Overlaying single cell readouts of cell cycle and apoptosis onto a multidimensional analysis of pulsed cisplatin signalling dynamics reveals targetable mechanisms of platinum resistance in lung adenocarcinoma.

Airway cells are required for the maintenance of the adult mouse lung and for carcinogen-induced lung adenocarcinoma development, and are thus marked therapeutic targets.

In lung adenocarcinoma, deleting one glucose transporter, whether it is Glut1 or Glut3 is insufficient, whereas their dual deletion reduces tumor growth.

Two of the most commonly mutated growth factor pathways induce a deadly feature of lung adenocarcinoma.

Cancer cells driven by mutations in KRAS or EGFR are dependent on DUSP6 to prevent ERK-induced cell death, creating a novel vulnerability for targeted therapy.

NFATc2 maintains the drug-induced TIC phenotypes through trans-activating SOX2/ALDH1A1 expression and scavenging stress from ROS.

Co-mutation of two powerful oncogenes in certain cell types may have a lethal effect that explains the mutual exclusivity of the mutations.

Combined EGFR and SOS1 inhibition synergize to inhibit NSCLC spheroid growth.

Experimental efforts to validate the output of a computational model that predicts new uses for existing drugs highlights the inherently complex nature of cancer biology.

Dissecting structural, cellular and molecular differences between transplanted and spontaneous mouse tumor models, highlighting their relevance for predicting the efficacy of anti-cancer treatments in patients.