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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 crosstalk between cancer cell genomic features and the tumor microenvironment (TME) to reveal the impact of genetic alterations on the TME phenotype.

Inhibiting KRAS^G12C and ULK-mediated autophagy is a novel treatment strategy to control the growth of KRAS^G12C-driven lung cancer in preclinical models of lung cancer.

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

Radiomics allows automated quantification of the radiographic phenotype of a tumor across diverse patient cohorts and is connected to the underlying molecular pathway activities, which together determine the clinical outcome.

Osteocytes, sensing mechanical stimulation generated by exercise, inhibit the proliferation of non-small cell lung cancer cells and sustain their dormancy by releasing small extracellular vesicles containing tumor-suppressive micro-RNAs.

Erlotinib-resistant AXL overexpressing cells are present in therapy-naive tumors, and expression of AXL in these cells is regulated through a stochastic mechanism centered on the epigenetic regulation of miR-335.

Genetically engineered, CD73-redirected human NK cells show potent antitumor activity in vivo by impairing adenosinergic activity of CD73 in cancer.

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