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.
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.
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.
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.