Walter Wang

TL;DR: It is shown that EGFR inhibition results in the activation of β-catenin signaling in a Notch3-dependent manner, which facilitates the survival of a subset of cells that the authors call “adaptive persisters”, and it is demonstrated that the combination of EGFR-TKI and a β-catsin inhibitor inhibits the development of these adaptive persisters.

TL;DR: The results suggest that mechanisms of innate and acquired therapeutic resistance are subtype-specific in SCLC and highlight the need for continued investigation to bolster therapy selection and development for this cancer.

TL;DR: In this paper, a small-molecule ROR1 inhibitor (KAN0441571C) was used in combination with the BCL2 inhibitor venetoclax for small cell lung cancer.

TL;DR: In this article, the authors identified a 16-gene signature for LKB1 loss of function through mutational and non-mutational mechanisms and applied this genetic signature to TCGA lung adenocarcinoma samples and discovered a novel association between LK1 loss and widespread DNA demethylation.

TL;DR: A non-canonical role of Notch3 is identified in response to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) therapy, whereby notch3 associates with β-catenin, resulting in increased catenin beta-1 (CTNNB1) stability and increased survival of drug persister cells (DPCs).