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.

Genetically engineered murine models reveal novel mechanisms of cell identity regulation in lung cancer and provide insights into the complex interplay between lineage specifiers and oncogenic signaling pathways in this disease.

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.

Platinum chemotherapy resistance is a complex process involving multiple signalling pathways and a novel, non-genetic, cell cycle-dependent mechanism that promotes tumour regrowth and highlights potential complications for combination therapies in human 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.

The MYC transcription factor network member MGA is a subunit of a non-canonical Polycomb complex, which, when inactivated, accelerates tumorigenesis in mouse models of cancer and proliferation in colon organoids.

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.