Monte M. Winslow

This study identifies CXCL-CXCR2 signaling as critical for SCLC liver metastasis by enhancing cancer cell migration and interactions with endothelial cells.

The paper analyzes ~9,100 tumors across 32 cancer types to determine if the transcriptional response to tumor mutational burden (TMB) is consistent across tissues, finding it to be largely consistent within each cancer type.

This study shows tumor suppressor genotype affects immune cell recruitment and tumor growth in KRAS-driven lung cancer with varying neoantigen expression.

This study shows aging suppresses lung tumor initiation and growth in mice, with age-dependent effects on tumor suppressor genes like PTEN and persistent age-related transcriptomic changes in tumors.

The paper identifies HBO1 and MLL1 complexes as key tumor suppressors in lung cancer using in vivo functional screens of epigenetic regulators.

The paper investigates functional differences between EML4-ALK variants V1 and V3 in lung cancer using mouse models and human data, showing variant-specific effects on tumorigenesis.

This study develops transgenic Cas12a mice to enable efficient, multiplexed somatic genome editing for studying complex genetic interactions in vivo.

The paper identifies ZMAT3 and CDKN1A as key hubs in the p53 tumor suppression network through integrative multiomic analyses in a mouse model.

The paper uses in vivo genome editing to study genetic interactions in lung cancer, finding widespread negative epistasis among tumor suppressor genes.

This study identifies a STAG2-PAXIP1/PAGR1 tumor-suppressive axis in lung cancer by showing their combined role in suppressing oncogenic KRAS-driven tumorigenesis.

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.