but it represents a substantial advantage and opportunity to further prolong progression free survival and probably could increase the response rate in comparison to the current standard of single therapy.

TL;DR: In this short review, existing knowledge on the immune role of STAT3 is reviewed and the possible implications that this may have for the discovery of new biomarkers to predict response to immunotherapy, as well as new partners to combine with and increase the efficacy of immune checkpoint inhibitors.