Crispin T Hiley

Main text (Cancer Cell 43, 1833–1849; October 13, 2025) This paper identifies subclonal immune escape in non-small cell lung cancer using clonally resolved organoid-immune cell co-cultures. We, the authors of this publication, have identified an error in the code used to process the organoid RNA sequencing (RNA-seq) data for patient 1 in our study.

Keywords lung cancer nonsmoking screening prevention Introduction Lung cancer is the leading cause of cancer-related deaths worldwide [1]. As smoking rates have decreased, lung cancer in never smokers (LCINS) (see Glossary) [2,3] accounts for an increasing proportion of patients [1]. Recent findings suggest that the absolute incidence of LCINS may be increasing [4,5].

Highlights • Micronuclei induced by DNA damage or mitotic errors fail to activate cGAS • Nucleosomes directly inhibit cGAS activation in cells • Micronuclei induced by DNA damage or mitotic errors contains histones Summary The cyclic guanosine monophosphate (GMP)-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway plays a pivotal role in innate immune responses to viral infection and inhibition of autoimmunity.