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.

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.

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.

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

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

Lineage specifiers FoxA1 and FoxA2 control lung cancer growth and identity by activating gastric differentiation and suppressing squamous cell carcinoma transdifferentiation.

The cancer testis antigen COX6B2 enhances cytochrome c oxidase activity thereby promoting proliferation and survival in cancer cells and represents a therapeutic target for inhibiting oxidative phosphorylation selectively in tumors.

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

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