Trudy G. Oliver

The paper identifies a KRT13+ hillock-like cell state in LUSC, driven by KLF4, which contributes to therapeutic resistance and heterogeneity.

The paper identifies basal cells as the origin of neuroendocrine-tuft-like tumors in SCLC, revealing lineage plasticity and transcriptional states that mirror human cancer and normal cell injury responses.

This study shows that TMPRSS11B promotes an acidified and immunosuppressive tumor microenvironment in lung squamous cell carcinoma, suggesting it as a therapeutic target.

The paper establishes a database of lung cancer mouse models to improve data comparison and translational relevance by aligning mouse mutations with human lung cancer mutations.

This study shows SCLC cells exist in a continuum of plastic states rather than discrete subtypes, with gene expression patterns linked to cancer hallmarks and potential therapeutic targets.