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

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

A novel Mendelian randomisation framework unravels one gene expression component, correlated with proliferation and genome stability-related features, associated with telomere length in lung adenocarcinoma tumours, which provides insights into how telomere length influences the genetic basis of lung cancer aetiology.

Prediagnostic RNA levels show early lung cancer progression.

Pembrolizumab activates innate immune metabolism and function in primary human non-small cell lung cancer, whereas Pembrolizumab and beta-glucan synergize in enhancing immune metabolism and tumoridical action in brain-metastasized lung cancer.

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.

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

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.

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.