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.

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

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

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.

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

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.

Genetic analyses reveal how CDX2 and BRAF defects seen in serrated colorectal cancer (CRCs), a poor prognosis CRC subset, cooperate in tumorigenesis in humans and in a mouse cancer model.

Extensive periodic regulation of alternative splicing during the cell cycle in genes is linked to cell cycle functions, and involves an auto-inhibitory mechanism that uses the protein kinase CLK1.

miR-34a prevents inflammation-induced colonic regeneration from oncogenesis by simultaneously targeting processes in both immune and epithelial cells, including T helper 17 cell differentiation, recruitment, and IL-17 induced epithelial proliferation.

Daple is a guanine nucleotide-exchange factor (GEF) for trimeric G proteins that enables Wnt/Frizzled receptors to transactivate G proteins during non-canonical Wnt signaling.