Lineage transformation in lung cancer is dictated by ERK activity and requires permissive chromatin alterations in the context of targeted therapy resistance.

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.

Targeting aberrant CRTC-CREB activation blocks the growth of LKB1-inactivated lung cancer.

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

SOX2 causes resistance to anti-EGFR therapies in EGFR-mutant lung cancer.

The chemokine CXCL13 is critical to the development of air pollution- and tobacco smoke-induced lung cancers.

Network topology and gene expression patterns in small cell lung cancer reveal two mutually opposing teams of regulators that enable multistability and consequent non-genetic heterogeneity, a clinically unsolved challenge.

Functional and mechanistic analysis of p53-regulated lncRNA PINCR and its interacting RNA-binding protein Matrin 3 uncovers context-dependent regulation of specific p53 target genes during DNA damage.

By increasing intracellular cysteine levels, NRF2 engages a tumor suppressive metabolic pathway mediated by cysteine dioxygenase 1.

In small cell lung cancer, the transition from a neuroendocrine state to a more neuronal state endows these cancer cells with increased migration and metastatic potential.